Midterm #1 Flashcards
(136 cards)
1
Q
what causes flow to occur
A
occurs because of the existence of an energy gradient between two points
2
Q
how is the magnitude of flow related to gradients
A
the magnitude of flow is a direct function of the magnitude of the energy gradient(s)
3
Q
define the key principles
A
- flow is the movement of “substances” from one point in the system to another point in the system
- flow occurs because of the existence of an energy gradient between two points
- the magnitude of flow is a direct function of the magnitude of the energy gradient that is present – the larger the gradient, the greater the flow.
- more than one gradient can determine the magnitude and direction of flow
- there is resistance or opposition to flow in all systems
4
Q
what is the structure of the cell membrane
A
phospholipid bilayer
5
Q
what is the function of the cell membrane
A
- selectively permeable barrier
- sense and respond to external stimulus
- create electric potentials (change permeability of ions)
6
Q
what helps the cell membrane carry out its functions
A
trans membrane proteins (proteins in the membrane that facilitate transport)
7
Q
describe the anatomy of a phospholipid
A
phospho molecule head (hydrophilic head) and a diacylglycerol tail (hydrophobic tail)
8
Q
simple diffusion
A
substance passes directly through the membrane from a high concentration to a low concentration. the movement across the membrane (lipid soluble or protein channel with varying levels of specificity). It is a passive process!
9
Q
facilitated diffusion
A
high conc. to low conc. diffusion through the membrane requiring a carrier protein interaction that binds and moves a substance across. it is a passive process!
10
Q
active transport
A
low conc. to high conc. energy input and ATP help move something across, against a concentration gradient (usually)
11
Q
can simple diffusion occur through a protein?
A
yes
12
Q
describe a simple diffusion vs facilitated diffusion graph
A
1.2 slide 28
simple diffusion keeps going, facilitated diffusion plateaus
13
Q
go over the diagram 1.2 slide 38
A
14
Q
what is membrane potential
A
electrical difference (voltage) across the membrane when comparing the outside and inside of the cell. the convention is to refer to the voltage inside the membrane relative to the outside
15
Q
explain how the relative concentrations of sodium and potassium differ across a membrane
A
1.2 slide 48
16
Q
what is the ratio of sodium to potassium that is entering / leaving the cell
A
3 sodium out
2 potassium in
17
Q
a sodium ion is small enough to pass through the membrane - true or false
A
false, it could fit but the amphipathic cell membrane doesn’t let it
18
Q
why might an ion move from one side of the membrane to another
A
concentration gradients and electrical gradients
19
Q
how does water move through a cell membrane
A
a water channel. water can use simple diffusion either through the membrane (slower process) or through aquaporins
20
Q
answer question on 2.1 slide 10
A
21
Q
what does a membrane potential of -70 mV indicate?
A
the electrical difference in charge across the cell membrane –> the inside of the cell is 70 mV more negative than the outside
22
Q
describe leak channels with reference to sodium and potassium entering / leaving the cell
A
2.1 slide 13
leak channels are always open –> there are more potassium channels, which contributes to more positive outside of the cell (there’s also more positive going out than negative going in)
23
Q
what is the equilibrium potential of potassium
A
around -90 mV
24
Q
what is the equilibrium potential of sodium
A
around 60 mV
25
draw membrane potential
2.1 slide 14
26
explain equilibrium potential
the electrical charge strong enough to oppose that ion moving down its concentration gradient. the concentration gradient is equal and opposite to electrical gradient --> positive charged potassium wants to stay in the more negative inside of the cell (electrical gradient), but since there is a high concentration of potassium inside, naturally it would want to flow out (concentration gradient).
27
draw a representation of equilibrium potential
2.1 slide 14
28
draw an action potential
2.1 slide 14
29
the equilibrium potential for an ion is reached when the concentrations are equal on both sides of the membrane -- true or false
false
30
why is the cell membrane becoming more negative during the repolarization phase of an action potential?
potassium is moving out
31
draw a permeanle membrane and how membrane potential effects a single ion
2.1 slide 21
32
draw the differences in concentration and electrical gradients for an equilibrium voltage of -91 mV for potassium
2.1 slide 22
33
Nernst equation
calculates the electrical membrane potential required to oppose a single ion's concentration gradient.
essentially, it is the voltage required to create equilibrium for an ion with a concentration difference across a membrane.
it refers to a single ion's effect on membrane charger when crossing a membrane --> must be an ion, and must be a permeable membrane.
