MT #1 Flashcards
(435 cards)
1
Q
what is ohm’s law
A
electric current through a conductor between two points is directly proportional to the voltage across the two points.
2
Q
what is the equation for voltage
A
V = I * R
V = voltage
I = current
R = resistance
3
Q
what is voltage
A
measures electrical potential –> potential energy per unit charge (voltz)
4
Q
what is current
A
charge per unit of time –> how much charge flowing past a point in a circuit in a unit of time
charge / time
5
Q
resistance
A
how much charge flow is impeded (ohm unit)
6
Q
conductance
A
Conductance is simply the inverse of resistance. Initially, even the units were inverted. measured in sieman (g)
7
Q
solve for I (current)
A
I = Q / t (where I = current; Q = charge; t = time)
I = V / R
I = V x g (since conductance is the inverse of resistance)
8
Q
solve for V (voltage)
A
V = E / Q (where V = voltage; E = energy; Q = charge)
V = I*R
9
Q
solve for R (resistance)
A
R = V / I (where R = resistance; V = voltage; I = current)
10
Q
If you know the electrical resistance (R) of something, how do you calculate its conductance (g)?
A
g = 1/R
11
Q
If the resistance in a circuit remains constant but the voltage increases, what happens to the current?
A
The current increases
12
Q
The video shows that water flowing through a pipe is analogous to an electrical circuit. According to the video, increases the resistance of a circuit is equivalent to:
A
Narrowing the pipe
13
Q
What is neurobiology
A
Neurobiology is the study of the structure and function of the nervous system, which interprets information and coordinates body activity in response to the environment.
14
Q
What are the main cellular units of the nervous system?
A
Neurons are the main active cellular units, responsible for processing and transmitting information.
15
Q
How does the nervous system communicate?
A
It uses electrical and chemical signals, with neurotransmitters passing information between neurons.
16
Q
What is the difference between Neurobiology and Neuroscience?
A
Neurobiology focuses on the biology of the brain, while Neuroscience is an integrative field that includes biology, psychology, chemistry, physics, medicine, and engineering.
17
Q
What are some biological approaches in Neuroscience?
A
Molecular neurobiology (proteins/gene regulation), cellular neurobiology (neuron networks), and cognitive neuroscience (behavioral studies).
18
Q
Major Cell Types in the Nervous System
A
Neurons: Cells that transmit electrical information.
Neuroglia: Supporting cells of the nervous system.
19
Q
Neuron Discovery
A
First described by Camillo Golgi using silver staining.
Golgi and Santiago Ramon-y-Cajal won the 1906 Nobel Prize for their contributions to neuroscience.
20
Q
Structure of a Typical Neuron
A
Dendrites: Branches that receive signals.
Cell body (Soma): Contains the nucleus and organelles.
Axon Hillock: Transition point from soma to axon.
Axon: Sends electrical signals.
Presynaptic Terminal: Communicates with other neurons.
21
Q
Neurons as Cells
A
Contain common cellular structures like the nucleus, mitochondria, and cytoplasm.
Surrounded by a phospholipid bilayer (cell membrane) that regulates ion movement.
22
Q
Unique Characteristics of Neurons
A
Electroactive: Can change charge.
Rapid Communication: Uses electrical and chemical signals.
“Forever” Cells: Rarely undergo neurogenesis, but some exceptions exist (olfactory system, hippocampus).
Plasticity: Neurons can change structure and function over time.
Regeneration: Some Peripheral Nervous System neurons can regrow after injury.
23
Q
Dendrites and Synaptic Input
A
Dendrites receive signals.
Dendritic spines increase surface area and play a role in plasticity.
24
Q
Soma (Cell Body)
A
Contains nucleus and organelles.
Integrates signals from dendrites.
Decides whether to send an action potential.
25
Axon and Signal Transmission
Axon: Main output pathway.
Axon Hillock: Initiates action potentials.
Axon Length: Varies from short (spinal interneurons) to long (sciatic nerve).
Axon Diameter: Affects signal speed.
Axoplasmic Transport:
Anterograde (to terminal) via kinesin.
Retrograde (to soma) via dynein.
26
Action Potential
Electrical signal that moves down the axon.
Changes membrane potential from negative to positive and back.
27
Myelin and Signal Speed
Myelin Sheath: Increases conduction speed.
Nodes of Ranvier: Gaps that regenerate action potential.
Saltatory Conduction: Signal jumps between nodes.
28
The Synapse
Electrical Synapse: Direct cytoplasmic connection, allows bidirectional ion flow.
Chemical Synapse: Uses neurotransmitters, unidirectional communication.
Presynaptic Terminal: Releases neurotransmitters.
Postsynaptic Membrane: Receives signals.
29
What are glial cells?
Non-neuronal cells in the nervous system that support and protect neurons.
Historically thought to act as "glue" for neurons.
Play crucial roles in maintaining homeostasis, forming myelin, and providing support and protection.
30
What are the main types of glial cells?
Astrocytes
Oligodendrocytes
Schwann Cells
Microglia
Ependymal Cells
31
Astrocytes
Named for their star-shaped morphology.
Maintain the blood-brain barrier using endfeet that interact with blood vessels.
Produce trophic factors that support neuron survival and synapse formation.
32
Oligodendrocytes
Found in the central nervous system (CNS).
Function: Myelinate multiple segments of axons, increasing signal conduction speed.
A single oligodendrocyte can myelinate up to 50 axon segments.
33
Schwann Cells
Found in the peripheral nervous system (PNS).
Function: Myelinate a single segment of an axon.
Aid in axon regeneration after injury.
34
Microglia
Act as the immune cells of the CNS.
Function: Identify and remove pathogens, dead cells, and protein aggregates.
React quickly to CNS injuries.
Make up 10-15% of all brain cells.
35
Ependymal Cells
Line the brain’s ventricles and spinal cord’s central canal.
Possess cilia that help circulate cerebrospinal fluid (CSF).
Part of the choroid plexus, which produces CSF (about 0.5 liters per day)
36
what is the name of the classic method used to count cells where you slice a whole brain and subsample a few brains under the microscope?
Stereology
37
T/F: we have ten times as many glial cells as neurons in the human brain
false
38
What is the name given to the new method by Professor Herculano-Houzel where the brain is dissolved into a solution and nuclei are counted?
brain soup
39
Why is neuroscience considered an integrative field of study?
Many different fields and disciplines contribute to our understanding of neuroscience
40
Which of the following describes brain plasticity?
1. The ability of the brain to change
2. Each area of the brain has one function that is incapable of change
3. The ability of the brain to learn new things
4. The ability of the skull to heal after trepanation
1. The ability of the brain to change
3. The ability of the brain to learn new things
41
Why is the “we only use 10% of our brain” myth incorrect?
Because we use nearly every part of our brain, but not at the same time
42
Which type of glial cell makes cerebral spinal fluid?
ependymal cells
43
Which cell types are found in the central nervous system?
Microglia
Astrocytes
Ependymal cells
Oligodendrocytes
44
Which two cell types are responsible for making the myelin sheath?
Oligodendrocytes and schwann cells
45
Which cell type would respond following an injury to the central nervous system?
Microglia
46
Leak / non-gated channels
channels that open spontaneously
47
Voltage gated channels
channels that open in response to membrane potential
48
Ligand gated channels
channels that open in response to chemicals binding
49
Which items are structural components of the cell that affect ion movement across the membrane? (Select all that apply)
1. Phospholipid bilayer
2. Ion channels
3. Concentration gradient
4. Electrical gradient
1. Phospholipid bilayer
2. Ion channels
50
does calcium tend to rest intra or extra cellularly
extracellular
51
what tends to be in extracellular solution at rest
sodium, calcium, and chloride are concentrated outside of the cell membrane in the extracellular solution
52
what tends to be in intracellular solution at rest
potassium and negatively-charged molecules like amino acids and proteins are concentrated inside in the intracellular solution.
53
equilibrium potential
The neuron’s membrane potential at which the electrical and concentration gradients for a given ion balance out
54
how do you calculate equilibrium potential
Nernst equation
55
assume there is a cell with a resting potential of -70 mV. Sodium has an equilibrium potential of +60 mV. What must sodium do to establish equilibrium
To reach equilibrium, sodium will need to enter the cell, bringing in positive charge.
56
assume there is a cell with a resting potential of -70 mV. Chloride has an equilibrium potential of -65 mV. What must chloride do to establish equilibrium
Since chloride is a negative ion, it will need to leave the cell in order to make the cell’s membrane potential more positive to move from -70 mV to -65 mV.
57
What is the equilibrium potential of sodium for a typical neuron?
+65 mV
58
What is the membrane potential?
The difference in charge between the inside and the outside of the neuron
59
What is the equilibrium potential of potassium for a typical neuron?
Great job! Potassium's equilibrium potential is approximately -80 mV.
60
A cell is at rest at -70 mV, and chloride channels open. In which direction does chloride flow and how does this affect the membrane potential?
chloride's equilibrium potential is -65 mV
Out of the cell; Makes the membrane potential more positive
61
A cell is at rest at -65 mV, and chloride channels open. In which direction does chloride flow and how does this affect the membrane potential?
chloride's equilibrium potential is -65 mV
No net movement; No change in membrane potential
62
When the cell is at rest, if sodium channels open, which direction does the electrical gradient try to move the ions?
Into the cell
63
When the cell is at rest, if sodium channels open, which direction does the concentration gradient try to move the ions?
Into the cell
64
Given the equilibrium potential of sodium, when the cell is at rest, if sodium channels open, which direction does the combined electrochemical gradient move the ion?
sodium's equilibrium potential = +60 mV
Into the cell
65
When the cell is at rest, if potassium channels open, which direction does the electrical gradient try to move the ions?
Into the cell
the inside is more negative than the outside
66
When the cell is at rest, if potassium channels open, which direction does the concentration gradient try to move the ions?
out of the cell
67
what gates are open when the neuron is at rest?
- non-gated ion channels (leak channels) are open
- Significantly more potassium channels are open than sodium channels, and this makes the membrane at rest more permeable to potassium than sodium.
68
can potassium cross the membrane at rest?
yes!
the membrane is permeable to potassium at rest due to the open non-gated channels. the electrochemical gradients at work will cause potassium to flow out of the cell in order to move the cell’s membrane potential toward potassium’s equilibrium potential of -80 mV.
69
if the cell has these open non-gated ion channels, and ions are moving at rest, won’t the cell eventually reach potassium’s equilibrium potential if the membrane is only permeable to potassium?
If the only structural element involved in ion flow present in the cell membrane were the open non-gated potassium channels, the membrane potential would eventually reach potassium’s equilibrium potential. However, the membrane has other open non-gated ion channels as well. There are fewer of these channels compared to the potassium channels, though. The permeability of chloride is about half of that of potassium, and the permeability of sodium is about 25 to 40 times less than that of potassium. This leads to enough chloride and sodium ion movement to keep the neuron at a resting membrane potential that is slightly more positive than potassium’s equilibrium potential.
70
goldman vs nernst equation
the Nernst equation is used to calculate one ion’s equilibrium potential. Knowing the equilibrium potential can help you predict which way one ion will move, and it also calculates the membrane potential value that the cell would reach if the membrane were only permeable to one ion. However, at rest, the membrane is permeable to potassium, chloride, and sodium. To calculate the membrane potential, the Goldman equation is needed.
71
The activity of the sodium-potassium pump can be evaluated by measuring how much sodium leaves the cell. If a cell was treated with a drug that prevented the synthesis of ATP, how would efflux of sodium change compared to baseline?
Sodium efflux would decrease
72
In a typical neuron, at rest, which ion channel has the most open non-gated (leak) channels?
Potassium
73
What structure is responsible for establishing and maintaining the presence of electrochemical gradients?
Sodium-potassium pump
74
passive membrane potential
changes in membrane potential that occur due to the movement of ions across the membrane in response to external stimuli. allow neurons to conduct electrical impulses without the use of voltage-gated ion channels.
75
input resistance
Input resistance determines how much the cell depolarizes in response to a steady current. It is the total resistance of the cell.
Therefore, if two cells are receiving the same current input, the neuron with the larger input resistance, will have the larger voltage response. Input resistance is more relevant at the soma than at the distal dendrites.
76
specific membrane resistance
Specific membrane resistance is dependent on the density of open channels. It is the membrane’s ability to pass current per unit membrane area, therefore you are only looking at segment of the neuron.
77
what is capacitance
the ability of a system to store an electrical charge for a given voltage. In the context of neurons, the cell membrane acts as a capacitor, storing charge across its two sides (intracellular and extracellular).
78
relationship of input capacitance to cell size
input capacitance is proportional to cell size. The bigger the cell, the higher the input capacitance.
79
what is input capacitance
The total capacitance of a neuron is called the input capacitance. It is derived from two factors: specific membrane capacitance and the size of the cell.
80
What does capacitance depend on?
Surface area of the cell
- Increases with the surface area of the cell
- The cell has a greater capacity to store
Distance between the bilayer
- Decreases with distance between the bilayer because there is a greater separation of charge
- The positive charges being stored intracellularly have a harder time attracting the negative extracellular charges
Insulation medium (composition of the bilayer)
- Typically does not change, therefore not a major contributing factor to cell-to-cell variation
81
axial resistance
Axial resistance is the resistance inside of the cell.
82
What are ways to increase conduction velocity?
- Decrease ra via increased diameter
- Decrease cm = myelination
83
According to the tutorial, a larger cell (with more membrane channels) will have:
Group of answer choices
A higher input resistance
A larger electrode
A lower input resistance
A lower input resistance
84
how would increasing the input capacitance change the time it takes for the membrane potential to change?
It would increase the time it takes for Vm to change
85
What is the effect of increasing the diameter of an axon?
A decreased axial resistance
86
Why is it useful to determine the "length constant"?
Because it tells us how far a change in membrane voltage will travel
87
what is the length constant
Taken together, axial resistance and membrane resistance help us determine a property known as the length constant, termed by λ.
88
what is a longer length constant indicative of
A longer length constant means the voltage response will travel further down the process.
89
what instrument was Emil du Bois-Reymond using to measure small currents?
A galvanometer
90
what was the speed of the nerve impulse estimated by Hermann Von Helmholtz?
33 m/s
91
post synaptic potential
changes in membrane potential that move the cell away from its resting state.
Ion channels that are opened by a stimulus allow brief ion flow across the membrane. A stimulus can range from neurotransmitters released by a presynaptic neuron, changes in the extracellular environment like exposure to heat or cold, interactions with sensory stimuli like light or odors, or other chemical or mechanical events. The change in membrane potential in response to the stimulus will depend on which ion channels are opened by the stimulus.
92
excitatory post synaptic potential
occurs when sodium channels open in response to a stimulus. The electrochemical gradient drives sodium to rush into the cell. When sodium brings its positive charge into the cell, the cell’s membrane potential becomes more positive, or depolarizes.
93
inhibitory post synaptic potential
caused by the opening of chloride channels.
Chloride brings its negative charge into the cell, causing the cell’s membrane potential to become more negative, or hyperpolarize. This change is called a hyperpolarization because the cell’s membrane potential is moving away from 0 mV
94
Temporal summation
occurs when one presynaptic input stimulates a postsynaptic neuron multiple times in a row.
can be excitatory or inhibitory
95
Spatial summation
occurs when multiple presynaptic inputs each stimulate the postsynaptic neuron at the same time.
can be excitatory or inhibitory
96
A neuron is at rest at -70 mV, and a stimulus causes sodium channels in the dendrites to open. What change in membrane potential would you expect to see?
Excitatory depolarization
97
A neuron is at rest at -55 mV, and a stimulus causes chloride channels in the dendrites to open. What change in membrane potential would you expect to see?
Inhibitory hyperpolarization
98
A neuron is at rest at -65 mV, and a stimulus causes chloride channels in the dendrites to open. What change in membrane potential would you expect to see?
None of the above
99
A neuron is at rest at -75 mV, and a stimulus causes chloride channels in the dendrites to open. What change in membrane potential would you expect to see?
Inhibitory depolarization
100
if you wanted to measure postsynaptic potentials, where would you place your recording electrode? (Select all that apply)
Myelin
Soma
Presynaptic terminal
Dendrites
Axon
Nucleus
Soma
Dendrites
101
A stimulus that opens ion channels that increase the permeability ____ ions of across the membrane will result in excitation of the neuron.
sodium
102
A stimulus that opens ion channels that increase the permeability of ____ ions across the membrane will result in inhibition of the neuron.
chloride
103
what is the main difference between voltage-gated channels and leak channels
how they are opened or “gated”. Voltage-gated channels open when the cell’s membrane potential reaches a specific value, called threshold.
104
What causes the rising phase of the action potential?
The opening of voltage-gated sodium channels, allowing Na⁺ to rush into the cell and depolarize the membrane.
105
When do voltage-gated sodium channels open?
Immediately after the membrane potential reaches threshold.
106
What causes the falling phase of the action potential?
Inactivation of sodium channels and delayed opening of potassium channels.
107
Why does potassium exit the cell during the falling phase?
The electrochemical gradient drives K⁺ out, repolarizing the membrane.
108
What is the undershoot phase?
A brief hyperpolarization after repolarization, caused by potassium channels staying open longer than needed.
109
How does the membrane return to its resting state after an action potential?
The sodium-potassium pump and leak channels reestablish the resting membrane potential.