34
what would happen if the electrical membrane potential inside the cell was -94
the electrical gradient would be strong enough to oppose the concentration gradient and prevent potassium ions from diffusing out of the cell.
35
describe which way potassium ions diffuse when Ek = -94 and Vm = -100
2.1 slide 27
into the cell
36
if the calculated Nernst equation value was negative, what would be true of the ion under consideration
the membrane potential will be a negative number when it stops flowing. the ion could be positive with a higher concentration inside of the cell. the ion could be negative with a higher concentration outside the cell.
37
draw the options for 2.1 slide 29
38
what does the goldman equation calculate / how is it different than the nernst equation
the goldman equation measures the membrane potential of the cell by combining information about multiple ions.
39
a negatively charged ion with a higher concentration outside the neuron membrane will have a negative nernst potential value -- true or false. draw it
2.1 slide 35
false
40
draw the electrical and concentration gradients of a cell during depolarization
2.1 slide 36
41
draw the electrical and concentration gradients of a cell during repolarization
2.1 slide 36
42
during a depolarization, what happens if the sodium gates are opened at +50 and the maximum is at +61
2.1 slide 36
the membrane potential voltage keeps increasing until it hits +61
43
volatage-gated channels normally close, if the channel remained open... will the ion continue diffuse until equal concentrations on both sides?
no, the interior would keep getting positive and eventually repel sodium
44
a negatively charged ion with a higher concentration inside the neuron will have a negative nernst potential value -- true or false
2.2 slide 6
false
45
draw what it looks like on a graph when you open a sodium channel
2.2 slide 8
46
draw what it looks like on a graph when you open a potassium channel
2.2 slide 8
47
which way do potassium ions diffuse when Ek = -94 and Vm = -94
2.2 slide 9
no net movement
48
which way do potassium ions diffuse when Ek = -94 and Vm = -100
2.2 slide 9
net movement in
49
A typical cell contains [140 mEq/L] K+ inside the cell and [4 mEq/L] K+ outside. This leads to an equilibrium potential of -94 mV.
If we increased the inside concentration to 160 mEq/L, what would happen to the equilibrium potential?
2.2 slide 11
becomes more negative (e.g. -100)
50
draw what happens to equilibrium potential if the inside concentration becomes higher
2.2 slide 12
51
you discover a cell that has an AP like electrical activity. It has a resting membrane potential of 0 mV. It’s also unique in that it’s hyperpolarization (-50 mV) is equivalent to it’s peak depolarization (+50 mV).
If the unknown ions are:
L- higher concentration inside with EL: +39 M- higher concentration inside with EM: +62 N+ higher concentration inside with EN: -86
Which ion(s) could be responsible for the entire depolarization phase? draw how they would all react
2.2 slide 12
M- is responsible
52
you discover a cell that has an AP like electrical activity. It has a resting membrane potential of 0 mV. It’s also unique in that it’s hyperpolarization (-50 mV) is equivalent to it’s peak depolarization (+50 mV).
If the unknown ions are:
L- higher concentration inside with EL: +39 M- higher concentration inside with EM: +62 N+ higher concentration inside with EN: -86
Which ion(s) could be responsible for the entire repolarization phase? draw how they would all react
2.2 slide 16
N+ is responsible
53
when the neuron is at rest, what is true regarding voltage-gated sodium channels?
- the activation gate is closed
- the inactivation gate is open
- no sodium is moving through the cell
54
draw how voltage-gated channels react to an action potential
2.2 slide 21 / 22
55
draw an action potential and draw vertical lines to show the refractory periods
2.2 slide 28
56
how is the absolute refractory period related to ion channels? draw it.
2.2 slide 30
because of channel orientation
57
how do absolute refractory periods relate to one-way propagation
2.2 slide 36 /37
newly activated channels can't reactivate old channels due to channel structure during absolute refractory period.
58
draw the sodium potassium pump and explain how it works
EB1 first page
59
define cotransport (aka symport)
EB1 first page
sodium and another solute are moved across the membrane in the same direction
- sodium binds to a transporter along with another molecule
- transporter changes shape allowing sodium to move down its concentration gradient, pushing other molecules into the cell.
60
define counter-transport (aka antiport)
EB1 first page
sodium and another solute move in opposite directions
- sodium binds to antiport transporter on the extracellular side and moves into the cell down the gradient
- another ion binds on the intracellular side and is moved out of the cell against its gradient
- the transporter uses energy from sodium movement to drive the other solute in the opposite direction.
61
where do action potentials originate from
the axon hillock
62
describe the all or nothing principle
describes the fact that for action potentials, once the membrane potential threshold required to depolarize the cell has been met, a full action potential will occur, regardless of the size of the trigger.
63
explain how the five principles in the flow down gradients core concepts relates to an action potential
EB2 pg 1
64
how do the characteristics of graded potentials and action potentials differ
graded potentials: small and localized changes in membrane potential
action potentials: large scale all-or-nothing depolarizations of the membrane
65
how do the amplitude of graded potentials and action potentials differ
graded potentials: can be small or large in magnitude
action potentials: always the same amplitude of +30 mV
66
how do the duration of graded potentials and action potentials differ
graded potentials: can be either brief or prolonged for longer
action potentials: rapidly occurs in a short timeframe of approximately one to two miliseconds
67
how do the propagation distance that must be traveled differ between graded potentials and action potentials differ
graded potentials: localized and diminishes with distance
action potentials: propagated along the length of the axon without deteriorating
68
how do the stimulus of graded potentials and action potentials differ
graded potentials: various stimuli can trigger it, such as, neurotransmitter binding or sensory stimuli
action potentials: triggered when a threshold level of depolarization is met
69
how do the involved channels of graded potentials and action potentials differ
graded potentials: involves ligand-gated ion channels (proteins in the membrane of a cell that can open or close to aid the passage of ions)
action potentials: voltage-gated ion channels
70
how do the direction of change (inhibition vs. excitation) of graded potentials and action potentials differ
graded potentials: may be depolarizing (excitatory) or hyperpolarizing (inhibitory)
action potentials: always depolarizing which is followed by repolarization
71
how do the functions of graded potentials and action potentials differ
graded potentials: locally signals areas and integrates inputs
action potentials: used for long-distance signaling and rapid communication
72
During an action potential, what causes the sodium and potassium channel activation
gates to open? How is it that they open at different times? How does the sodium channel
close and what triggers this to happen?
an action potential triggers the conformational change of the sodium / potassium pump (which are voltage gated), allowing sodium ions to rush in. after the activation gate snaps open, the inactivation gate (which was already open) slowly closes. simultaneously, the potassium activation gate begins to open as the sodium inactivation gate closes.
73
draw the activation gates at different steps
EB2 pg.5
74
explain how once an
action potential is triggered, they then spread along a membrane
An action potential is initiated at a specific location (e.g., the axon hillock) when sodium ions enter the neuron, causing local depolarization. This depolarization spreads to neighboring areas, which, upon reaching a threshold, triggers the opening of voltage-gated sodium channels and regenerates the action potential in adjacent regions. This process repeats along the axon. The refractory period ensures that the action potential travels in one direction, preventing backward propagation. During the absolute refractory period, no new action potential can occur, while during the relative refractory period, it's harder but possible. Repolarization follows as potassium ions exit the neuron, restoring resting potential. In unmyelinated axons, this process occurs continuously, while in myelinated axons, the signal jumps between Nodes of Ranvier, speeding up propagation.
75
Unmyelinated Axons
Action potentials are regenerated at every point along the axon in a continuous
process. The signal travels slowly because it must depolarize each successive
section of the membrane.
76
Myelinated Axons
In myelinated axons, the axon is covered by a myelin sheath that acts as an
insulator to prevent ions from leaking out of the axon. The action potentials only
occur at the Nodes of Ranvier – a section in the myelin sheath where the voltage-
gated sodium and potassium channels are concentrated.
The action potential jumps from one node to another to significantly speed up the
propagation of the signal. This facilitates rapid communication along larger
distances.
77
how does axon diameter influence speed of action potential conduction velocity
Axons with larger diameters conduct action potentials more rapidly than
axons with smaller diameters. Larger diameters reduce the internal
resistance to the flow of ions (ex. sodium and potassium) within the axon,
which allows the electrical signal to travel faster. The greater the space
within the axon, the greater the efficacy of ion movement → increases
conduction speed.