110
What is saltatory conduction?
The jumping of the action potential between Nodes of Ranvier in myelinated axons, increasing conduction speed.
111
How does myelin affect action potential speed?
It insulates the axon, reduces charge loss, and increases speed.
112
How does axon diameter affect conduction speed?
Larger axons have less resistance, allowing faster propagation of the action potential.
113
What causes the action potential to move forward along the axon?
Sodium influx depolarizes adjacent axon segments to threshold.
114
Why doesn’t the action potential move backward?
Sodium channels behind the action potential are inactivated (refractory), preventing backward flow.
115
How is stimulus strength encoded by neurons?
By the frequency (rate) of action potential firing, not amplitude.
116
What is the absolute refractory period?
A period when a second action potential cannot occur due to sodium channels being open or inactivated.
117
What is the relative refractory period?
A period when a stronger-than-normal stimulus is needed to initiate another action potential due to hyperpolarization.
118
Can the characteristics of an action potential change in a neuron?
Yes, changes in extracellular ion concentrations (e.g., less external sodium) can alter shape and amplitude.
119
Where are the voltage-gated ion channels located in the cell?
in the axon and axon hillock
120
What triggers the voltage-gated sodium channels to open?
Reaching threshold
121
What triggers the voltage-gated potassium channels to open?
Reaching threshold
122
Which ion is responsible for the rising phase of the action potential?
Sodium
123
Which ion is responsible for the falling phase of the action potential?
Potassium
124
Which statement best describes the relationship between the external sodium concentration and the shape of the action potential?
If the external sodium concentration were decreased, the amplitude of the action potential would also decrease.
125
How is stimulus intensity encoded by the action potential?
The stronger the stimulus the faster the action potential frequency
126
Which statement(s) is/are true regarding action potential propagation speed?
Group of answer choices
1. The presence of myelin insulates the axon, which increases action potential speed
2. A larger diameter axon causes less resistance and therefore increases action potential speed
3. Saltatory conduction, the process of action potential propagation in unmyelinated neurons, is slower than normal conduction
4. An increased density of non-gated potassium channels decreases the length of the absolute refractory period, increasing action potential speed
1. The presence of myelin insulates the axon, which increases action potential speed
2. A larger diameter axon causes less resistance and therefore increases action potential speed
127
Which factor is responsible for preventing the action potential from going backward down the axon?
Inactivated sodium channels
128
voltage clamp experiment purpose
The voltage clamp method allows researchers to study voltage-gated ion channels by controlling the membrane potential of a neuron.
129
What is the purpose of a voltage clamp experiment?
To control (clamp) the membrane potential of a neuron while measuring the ionic currents that flow through voltage-gated ion channels.
130
What is the first step in a voltage clamp experiment?
Measuring the membrane potential using a recording electrode inside the axon and a reference electrode in the extracellular solution.
131
What happens if the actual membrane potential differs from the set (desired) membrane potential in a voltage clamp?
Current is injected into the axon to bring the actual membrane potential to the set value.
132
What maintains the membrane potential at the set value during the experiment?
The equipment continuously compares actual vs. desired membrane potential and adjusts by injecting current.
133
What is the typical resting membrane potential of the axon used in the example?
-65 mV.
134
What happens when the desired membrane potential is set to 0 mV?
The equipment injects positive current to depolarize the axon from -65 mV to 0 mV.
135
Why do voltage-gated sodium channels open in the experiment example?
Because the membrane is depolarized above threshold due to the injected current.
136
How does the equipment respond to sodium influx during the voltage clamp?
It injects an equal and opposite current to offset the sodium influx and keep the membrane potential steady.
137
What happens after sodium channels inactivate in a voltage clamp?
Voltage-gated potassium channels open, and potassium flows out of the axon.
138
How does the equipment respond to potassium efflux?
It injects current equal in strength and opposite in charge to maintain the membrane potential at 0 mV.
139
How do researchers determine how much ionic current is flowing?
By measuring how much current the equipment must inject to keep the membrane potential constant.
140
in the voltage clamp experiment, Why is a reference electrode necessary?
To compare the voltage on the inside and outside of the cell
141
in the voltage clamp experiment, to investigate ion flow through voltage-gated ion channels that open during an action potential, the membrane must be clamped at which value?
any value above threshold
142
When ions flow across the membrane during a voltage clamp experiment, what happens to the membrane potential?
The membrane potential does not change
143
In the example in the video, what is the fastest the recorded neuron can fire action potentials (APs) because of the refractory period? (note that since we don't know the setting in the oscilloscope shown, we just refer to each line in the oscilloscope grid as a time unit).
1 AP every 2 time units
144
In the video, what happened to the neural signal when the stimulus intensity (the pressure on the animal's paw) was increased?
The recorded nerve fiber produced more action potentials
145
describe the role of calcium in neurotransmission
When the action potential reaches the terminal, there is an influx of sodium ions. This inward positive current causes a depolarization of the terminal, activating voltage-gated calcium channels that are embedded in the cell membrane of the axon terminals. Due to the electrochemical gradient of calcium, when the voltage-gated calcium channels are opened, calcium will rush into the cell. The concentration of intracellular calcium, generally in the range of 100 nM, is much lower than the concentration outside the cell, therefore there is a strong electrochemical gradient that moves calcium into the terminal. As it turns out, an elevation of Ca2+ in the intracellular space is the “go ahead” signal that causes neurotransmitter release.
146
active zones
The voltage-gated calcium channels are concentrated in the presynaptic terminal at active zones, the regions of the membrane where small molecule neurotransmitters are released. At active zones, some synaptic vesicles are docked and are ready for immediate release upon arrival of the action potential. Other neurotransmitter-filled vesicles remain in a reserve pool outside of the active zone.
Vesicles filled with neuropeptides do not dock at active zones. They are located outside of the active zone, further away from the membrane and the high density of voltage-gated calcium channels. They are, therefore, slower to release than the small molecule transmitters.
147
what are the three places vessicles can be found in the synaptic terminal
1. Readily releasable pool.
vesicles are located close to the cell membrane at the axon terminal. Many of them are already “docked”, meaning that their coat proteins are already interacting closely with the proteins on the inside of the cell membrane. When the depolarizing charge of an action potential reaches the terminal, these vesicles at the readily releasable pool are the first ones that fuse with the cell membrane and release their contents.
2. Recycling pool.
These vesicles are the ones that have been depleted due to release. They are currently in the process of being refilled or reloaded with neurotransmitter. They are farther from the cell membrane, and the protein machinery is not primed for release, so it requires a more intense stimulation to release the contents of these vesicles.
3. Reserve pool.
These vesicles are the farthest from the surface of the cell membrane, and most vesicles are held in this reserve pool. For these neurotransmitters to be released, very intense stimulation is required.
148
SNARE proteins
Docking of synaptic vesicles packaged with small molecule neurotransmitters occurs through the interaction of three membrane-bound proteins called SNARE proteins. Synaptobrevin is called a v-SNARE because it is located on the Vesicular membrane. Syntaxin and SNAP-25 are called t-SNARES because they are located on the terminal membrane, which is the Target membrane. The interaction of these three proteins leads to vesicle docking at the active zone.
149
the role of calcium in exocytosis
The influx of calcium through the voltage-gated calcium channels initiates the exocytosis process that leads to neurotransmitter release. Calcium enters the cell and interacts with a vesicle-bound protein called synaptotagmin. Synaptotagmin is a calcium sensor that detects elevated levels of calcium in the axon terminal.
150
SNARE complex
In the presences of calcium, the v-SNAREs and the t-SNAREs interact with one another, forming a molecular structure called a SNARE complex. The SNARE complex looks a lot like two twist ties that are wound tightly together. As they twist tighter together, it causes the vesicle membrane to approach the inside of the cell membrane, which results in vesicular fusion.
151
what is the last step of neurotransmitter release is
it is the fusing of the cell membrane. In order to release their chemical contents into the synapse, vesicles need to fuse with the cell membrane. As the vesicular membrane merges with the interior of the neuronal membrane, the membranes fuse and the contents of the vesicle become exposed to the extracellular space. The neurotransmitters then float across the aqueous synapse, giving them the opportunity to interact with postsynaptic receptors.
152
what are the four steps in neurotransmitter release
Step 1: An action potential arrives at the axon terminal
Step 2: Membrane depolarization from action potential causes influx of calcium ions
Step 3: Docking of synaptic vesicles at the membrane
Step 4: Release of neurotransmitters into the synapse
153
what happens after exocytosis
transmitter molecules, neurotransmitters traverse across the synapse and bind to receptors on the postsynaptic membrane.
154
what are the two main receptor categories
ionotropic receptors (also called ligand-gated channels) and metabotropic receptors (also called G-protein coupled receptors).