78
how does myelination influence speed of action potential conduction velocity
Axons are insulated by myelin sheaths (myelination), which are produced
by Schwann cells in the peripheral nervous system and oligodendrocytes
in the central nervous system. Myelination increases the conduction
velocity because myelin acts as an insulator to prevent the leakage of
electrical signals. This process results in saltatory conduction, where
action potentials jump from one node of Ranvier (gaps in the myelin
sheath) to the next, specifically bypassing the myelinated sections. The
“jumping” of the signals dramatically increases the transmission speed,
compared to continuous conduction along unmyelinated fibers. Saltatory
conduction reduces the number of times the action potential must be
regenerated along the axon, whereas unmyelinated fibers must
continuously regenerate the action potential at every point along the
axon’s membrane in a much slower process
79
What is the role of calcium at the axon terminal of synaptic junctions?
* depolarization causes voltage-gated calcium channels to open, which allows calcium ions to flow into the axon terminal from the extracellular space.
* influx of calcium ions triggers calcium to bind to proteins on synaptic vesicles, such as synaptotagmin, which is involved in vesicle fusion with the presynaptic membrane. The interaction causes the synaptic vesicles, which contain neurotransmitters, to move toward and fuse with the presynaptic membrane in the process of exocytosis.
* Once the synaptic vesicles fuse with the membrane, the neurotransmitter contents
are released into the synaptic cleft.
* The released neurotransmitters diffuse across the synaptic cleft and bind to receptors on the postsynaptic membrane, which triggers a response in the
postsynaptic neuron.
80
Describe anion channels found in the postsynaptic membrane and the most
common ion to travel
* Primarily permit the flow of anions into the postsynaptic cell.
* Usually involved in inhibitory postsynaptic potentials (IPSPs).
When anions enter the cell, they make the membrane potential more negative (hyperpolarized), which reduces the likelihood that the action potential threshold is met and inhibits neuronal firing.
* The most common ion that travels through anion channels is chloride. When inhibitory neurotransmitters (ex. GABA or glycine) bind to receptors, chlorine channels open, which allows the chlorine ions to enter the postsynaptic
neuron → this hyperpolarizes the membrane and leads to inhibition
81
Describe cation channels found in the postsynaptic membrane and the most common ion to travel (does something bind to it?)
* Usually involved in excitatory postsynaptic potentials (EPSPs).
* When cations enter the cell, they make the membrane potential more positive, bringing it closer to the threshold for triggering an action potential.
* The most common ion that travels through cation channels is sodium → when a neurotransmitter (ex. glutamate or acetylcholine) binds to the
postsynaptic receptors, sodium channels open, which allows the sodium ions to flow into the cell. The influx of sodium depolarizes the postsynaptic
membrane, which contributes to the excitation
82
What happens *to the receptor* (and what type of receptor) when acetylcholine attaches to the channels on the post-synaptic membrane?
Acetylcholine binds to the nicotinic acetylcholine receptors that are located on the postsynaptic membrane, which causes a conformational change in the receptor and opens the ion channel.
83
When acetylcholine attaches to the channels on the post synaptic membrane, which ions can pass through, which cannot, and which ion has the greatest
number of particles move across the postsynaptic membrane?
* The nicotinic receptor (on post synaptic receptor) is a non-selective cation channel, so it allows the passage of multiple types of cations
* However, the nicotinic acetylcholine receptor is
not permeable to anions.
* Overall, sodium ions have the greatest net movement because there is a much stronger electrochemical gradient for sodium; both the concentration gradient (higher outside the cell) and the electrical gradient (negative inside the cell) favor sodium entering the postsynaptic cell.
* Potassium also moves but to a lesser extent. The concentration gradient drives it out of the cell; however, the electrical gradient (negative inside)
opposes its movement, which results in less overall potassium movement, compared to sodium
84
Explain what “excitatory postsynaptic potentials” (EPSP)
- An EPSP is a type of electrical signal that makes a postsynaptic neuron more likely to fire an action potential.
- Occurs when a neurotransmitter binds to the postsynaptic membrane and opens ion channels that allow positively charged ions to flow into the cell (ex. sodium).
- Causes a slight depolarization → the inside of the neuron becomes more positive. If enough EPSPs occur, they can bring the neuron’s membrane
potential closer to the threshold needed to trigger an action potential.