155
where in the neuron do signals summate
The postsynaptic potentials generated from neurotransmitter binding summate at the axon hillock. If the membrane potential is over threshold potential for the cell, then a new action potential will be generated in the postsynaptic cell.
156
describe neurotransmitter inactivation
1. After being released, neurotransmitters can be altered into inactive substances.
2. Neurotransmitters can go through the reuptake process, where they are recycled by being transported back into the presynaptic cell and repackaged into synaptic vesicles.
3. Some neurotransmitters simply float away from the synapse due to the aqueous environment surrounding neurons.
157
When a depolarizing stimulus arrives at the axon terminal, what type of channels are opened that allow for neurotransmitter release?
voltage-gated calcium channel
158
Which protein(s) is/are t-SNARES?
Syntaxin
SNAP-25
159
what is true about small molecule vesicles
dock at active zones
smaller vessicle size
160
what is true about neuropeptide vesicles
slower release of neurotransmitter
must travel from cell body to terminal
161
Which protein(s) is/are v-SNARES?
Synaptobrevin
162
Which of the following are ways that neurotransmitter signaling is terminated?
Reuptake
Diffusion away from the synapse
chemical degradation
all of the above
163
Which protein(s) function as a calcum sensor in the terminal?
Synaptotagmin
164
qualities of every neurotransmitter
First, the transmitter must be synthesized within in the presynaptic neuron. Second, the transmitter must be released by the presynaptic neuron in response to stimulation. Third, when a postsynaptic neuron is treated with the transmitter by a researcher, the molecule must cause the same effect in the postsynaptic neuron as when it is released by a presynaptic neuron.
165
two main categories of neurotransmitters
small molecule transmitters and peptide transmitters
166
small molecule transmitters (overview)
can be divided into two main groups: amino acid neurotransmitters and biogenic amines, also called monoamines. In addition to acting as neurotransmitters, the amino acids glutamate and glycine are used to synthesize proteins in all cell types throughout the body. GABA (Ɣ-Aminobutyric acid) is a metabolite of glutamate but is not used in protein synthesis in the body. The biogenic amines include serotonin and histamine, and the subgroup the catecholamines dopamine, norepinephrine, and epinephrine. Acetylcholine does not fit into either division but is still considered a small molecule neurotransmitter.
167
where are small molecule tramsmitters synthesized
Small molecule transmitters are synthesized in the synaptic terminal
168
describe the Synthesis and Storage of Small Molecule Transmitters
Most small molecule neurotransmitters are synthesized by enzymes that are located in the cytoplasm (the exception is norepinephrine, see below). This means that small molecule neurotransmitters can be synthesized and packaged for storage in the presynaptic terminal using enzymes present in the terminal.
169
acetylcholine function
Acetylcholine is best known for its role at the neuromuscular junction, the synapse between a motor neuron and the muscle fiber.
170
what is acetylcholine synthesized from and by what
In the presynaptic terminal, acetylcholine is synthesized from acetyl coenzyme A (acetyl CoA) and choline via the enzyme choline acetyltransferase. The level of enzyme activity is the rate-limiting step in the synthesis pathway.
171
what packages acetylcholine
Acetylcholine is packaged into vesicles for storage in the terminal via the vesicular acetylcholine transporter (VAChT).
172
function of glutamate
Glutamate is an amino acid transmitter and is the primary excitatory neurotransmitter in the brain.
173
what converts glutamate
In the presynaptic terminal, glutamine is converted into glutamate via the enzyme glutaminase, which is the rate-limiting step in the synthesis pathway.
174
what packages glutamate into vessicles
Glutamate is packaged into vesicles for storage via the vesicular glutamate transporter.
175
what synthesizes GABA
Glutamate is then used to synthesize GABA
176
what is GABA
amino acid transmitter and the primary inhibitory neurotransmitter in the brain.
177
What converts into GABA and what does it used to do this
In the presynaptic terminal, glutamate is converted into GABA via the enzyme glutamic acid decarboxylase, which like the other synthesis pathways is the rate-limiting step.
178
how is GABA packaged into vessicles
GABA is packaged into vesicles for storage in the terminal via the vesicular inhibitory amino acid transporter.
179
what is glycine
Glycine is another inhibitory amino acid neurotransmitter, but unlike GABA, it is more common in the spinal cord than in the brain.
180
how is glycine produced
Serine hydroxymethyltransferase converts the amino acid serine into glycine in the presynaptic terminal. The rate limiting step for glycine synthesis occurs earlier in the pathway prior to serine synthesis.
181
how is glycine packaged into vessicles
Glycine is packaged into vesicles by the vesicular inhibitory amino acid transporter like GABA
182
what is dopamine
Dopamine, a catecholamine transmitter, plays many roles in the nervous system, but it is best known for its roles in reward and movement.
183
what is converted to produce dopamine and by what
In the presynaptic terminal, the amino acid tyrosine is converted into DOPA via tyrosine hydroxylase, which is the rate limiting step in the synthesis of all the catecholamines. DOPA is then converted to dopamine by DOPA decarboxylase.
184
how is dopamine packaged into vessicles
Dopamine is packaged into synaptic vesicles by the vesicular monoamine transporter.
185
norepinephrine
a catecholamine transmitter that plays an important role in your body's “fight-or-flight” response.
186
how is norepinephrine produced and packaged into vessicles
once dopamine is packaged into the synaptic vesicles, a membrane-bound enzyme called dopamine beta-hydroxylase converts dopamine into norepinephrine. Therefore, unlike the other small molecule neurotransmitters, norepinephrine is synthesized within the vesicles, not in the cytoplasm. Like dopamine, the rate limiting step of this synthesis pathway is the activity of tyrosine hydroxylase.
187
what is epinephrine
Epinephrine, also called adrenaline, is a catecholamine, but it is often considered a hormone instead of a neurotransmitter.
188
where is epinephrine released from
Epinephrine is primarily released by the adrenal medulla into the circulation; it is used as a neurotransmitter in only a small number of neurons.
189
how is epinephrine synthesized
Epinephrine is synthesized from norepinephrine in the cytoplasm by the enzyme phenylethanolamine-N-methyltransferase, so epinephrine synthesis requires norepinephrine to exit the vesicles where it was synthesized.
190
how is epinephrine packaged and stored
After synthesis in the cytoplasm, epinephrine is repackaged into vesicles via the vesicular monoamine transporter.
191
what is serotonin
Serotonin, a biogenic amine neurotransmitter, is known for its role in mood.
192
how is serotonin synthesized
Tryptophan is converted into 5-hydroxytryptophan by tryptophan hydroxylase. This is also the rate-limiting step of the synthesis pathway. Then aromatic L-amino acid decarboxylase converts the 5-hydroxytryptophan into serotonin.
193
how is serotonin packaged into vessicles
Serotonin is packaged into vesicles by the vesicular monoamine transporter similar to the other monoamine neurotransmitters: dopamine and epinephrine.
194
what is histamine
another biogenic amine transmitter involved in inflammation and immune responses
195
how is histamine synthesized
synthesized from histidine through the action of histadine decarboxylase, the rate limiting step of the pathway.
196
how is histamine packaged
Like the other monoamine neurotransmitters, it is packaged into synaptic vesicles via the vesicular monoamine transporter.
197
describe the Synthesis and Storage of Neuropeptides
Neuropeptides are synthesized in the cell body and transported to the synaptic terminal
198
what are neuropeptides
Neuropeptides are a short string of amino acids and are known to have a wide range of effects from emotions to pain perception.
199
how do neuropeptides and small molecule transmitters differ
Unlike small molecule neurotransmitters, neuropeptides are synthesized in the cell body and transported to the axon terminal.
200
how are neuropeptides synthesized and packaged
Like other proteins, neuropeptides are synthesized from mRNA into peptide chains made from amino acids. In most cases, a larger precursor molecule called the prepropeptide is translated into the original amino acid sequence in the rough endoplasmic reticulum. The prepropeptide is processed further to the propeptide stage. The remaining processing and packaging of the final neuropeptide into a vesicle occurs in the Golgi apparatus. The peptides are packaged into vesicles that are significantly larger that the vesicles that store the small molecule transmitters. These large vesicles must then move from the soma to the terminal.
201
describe axonal transport
The packaged peptides need to be transported to the presynaptic terminals to be released into the synaptic cleft. Organelles, vesicles, and proteins can be moved from the cell body to the terminal via anterograde transport or from the terminal to the cell body via retrograde transport.
202
anterograde transport
Toward the axon from the cell body. Anterograde transport can be either fast or slow.
203
retrograde transport
toward the cell body from the axons
204
Which neurotransmitter(s) is/are biogenic amine(s)?
Histamine
Serotonin
Norepinephrine
Dopamine
205
Which small molecule neurotransmitter is not synthesized in the cytoplasm of the cell?
norepinephrine
206
Which neurotransmitter(s) is/are amino acid(s)?
glycine
glutamate
GABA
207
Where are peptide neurotransmitters synthesized?
in the cell body
208
Which neurotransmitter(s) is/are catecholamine(s)?
dopamine
norepinephrine
209
what are Catecholamines
a group of chemicals, including dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline), that are produced by the brain, nerve tissues, and adrenal glands. They are primarily known for their role in the body's "fight-or-flight" response to stress
210
Which neurotransmitter(s) is/are peptide(s)?
oxytocin
211
How do peptide vesicles move from the cell body to the terminal?
fast anterograde axonal transport mechanisms
212
describe the ion flow in the terminal
When the action potential reaches the terminal, there is an influx of sodium ions, just like when the action potential moves down the axon. This inward current causes a depolarization of the terminal, and that depolarization activates voltage-gated calcium channels. There is a strong electrochemical gradient that moves calcium into the terminal.
213
Which protein(s) function as a calcum sensor in the terminal?
Synaptotagmin
214
Which protein(s) is/are t-SNARES?
SNAP-25
Syntaxin
215
You conduct a voltage clamp experiment where you hold the presynaptic terminal of a neuron at 0 mV. Additionally, you treat the terminal with TTX to block the voltage-gated sodium channels and TEA to block the voltage-gated potassium channels. You record an inward ion flow while the cell is held at 0 mV as displayed in the image.
calcium
If the terminal is clamped above threshold, the voltage-gated calcium channels will open even if the sodium and potassium channels are blocked.
216
Which protein(s) is/are v-SNARES?
Synaptobrevin
217
ionotropic receptors
ligand-gated channels --> are ion channels that open in response to the binding of a neurotransmitter. They are primarily located along the dendrites or cell body, but they can be present anywhere along the neuron if there is a synapse. Ligand-gated channels are important for receiving incoming information from other neurons.
218
glutamate receptor mechanism
Glutamate causes EPSPs by opening cation channels that increase sodium permeability across the membrane
219
glutamate receptor subtypes and how sodium and potassium flow
There are three subtypes of glutamate receptors. The NMDA, AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid), and kainate receptors
220
explain NMDA recepto
NMDA (N-methyl-D-aspartate) receptor requires the binding of glutamate to open, but it is also dependent on voltage. When the membrane potential is below, at, or near rest, a magnesium ion blocks the open NMDA receptor and prevents other ions from moving through the channel. Once the cell depolarizes, the magnesium block is expelled from the receptor, which allows sodium, potassium, and calcium to cross the membrane. The voltage change needed to open the NMDA receptor is usually a result of AMPA receptor activation. Released glutamate binds to both AMPA and NMDA receptors, sodium influx occurs through open AMPA channels, which depolarizes the cell enough to expel the magnesium ion and allow ion flow through the NMDA receptors.
221
explain AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and kainate receptors
allow both sodium and potassium to cross the membrane. Although potassium can leave the cell when the receptors open, the electrochemical gradient driving sodium ion movement is stronger than the gradient driving potassium movement, resulting in a depolarization of the membrane potential.
222
Nicotinic Acetylcholine Receptors
Like glutamate receptors, nicotinic acetylcholine receptors are non-selective cation channels. Nicotinic receptors, though, are located primarily outside of the central nervous system and are primarily used at the neuromuscular junction.
223
describe mechanism of GABA and Glycine Receptors
GABA and glycine receptors are chloride channels. Since an increase chloride permeability across the membrane is inhibitory, the binding of GABA or glycine to their respective ionotropic receptor will cause inhibition.
224
What type of receptor causes postsynaptic potentials?
Ionotropic receptors.
225
What do excitatory ionotropic receptors increase permeability to?
Sodium (Na⁺).
226
What do inhibitory ionotropic receptors increase permeability to?
Chloride (Cl⁻).
227
What is the equilibrium potential?
The membrane potential at which the chemical and electrical gradients for an ion are balanced.
228
What is the reversal potential of a receptor?
The membrane potential at which there is no net ion flow through the receptor.
229
How does reversal potential relate to equilibrium potential when only one ion is involved?
The reversal potential equals the equilibrium potential of that ion.
230
What type of postsynaptic potential does GABA binding to its receptor cause?
An inhibitory postsynaptic potential (IPSP).
231
What ion do GABA and glycine receptors allow to pass through?
Chloride (Cl⁻).
232
What is the approximate reversal potential for GABA receptors?
About -65 mV (same as chloride’s equilibrium potential).
233
What type of ion channel is the glutamate receptor?
A non-selective cation channel.
ionotropic glutamate receptors
234
What ions can flow through glutamate receptors?
Sodium (Na⁺) and Potassium (K⁺).
235
What is the reversal potential of the glutamate receptor?
Approximately 0 mV.
236
Why does glutamate cause an excitatory postsynaptic potential (EPSP)?
More Na⁺ flows in than K⁺ flows out, causing depolarization.
237
What happens to net ion movement when the membrane potential reaches the receptor’s reversal potential?
Net ion movement stops; inward and outward flows balance.
238
A neurotransmitter that opens ionotropic receptors with which reversal potential would be excitatory transmitters?
0 mV
Ions will flow through the receptor in order to to make the membrane potential move toward 0 mV. 0 mV is above threshold, so that change in potential is excitatory.
239
Which ions move through ionotropic GABA receptors?
chloride
240
Which ions move through AMPA receptors?
potassium and sodium
241
Which ions move through NMDA receptors?
potassium, sodium, calcium
242
Which neurotransmitter is responsible for causing an EPSP in a postsynaptic neuron in the CNS?
Acetylcholine
Glutamate
GABA
Glycine
Glutamate
243
Which neurotransmitter(s) is/are responsible for causing an IPSP in a postsynaptic neuron in the CNS? Select all that apply.
Glycine
GABA
Acetylcholine
Glutamate
GABA and glycine
Acetycholine opens ionotropic nicotinic receptors, which are non-selective cation channels that cause depolarization in the postsynaptic membrane. These receptors are located primarily outside of the central nervous system at neuromuscular junctions. this is why Ach isnt an answer
244
What are G-protein-coupled receptors (GPCRs) also known as?
Metabotropic receptors.
245
Where are metabotropic receptors primarily located on a neuron?
Along the dendrites and cell body.
246
How do the effects of metabotropic receptors compare to ionotropic receptors?
They are slower but can produce longer-lasting effects.
247
What activates a G-protein?
Neurotransmitter binding to a GPCR, leading to GDP-GTP exchange on the alpha subunit.
248
What are the three subunits of a G-protein?
Alpha, beta, and gamma.
249
What happens when a G-protein is activated?
It splits into alpha-GTP and beta-gamma subunits, which can affect cellular effector proteins.
250
What is the role of the beta-gamma subunit in GPCR signaling?
It can open ion channels, such as GIRK channels in the heart.
251
What does the alpha subunit of Gs do?
Activates adenylyl cyclase, increasing cAMP production.
252
What does the alpha subunit of Gi do?
Inhibits adenylyl cyclase, reducing cAMP levels.
253
What does the alpha subunit of Gq activate?
Phospholipase C, leading to the IP3/DAG pathway.
254
What are the products of phospholipase C acting on PIP2?
IP3 and DAG.
255
What does IP3 do in the cell?
Opens calcium channels in the endoplasmic reticulum.
256
What is the function of DAG in the GPCR pathway?
Activates protein kinase C (PKC).
257
What happens when cAMP binds to protein kinase A (PKA)?
It activates PKA by releasing its catalytic subunits.
258
What is the role of PKA in the cell?
Phosphorylates target proteins, affecting ion channels, CREB, and other cellular functions.
259
What transcription factor does PKA phosphorylate?
CREB (cAMP Response Element Binding Protein).
260
What does phosphorylated CREB do?
Initiates transcription of new genes, producing long-term changes in the neuron.
261
How does signal amplification occur in GPCR pathways?
One receptor activates multiple G-proteins, each producing many second messengers, amplifying the signal.
262
What enzyme converts ATP to cAMP?
Adenylyl cyclase.
263
How is a GPCR signal terminated?
GTP is hydrolyzed back to GDP by the alpha subunit; phosphatases remove phosphates; calcium and second messengers are cleared.
264
Which outcome(s) could result from a neurotransmitter binding to a GPCR? Select all that apply.
Synthesis of new proteins
Opening ion channels
Altering cellular protein function
all of the above
265
What is the outcome of activation of a Gq alpha subunit?
1. Inhibition of the phospholipase C / DAG / IP3 signaling cascade
2. Initiation of the adenylyl cylcase / cAMP signaling cascade
3. Initiation of the phospholipase C / DAG / IP3 signaling cascade
4. Inhibition of the adenylyl cylcase / cAMP signaling cascade
3. Initiation of the phospholipase C / DAG / IP3 signaling cascade
266
Which enzyme is a transcription factor that can initiate gene transcription?