85
“inhibitory postsynaptic potentials “(IPSP)
* An IPSP is a signal that makes the postsynaptic neuron less likely to fire an action potential.
* Occurs when neurotransmitters open ion channels that allow negatively charged ions to enter the neuron (ex. chlorine) or positively charged ions to
exit the neuron (ex. potassium).
* Causes hyperpolarization, which makes the inside of the cell more negative and further from the threshold needed to fire an action potential.
86
How Graded Potentials Summate: spatial summation
a. Occurs when multiple synapses on the neuron are active at the same
time. The graded potentials from different locations on the
membrane of the neuron add up together.
b. If several EPSPs from different synapses add up, they can depolarize
the neuron enough to trigger an action potential. If multiple IPSPs
occur at the same time, they can combine to strongly hyperpolarize
the neuron and prevent it from firing.
c. Ex. if neurons A, B, and C all send EPSPs to a postsynaptic neuron
simultaneously, the combined effect may be strong enough to reach
the threshold.
87
How Graded Potentials Summate: temporal summation
a. Occurs when one synapse produces multiple signals in rapid
succession. The grade potentials generated in each accumulate over
time.
b. If EPSPs are generated close enough together in time, they can
combine to push the neuron over the action potential threshold.
Rapid IPSPs can sum to make the neuron more inhibited.
c. Ex. if neuron A fires several EPSPs in rapid sequence, each EPSP can
build on the last, which eventually leads to a depolarization that
triggers an action potential
88
draw spatial vs temporal summation and how they look on a graph
EB3 pg. 7
89
Axodendritic
A type of synapse where the axon of the presynaptic neuron connects to the dendrite of the postsynaptic neuron.
This is the most common type of
synapse and it typically involves the transmission of excitatory or inhibitory signals from one neuron to another.
Ex. the presynaptic axon releases neurotransmitters that bind to
receptors on the dendrites of the postsynaptic neuron.
90
Axoaxonal
The axon of the presynaptic neuron connects to the axon of another
neuron. Oftentimes, these types of synapses are modulatory in that they
can influence the strength or efficacy of signals being transmitted along
the postsynaptic axon when it fires
91
Axosomatic
Occurs when the axon of the presynaptic neuron forms a connection
directly with the soma of the postsynaptic neuron. Often, these synapses
have a strong influence on whether the postsynaptic neuron fires an
action potential because they are located close to the trigger zone of the
neuron (axon hillock)
92
One-Way Conductance (Unidirectional Propagation)
o The principle that the flow of information between neurons travels in
only one direction: from the presynaptic neuron to the postsynaptic
neuron.
▪ The presynaptic neuron sends the signal. When an action
potential reaches the axon terminal of the presynaptic neuron, it
causes the release of neurotransmitters into the synaptic cleft.
▪ The postsynaptic neuron receives the signal. The
neurotransmitters released by the presynaptic neuron bind to the
receptors on the postsynaptic membrane, which triggers the ion
channel gates to open, further leading to either depolarization
(EPSP) or hyperpolarization (IPSP) of the postsynaptic cell.
93
draw axodendritic vs. axosomatic vs. axoaxonic
EB 3 pg 9
94
where do neurotransmitters originate
released by neurons in the brain or nervous system
95
where do hormones originate
released by endocrine glands (e.g. adrenal glands, thyroid) into the bloodstream
96
where do neurohormones originate
released by neurons but functions more like hormones
They are produced in other areas of the brain, mainly in the hypothalamus, cerebral cortex and cerebellum.
97
how are neurotransmitters released
transmits signals across a synapse to target cells such as other neurons, muscles, or glands
98
how are hormones released
travels through the blood to distant organs or tissues where it exerts its effects
99
how are neurohormones released
released into the bloodstream
100
what is the function of neurotransmitters
facilitate fast, localized communication between neurons
101
what is the function of hormone
typically regulate long-term processes like metabolism, growth, and reproduction. they affect specific target cells that have receptors for certain hormones, often affacting the body more slowly than neurotransmitters
102
what is the function of neurohormone
Often regulate more
widespread physiological
processes. Combines
characteristics of both
neurotransmitters and
hormones, influencing distant
targets via the blood.