CREB
PKA
Calmodulin
Adenylyl cyclase
CREB
267
What is the outcome of activation of a Gs alpha subunit?
Initiation of the adenylyl cylcase / cAMP signaling cascade
268
While at rest, which cellular molecule is bound to the G-protein complex?
GDP
269
What is the outcome of activation of a Gi alpha subunit?
Inhibition of the adenylyl cylcase / cAMP signaling cascade
270
What are the two main mechanisms that terminate neurotransmitter action?
Transport (removal from synaptic cleft) and degradation (enzyme breakdown).
271
Why must neurotransmitter action be terminated?
To ensure proper and timely neuronal communication.
272
What enzyme terminates acetylcholine action?
Acetylcholinesterase.
273
What are the breakdown products of acetylcholine?
Choline and acetate.
274
What happens to choline after acetylcholine degradation?
It is transported back into the presynaptic terminal for new ACh synthesis.
275
How is glutamate action terminated?
By reuptake into the presynaptic terminal or transport into glial cells.
276
What transporter helps remove glutamate from the synaptic cleft?
Excitatory amino acid transporter (sodium co-transporter).
277
What happens to glutamate in glial cells?
It's converted to glutamine by glutamine synthetase.
278
What is the fate of glutamine after its formation in glial cells?
It is transported back to the presynaptic terminal for new glutamate synthesis.
279
How are GABA and glycine actions terminated?
By reuptake into the presynaptic terminal or glial cells via sodium co-transporters.
280
What happens to GABA and glycine after reuptake?
They are either degraded by enzymes or repackaged into vesicles.
281
What transporter reuptakes dopamine into the presynaptic terminal?
Dopamine transporter (DAT).
282
What enzymes degrade dopamine?
Monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT).
283
What are the two fates of dopamine after reuptake?
Degradation or repackaging into synaptic vesicles.
284
What transporter reuptakes norepinephrine?
Norepinephrine transporter (NET).
285
What enzymes degrade norepinephrine?
MAO and COMT.
286
What are the fates of norepinephrine after reuptake?
Degraded or repackaged into vesicles.
287
What transporter reuptakes serotonin?
Serotonin transporter (SERT).
288
What enzyme degrades serotonin?
Monoamine oxidase (MAO) only.
289
Which neurotransmitter(s) can be transported into glial cells? Select all that apply
Glutamate
Glycine
GABA
Dopamine
Norepinephrine
Acetylcholine
Serotonin
GABA, glycine, glutamate
290
SSRIs block the function of SERT. Compared to before treatment, which outcome would you expect to see after SSRI treatment?
Increased acetylcholine levels in the synapse
Decreased serotonin levels in the synapse
Increased serotonin levels in the synapse
Decreased dopamine levels in the synapse
Increased serotonin levels in the synapse
291
Which neurotransmitter(s) is/are degraded in the synapse? Select all that apply
Dopamine
Serotonin
Acetylcholine
GABA
Glycine
Glutamate
Norepinephrine
Acetylcholine
Acetylcholine is broken down in the synaptic cleft by acetylcholinesterase.
292
Which neurotransmitter(s) can be broken down by COMT? Select all that apply
GABA
Norepinephrine
Glycine
Acetylcholine
Glutamate
Dopamine
Serotonin
Dopamine and Norepinephrine
293
In what three general ways can drugs and toxins affect neurons?
Excitatory, inhibitory, or modulatory effects.
294
Why are synapses common targets for drug action?
Because neurotransmitter synthesis, packaging, release, action, and termination all occur there.
295
How can drugs affect neurotransmitter synthesis?
By increasing or decreasing the amount of neurotransmitter produced in the terminal.
296
What is an example of a drug that increases neurotransmitter synthesis?
L-DOPA increases dopamine synthesis and is used to treat Parkinson’s Disease.
297
How can drugs affect neurotransmitter packaging?
By inhibiting the transport of neurotransmitters into vesicles.
298
What drug blocks neurotransmitter packaging into vesicles?
Reserpine inhibits VMAT, reducing monoamine transmitter storage.
299
What is an agonist in terms of neurotransmitter receptors?
A substance that mimics the effects of a neurotransmitter.
300
What is an antagonist?
A substance that blocks the effects of a neurotransmitter.
301
What is muscimol and its effect?
A GABA receptor agonist that mimics GABA and causes IPSPs.
302
What is bicuculine and its effect?
A GABA receptor antagonist that blocks GABA action, preventing IPSPs.
303
How does alcohol affect GABA receptors?
It positively modulates them, increasing receptor opening time when GABA binds.
304
How can drugs affect neurotransmitter degradation?
By inhibiting enzymes that break down neurotransmitters.
305
What do organophosphates do?
Inhibit acetylcholinesterase, increasing acetylcholine action.
306
What do monoamine oxidase inhibitors (MAOIs) do?
Block MAO enzyme, increasing levels of monoamine neurotransmitters.
307
How does cocaine affect neurotransmitter reuptake?
It blocks the dopamine transporter (DAT), increasing dopamine levels in the synapse.
308
Can drugs affect neurons outside the synapse?
Yes, such as by altering ion channel behavior.
309
What is veratridine's effect on sodium channels?
It prevents voltage-gated sodium channel inactivation, initially increasing neurotransmitter release.
310
What dangerous condition can veratridine lead to?
Excitotoxicity due to prolonged depolarization.
311
what are examples of increasing transmitter action
agonist
antagonist
block reuptake
block packaging
increase synthesis
block degradation
agonist
block reuptake
increase synthesis
block degradation
312
what are examples of decreasing transmitter action
agonist
antagonist
block reuptake
block packaging
increase synthesis
block degradation
antagonist
block packaging
313
SSRIs block the function of SERT. Compared to before treatment, which outcome would you expect to see after SSRI treatment?
1. Decreased serotonin levels in the synapse
2. Increased acetylcholine levels in the synapse
3. Increased serotonin levels in the synapse
4. Decreased dopamine levels in the synapse
3. Increased serotonin levels in the synapse
314
Benzodiazepines bind to the ionotropic GABA receptors and increase the effects of GABA. Which effect would you predict to see after treatment with benzodiazepines.
1. Increased chloride flow after binding of the benzodiazepines
2. Increased chloride flow after GABA binds to the receptor
3. Increased potassium flow after GABA binds to the receptor
4. Increased Gs subunit action
2. Increased chloride flow after GABA binds to the receptor
315
What is the role of magnesium in the function of NMDA receptors, and why is it important for synaptic plasticity?
Magnesium is attracted to the NMDA receptor channel pore and blocks it, even if glutamate has bound. This blockage prevents ion flow (specifically Ca²⁺) until the postsynaptic neuron is sufficiently depolarized, which expels the magnesium ion. This mechanism is biologically useful because it ensures that NMDA receptors only allow ion flow when both presynaptic glutamate release and postsynaptic depolarization occur simultaneously. This process is essential for synaptic plasticity, particularly in long-term potentiation (LTP), which is critical for learning and memory formation.
316
A researcher is studying a brain region where GABAergic inhibition is particularly prominent. They apply a GABA agonist to the postsynaptic neuron and observe a hyperpolarization of the membrane potential.
What type of receptor is most likely being activated by this GABA agonist, and how does this receptor mediate the observed effect?
The GABA(A) receptor is most likely being activated in this case. GABA(A) receptors are ionotropic receptors that open chloride (Cl⁻) channels when GABA binds. The influx of chloride ions leads to hyperpolarization of the postsynaptic neuron, making it less likely to fire an action potential. GABA(B) receptors are metabotropic and tend to mediate slower, longer-lasting effects, often involving K⁺ channel opening, but in this case, the fast, direct hyperpolarization is more consistent with GABA(A) receptor activation.
317
In an experiment, a researcher wants to determine whether a specific neuron has an excitatory or inhibitory effect on a target neuron.
They apply glutamate to the target neuron and observe depolarization. Then, they apply GABA to the same target neuron and observe hyperpolarization.
Based on this information, how would you classify the effect of the original neuron on the target neuron (excitatory or inhibitory), and why?
What role do the types of neurotransmitters (glutamate and GABA) play in determining whether the effect is excitatory or inhibitory?
The neuron releasing glutamate is excitatory because glutamate binding to its receptors (such as AMPA or NMDA) leads to depolarization of the postsynaptic neuron. The neuron releasing GABA is inhibitory because GABA binding to its receptors (such as GABA(A)) leads to hyperpolarization. Thus, the original neuron’s effect on the target neuron can be classified as excitatory or inhibitory depending on the neurotransmitter it releases.
318
In a study of neuronal communication, a researcher manipulates the postsynaptic neuron to express a mutant version of the AMPA receptor that has reduced ion conductivity.
When glutamate is applied to the neuron, the expected excitatory postsynaptic potential (EPSP) is smaller than normal.
How would you explain the observed decrease in EPSP? What is the role of AMPA receptors in mediating excitatory synaptic transmission, and how does reduced ion conductivity affect their function?
AMPA receptors are ionotropic glutamate receptors that mediate fast depolarization (EPSPs) by allowing Na⁺ ions to flow into the postsynaptic neuron. When the mutant AMPA receptor has reduced ion conductivity, fewer ions (such as Na⁺) are able to enter the cell, leading to a smaller depolarization. This results in a weaker EPSP, meaning the postsynaptic neuron is less likely to fire an action potential. Reduced ion conductivity in AMPA receptors diminishes their ability to mediate strong excitatory responses.
319
A researcher is studying the effects of presynaptic modulation on neurotransmitter release. They apply a drug that enhances voltage-gated calcium channels in the presynaptic neuron, leading to a greater influx of calcium ions during an action potential.
How would this enhanced calcium influx affect the postsynaptic response? Why is calcium influx so important for neurotransmitter release at the synapse?
Enhancing calcium influx would lead to a greater release of neurotransmitters because calcium is essential for the fusion of synaptic vesicles with the presynaptic membrane. When calcium ions enter the presynaptic terminal, they trigger the SNARE complex to facilitate vesicle fusion, leading to neurotransmitter release. This would result in a stronger postsynaptic response due to the increased neurotransmitter concentration in the synaptic cleft. However, if calcium influx is excessive, it could lead to excitotoxicity, potentially damaging the neuron, as too much calcium can activate harmful cellular pathways.
320
What are the parts of the eye that light encounters first?
Cornea, pupil, iris, and lens.
321
What is the function of the cornea?
It refracts light and covers the iris and pupil.
322
What controls the amount of light entering the eye?
The iris and its associated muscles, by adjusting the pupil size.
323
What is accommodation in vision?
The process of the lens changing shape to focus light on the retina.
324
Where are photoreceptors located?
In the retina at the back of the eye.
325
What is the fovea?
A small region of the retina with the highest visual acuity.
326
What is the optic disc?
The blind spot where the optic nerve exits the eye; it contains no photoreceptors.
327
What are the 5 primary cell types in the retina?
Photoreceptors, bipolar cells, ganglion cells, horizontal cells, and amacrine cells.
328
What is the direction of information flow in the retina?
Light → photoreceptors → bipolar cells → ganglion cells → brain (via optic nerve).
329
What are the two types of photoreceptors?
Rods and cones.
330
What is the function of rods?
Vision in low light (scotopic vision).
331
What is the function of cones?
Color vision and sharp central vision in bright light.
332
Where are cones most densely located?
In the fovea.
333
How do photoreceptors respond to light?
They hyperpolarize in light and depolarize in darkness.
334
What neurotransmitter do photoreceptors release?
Glutamate.
335
What happens in the dark in photoreceptors?
cGMP-gated channels are open, allowing Na⁺ and Ca²⁺ influx; cell is depolarized (~ -40 mV).
336
What happens when photoreceptors are exposed to light?
Opsin activates transducin → activates PDE → reduces cGMP → closes cation channels → hyperpolarization.
337
How do OFF bipolar cells respond in the dark?
They depolarize due to excitatory glutamate binding to ionotropic receptors.
338
How do ON bipolar cells respond in the dark?
They hyperpolarize due to inhibitory glutamate binding to metabotropic receptors.
339
What do ON bipolar cells do in the light?
They depolarize due to reduced glutamate inhibition.
340
What are the only retinal cells that fire action potentials?
Ganglion cells.
341
What happens to ON-center ganglion cells in light?
Their firing rate increases.
342
What happens to OFF-center ganglion cells in light?
Their firing rate decreases.
343
What is a receptive field?
The area of the retina a neuron responds to.
344
Where are receptive fields smallest?
In the fovea.
345
What causes receptive field size differences?
The amount of photoreceptor convergence onto bipolar and ganglion cells.
346
What effect does light in the center of an ON bipolar cell’s receptive field have?
It depolarizes the ON bipolar cell.
347
What effect does light in the surround of an ON bipolar cell’s receptive field have?
It hyperpolarizes the ON bipolar cell (indirect pathway via horizontal cells).
348
What is lateral inhibition?
A mechanism that enhances contrast and edge detection in vision.
349
How does lateral inhibition work in the retina?
Surround photoreceptors indirectly inhibit the center response via horizontal and amacrine cells.
350
Using the figure above, neuron #3 is an OFF bipolar cell. If photoreceptor #1, which synapses on neuron #3, moves from the dark to the light, what response would you expect to see in neuron #3?
Hyperpolarization
351
Using the figure above, neuron #6 is an ON-center ganglion cell. If photoreceptor #2, which is upstream of neuron #6, moves from the dark to the light, what response would you expect to see in neuron #6?
An increase in action potential firing
352
Using the figure above, neuron #5 is an OFF-center ganglion cell. If photoreceptor #1, which is upstream of neuron #5, moves from the dark to the light, what response would you expect to see in neuron #5?
A decrease in action potential firing
353
Which receptive field would lead to the highest action potential firing rate for a OFF-center ganglion cell?
Light in center, dark in surrond
Dark in both center and surround
Light in both center and surround
Dark in center, light in surround
Dark in center, light in surround
354
Which receptive field would lead to the lowest action potential firing rate for a OFF-center ganglion cell?
Light in center, dark in surrond
Dark in both center and surround
Light in both center and surround
Dark in center, light in surround
Light in center, dark in surrond
355
How do photoreceptors differ from the "typical" brain neuron we have previously covered?
Group of answer choices
1. The photoreceptor has higher chloride permeability in the dark compared to the typical neuron at rest
2. The photoreceptor is more depolarized than the typical neuron at rest
3. The photoreceptor has higher sodium permeability in the dark compared to the typical neuron at rest
4. The photoreceptor hyperpolarizes in response to stimuli
2. The photoreceptor is more depolarized than the typical neuron at rest
3. The photoreceptor has higher sodium permeability in the dark compared to the typical neuron at rest
4. The photoreceptor hyperpolarizes in response to stimuli
356
What neurotransmitter is released by the photoreceptors?
Glutamate
GABA
Acetylcholine
Dopamine
Glutamate
357
The opsin protein in the photoreceptors uses mechanisms similar to what other protein we have learned about?
Voltage-gated channels
Ionotropic receptors
SNARE proteins
Metabotropic neurotransmitter receptors
Metabotropic neurotransmitter receptors
358
Which retinal cells fire action potentials?
Amacrine cells
Photoreceptors
Bipolar cells
Horizontal cells
Ganglion cells
Ganglion cells
359
Which region of the retina has no photoreceptors?
Optic disc
Iris
Cornea
Fovea
Optic disc
360
Which statements are true about OFF bipolar cells? Select all that apply.
1. OFF bipolar cells have a 1:1 pairing with photoreceptors.
2. OFF bipolar cells express ionotropic glutamate receptors
3. A light in the surround of an OFF-bipolar cell's receptive field would be excitatory
4. OFF bipolar cells hyperpolarize in the light
5. When moving from dark to light, glutamate will cause an increase in sodium permeability in OFF bipolar cells
2. OFF bipolar cells express ionotropic glutamate receptors
3. A light in the surround of an OFF-bipolar cell's receptive field would be excitatory
4. OFF bipolar cells hyperpolarize in the light
361
Which location would have the lowest amount of convergence between photoreceptors and bipolar cells?
Optic disc
Peripheral retina
Fovea
Fovea
362
What are the three main divisions of sensory modalities in the somatosensory system?
External stimuli, internal stimuli, and proprioception (sense of body in space).
363
What types of receptors detect touch, pain, and temperature?
Touch: mechanoreceptors, Pain: nociceptors, Temperature: thermal receptors.
364
What is proprioception and which receptors mediate it?
Proprioception is the sense of body position in space, mediated by proprioceptors.
365
What is equilibrioception and how is it mediated?
Equilibrioception is the sense of head and body orientation relative to gravity; mediated by somatosensory and inner ear receptors.
366
Where are the cell bodies of all somatosensory receptor neurons located?
In the dorsal root ganglion.
367
What type of neuron are somatosensory primary afferent fibers?
Bipolar neurons.
368
What are the two branches of somatosensory primary afferent fibers?
One branch goes to the receptor (e.g., skin), the other enters the spinal cord.
369
What are the four types of primary afferent axons from the skin, and their order of conduction speed?
Aα (fastest), Aβ, Aδ, C (slowest).