103
example of neurotransmitter
dopamine / acetylcholine
104
example of hormone
insulin
105
example of neurohormone
oxytocin
106
signal transduction
the process by which a cell responds to signals (such as hormones, neurotransmitters, or other signaling molecules) by converting the signal from outside the cell into a functional response inside the cell. The process typically. Involves binding of a signaling
molecule (the “first messenger”) to a receptor, which triggers a cascade of biochemical events
inside the cell → this leads to a specific cellular response. Signal molecules activate receptors
based on solubility
107
signal molecules activate receptors based on solubility --> lipid-Soluble Molecules
Lipid-soluble molecules (ex. steroid hormones like cortisol and testosterone)
can pass directly through the cell membrane because the membrane is
composed of a lipid bilayer. Once inside the cell, they bind to intracellular
receptors in the cytoplasm or nucleus.
b. The lipid-soluble signaling molecule-receptor complex often acts as a
transcription factor, directly influencing gene expression by binding to DNA and
regulating the production of specific proteins.
c. For example, cortisol enters the cell and binds to glucocorticoid receptors
inside the cytoplasm—the complex moves into the nucleus to regulate genes
that control metabolism and immune response.
108
signal molecules activate receptors based on solubility --> water-Soluble Molecules
a. Water-soluble molecules (ex. peptide hormones like insulin or
neurotransmitters like dopamine) cannot pass through the lipid bilayer of the
cell membrane. Instead, they bind to cell-surface receptors embedded in the
membrane.
b. When the signaling molecule binds to the cell-surface receptor, a signal
transduction pathway initiates, which often involves a second messenger (ex.
cAMP or calcium ions) that relays the signal inside the cell. The pathways can
trigger changes in enzyme activity, ion channel opening, or other cellular
responses.
c. For example, insulin binds to its receptor on the cell surface, which triggers a
cascade of events that leads to glucose uptake by the cell.
109
ionotropic receptors structure (what type of channel is it)
Ligand-gated ion channels (they are proteins that form a pore through the cell membrane)
110
metabotropic receptors structure
These are G-protein-coupled receptors or other similar proteins that do not form ion channels them themselves
111
ionotropic receptors mechanism
When a neurotransmitter or signaling molecule (the
ligand) binds to an ionotropic receptor, the
receptor undergoes a confirmational change, causing the channel to open and allow specific ions to flow through (ex. sodium or potassium).
112
what type of response is initiated by metabotropic receptors mechanism
* When a neurotransmitter binds to a metabotropic receptor, the receptor activates a G-protein on the inside of the cell membrane.
* This initiates a cascade of intracellular signaling, which often involves second messengers like cAMP or calcium ions → this then effects various cellular processes
113
ionotropic receptors speed
The action is fast, rapid, short lasting responses because ion flow directly affects the cell’s electrical state.
114
how long does metabotropic receptors mechanism last
Have a slower onset compared to ionotropic receptors, but their effects are usually longer lasting because they activate complex signaling pathways inside the cell.
115
what types of processes do ionotropic receptors control (what is their speed - what areas of the body use these)
Typically control immediate processes, such as muscle contraction or the propagation of action potentials in neurons
116
what is the speed of metabotropic receptors mechanism (what kind of responses do they mediate)
Involved in regulating longer-term cellular responses, such as changes in gene expression, metabolism, or modulating the sensitivity of neurons
117
draw ligand-agetd ion channel vs G-protein coupled receptors
EB1D pg. 5
118
describe a fast synapse
* Mediated by ionotropic receptors. When a neurotransmitter binds to an ionotropic receptor, the receptor acts as a ligand-gated ion channel that allows ions to flow directly through the membrane.
* An almost immediate change in the electrical potential of the postsynaptic neuron occurs, which makes the response very fast (within milliseconds).
119
describe a slow synapse
Involve metabotropic receptors that activate intracellular signaling cascades through G-proteins and second messengers
This process is slower (seconds to minutes) because it involves multiple steps before ion channels or other cellular processes are affected.
Slow synaptic responses regulate more sustained, long-term functions
The neurotransmitter dopamine acts on metabotropic receptors, which initiates a
slower effect on neuron function and behavior.
120
What are the two types of cholinergic receptors?