370
What axon types carry proprioception, touch, pain, and temperature?
Proprioception: Group I / Aα
Touch: Aβ
Pain & temperature: Aδ and C
Itch & chemoreception: C
371
Which axon type is unmyelinated and has the slowest conduction speed?
C fibers.
372
What is a dermatome?
A region of skin innervated by the axons of a single spinal nerve.
373
What are the four spinal nerve groups, and how many segments does each have?
Cervical: 7
Thoracic: 12
Lumbar: 5
Sacral: 5
374
Primary afferent somatosensory fibers ascend to the brainstem via which spinal cord structure?
Dorsal column
The dorsal column is a white matter tract on the dorsal aspect of the spinal cord and is the location of ascending somatosensory fibers.
375
Which options correctly pairs afferent axon type with its appropriate sensory modality?
Group I - Proprioception
A delta - Itch
Group IV - Temperature
A beta - Touch
Group I - Proprioception
A beta - Touch
376
Where are the cell bodies of primary somatosensory neurons located?
Dorsal root ganglion
Dorsal column
Dorsal horn
Dorsal root ganglion
377
What characteristics of objects can touch receptors help determine?
Location, strength, duration, movement, shape, and texture.
378
What are mechanoreceptors?
Specialized sensory receptors in the skin that detect different modalities of touch.
379
Which mechanoreceptor detects vibration and where is it located?
Pacinian corpuscles; deep in the dermis.
380
Which mechanoreceptor detects skin stretch?
Ruffini endings.
381
Which mechanoreceptor detects skin motion?
Meissner corpuscles.
382
Which mechanoreceptor detects edges and points?
Merkel cells.
383
What is a receptive field in somatosensation?
The area of skin that activates a particular mechanoreceptor.
384
Which mechanoreceptors have small receptive fields?
Merkel cells and Meissner corpuscles.
385
Which mechanoreceptors have large receptive fields?
Pacinian corpuscles and Ruffini endings.
386
How does receptor density affect receptive field size?
Higher density leads to smaller receptive fields, increasing spatial resolution.
387
What is the two-point discrimination test?
A method to measure receptive field size by determining the minimum distance to perceive two separate stimuli.
388
Which mechanoreceptors are slowly adapting?
Merkel cells and Ruffini endings.
389
What do slowly adapting mechanoreceptors help determine?
Pressure and shape of a stimulus.
390
Which mechanoreceptors are rapidly adapting?
Meissner corpuscles and Pacinian corpuscles.
391
What do rapidly adapting mechanoreceptors detect?
Changes in stimuli, such as onset and offset of touch or vibration.
392
What gates ion channels in the somatosensory system?
Physical distortion or stretch of the membrane.
393
What ions enter the mechanoreceptor during stimulation?
Sodium (Na⁺) and calcium (Ca²⁺).
394
which of the following is a mechanoreceptor
Ruffini endings
Pacinian corpuscle
Merkle Cells
Meisner Corpuscle
Ruffini endings
Pacinian corpuscle
395
do Ruffinin endings have large or small receptor fields
large
396
do Pacinian corpuscle have large or small receptor fields
large
397
which of the following are rapidly adapting:
Ruffini endings
Pacinian corpuscle
Merkle Cells
Meisner Corpuscle
Pacinian corpuscle
Meisner Corpuscle
398
which of the following are slowly adapting:
Ruffini endings
Pacinian corpuscle
Merkle Cells
Meisner Corpuscle
Merkle Cells
Ruffini endings
399
Which mechanoreceptors are located near the skin surface? (Select all that apply)
Ruffini endings
Meissner corpuscle
Pacinian corpuscles
Merkel cells
Meissner corpuscle
Merkel cells
400
Which ions are responsible for the depolarization of mechanoreceptors during sensory transduction?
Calcium
Chloride
Sodium
Sodium
Calcium
401
Which of the following is not a chamber in the cochlea:
scala tympani
scala media
scala tectorial
scala vestibuli
scala tectorial
402
What is the main ion flowing into hair cells through mechanically-gated channels to depolarize these cells? (Note that the answer is not in the video)
Group of answer choices
sodium
chloride
calcium
potassium
potassium
403
What is a reflex?
A reflex is an involuntary motor response to a stimulus that occurs automatically and without input from the brain.
404
Where do spinal reflexes occur?
In the spinal cord, often involving simple circuits between sensory and motor neurons.
405
Can reflexes be voluntarily suppressed?
Some can be suppressed with effort, but many, like the stretch reflex, cannot.
406
What triggers the stretch reflex?
Stretching of a muscle spindle in response to muscle stretch (e.g., tapping the knee tendon).
407
What sensory neuron is involved in the stretch reflex?
A 1a sensory afferent neuron from the muscle spindle.
408
What is the path of the stretch reflex?
The 1a afferent neuron synapses directly on a motor neuron (monosynaptic) and on an inhibitory interneuron that inhibits the antagonist muscle.
409
What does the motor neuron do in the stretch reflex?
It causes contraction of the stretched muscle (e.g., quadriceps), resulting in leg extension.
410
What is reciprocal inhibition?
Inhibition of the antagonist muscle (e.g., hamstrings) via inhibitory interneurons, allowing the agonist muscle to contract more effectively.
411
Why is the stretch reflex considered monosynaptic?
Because there is a single synapse between the sensory and motor neuron for the agonist muscle.
412
What sensory receptor initiates the withdrawal reflex?
Nociceptors (pain receptors).
413
Is the withdrawal reflex monosynaptic or polysynaptic?
Polysynaptic – it involves interneurons between sensory and motor neurons.
414
What is the outcome of the withdrawal reflex?
Flexion of the limb away from the painful stimulus.
415
How are muscles coordinated in the withdrawal reflex?
Excitatory interneurons activate flexor motor neurons, and inhibitory interneurons inhibit extensor motor neurons.
416
When is the crossed-extensor reflex activated?
Alongside the withdrawal reflex, when one leg lifts in response to pain and the other must support the body.
417
What distinguishes the crossed-extensor reflex?
It involves interneurons that cross the spinal cord midline to coordinate movement on the opposite side.
418
What happens on the contralateral side during the crossed-extensor reflex?
Extensors are activated and flexors inhibited to support posture and prevent falling.
419
What neurotransmitter is released by inhibitory interneurons in these reflexes?
GABA.
420
What type of motor neuron is involved in muscle contraction in these reflexes?
Alpha motor neurons.
421
Why is the patellar reflex clinically significant?
It is used to assess spinal cord integrity and peripheral nerve function.
421
What are central pattern generators (CPGs)?
CPGs are networks of neurons that produce intrinsic, rhythmic motor responses without input from the brain or sensory systems.
422
Can CPGs function without brain or sensory input?
Yes, they generate unconscious, repetitive motor outputs independently, but can be modified by brain signals.
423
Name three behaviors controlled by CPGs.
Breathing (diaphragm movement), walking (alternating leg motion), and swallowing (coordinated tongue/mouth muscle contraction).
424
Where are some CPGs located in the body?
In the brainstem (e.g., for respiration) and spinal cord (e.g., for locomotion).
425
How can CPG output be changed?
Descending signals from the brain can override or alter CPG activity (e.g., holding breath, changing walking style).
426
What is reciprocal inhibition in CPG circuits?
It's when activation of one muscle group (e.g., flexor) is accompanied by inhibition of its antagonist (e.g., extensor) on the same or opposite side.
427
How was CPG function demonstrated in cats with spinal cord transection?
Cats with thoracic spinal cord injury could still walk on a treadmill using only spinal CPGs, despite lacking brain input.
428
Describe the human case that supported the existence of spinal CPGs.
A paralyzed man developed involuntary rhythmic leg movements after rehab, consistent with locomotor patterns, despite no voluntary control.
429
How do CPGs contribute to locomotion?
They coordinate alternating contraction and relaxation of flexor and extensor muscles across both legs for smooth walking.
430
What role do excitatory and inhibitory interneurons play in CPGs?
They create reciprocal patterns by activating some motor neurons while inhibiting others, ensuring proper coordination of movement.
431
How do neurons in CPGs sustain rhythmic activity?
Some have pacemaker properties, allowing continuous depolarization and repolarization without external input.
432
Can sensory feedback or brain input influence CPG activity?
Yes, input from sensory neurons or brainstem can modulate CPGs to adjust speed, stop/start, or change direction.
433
During the patellar reflex, you measure a membrane potential change in the ipsilateral (same side of the body as the tapped knee) extensor motor neuron. What would you expect to measure?
IPSP
EPSP
EPSP
434
Proper functioning of a central pattern generator is dependent upon which of the following?
Motor neurons that cross the spinal cord midline
Inhibitory interneurons that cross the spinal cord midline
Input from the brain and brainstem
Inhibitory interneurons that cross the spinal cord midline