Nicotinic Cholinergic Receptors and Muscarinic Cholinergic Receptors
121
describe Nicotinic Cholinergic Receptors
onotropic receptor
b. When acetylcholine binds to nicotinic receptors, they function as ligand-gated ion
channels. Upon binding, the receptor undergoes a conformational change, opening
the channel and allowing ions (such as sodium or potassium) to flow through the
membrane.
c. The response is fast, and the binding of acetylcholine typically results in
depolarization of the postsynaptic cell, which leads to excitatory effects (ex.
muscle contraction).
d. Found in the neuromuscular junction (in skeletal muscles), the central nervous
system, and the autonomic ganglia
122
describe Muscarinic Cholinergic Receptors
* acetylcholine binds to muscarinic receptors, activating signaling pathways via G-proteins, which leads to a cascade of cellular events
* Slower response compared to nicotinic receptors and can result in either excitatory or inhibitory effects, depending on the receptor subtype.
* found in PNS (ex. heart, smooth muscles) and the
CNS.
* slow down the heart rate (inhibitory) or cause smooth muscle contractions (excitatory)
123
What are the two main classes of adrenergic receptors?
Alpha-Adrenergic Receptors and Beta-Adrenergic Receptors
124
Alpha-Adrenergic Receptors subtypes
Alpha one and alpha two receptors
125
Beta-Adrenergic Receptors subtypes
Beta one, beta two, and beta three receptors
126
what is the effect of Alpha-Adrenergic Receptors on the body
* Alpha one receptors typically cause vasoconstriction (narrowing of the blood vessels) when activated by norepinephrine or epinephrine, increasing blood pressure.
* Alpha two receptors often have inhibitory effects, reducing the release of neurotransmitters and decreasing sympathetic nervous system activity.
127
where are the different Beta-Adrenergic Receptors found
Beta one receptors --> the heart, where activation by norepinephrine and epinephrine increases heart rate and force of contraction (excitatory).
Beta two receptors --> smooth muscle (ex. bronchioles, blood vessels), where activation cause relaxation.
Beta receptors found in adipose tissue --> involved in lipolysis (breakdown of fat).
128
speed of Alpha-Adrenergic Receptors response
involves slower more sustained effects due to G-protein-coupled signaling pathways.
129
Beta-Adrenergic Receptors response
These receptors activate G- proteins that
stimulate or inhibit second messengers (like cAMP), resulting in diverse effects like increasing cardiac output or relaxing smooth muscle
130
where are Alpha-Adrenergic Receptors found
Found in various smooth muscles, blood vessels, and certain parts of the CNS
131
Beta-Adrenergic Receptors location
Primarily in the heart, lungs, and blood vessels
132
Alpha-Adrenergic Receptors type
Metabotropic
receptors (G-
protein
coupled)
133
Beta-Adrenergic Receptors location
Metabotropic
receptors (G-
protein
coupled)
134
Explain the basic mechanism of the G protein-coupled receptor system, including what happens
to an inactive G and the bound GDP when its associated receptor is activated
Resting (Inactive) State
o The G-proteins (composed of Gα, Gβ, and Gγ subunits) are associated with the GPCR
on the inside of the cell membrane.
o The Gα subunit is bound to GDP (guanosine diphosphate), which keeps the G-
protein in its inactive form.
2. Activation of the GPCR
o When a signaling molecule, such as a neurotransmitter or hormone (the ligand),
binds to the GPCR on the extracellular side of the cell membrane, the receptor
undergoes a conformational change. This change in the receptor’s shape allows it to
interact with the inactive G-protein (specifically the Gα subunit bound to GDP).
3. Exchange of GDP for GTP
o The conformational change in the GPCR triggers the Gα subunit to release GDP.
o Once the GDP is released, the Gα subunit binds to GTP (guanosine triphosphate),
which is abundant in the cell.
o Binding of GTP to the Gα subunit causes the G-protein to become activated.
4. Dissociation of the G-Protein
o Once the Gα subunit is bound to GTP, the G-protein undergoes a structural change
that causes the Gα subunit to dissociate from the Gβγ dimer.
o Both the Gα-GTP complex and the free Gβγ dimer can interact with downstream
target proteins in the cell, such as enzymes (ex. adenylyl cyclase) or ion channels, to
propagate the signal.
5. Signal Transduction
o The activated Gα-GTP and Gβγ subunits regulate various intracellular signaling
pathways:
▪ Gα-GTP often activates or inhibits enzymes that produce second messengers
(ex. cAMP).
▪ The Gβγ dimer can modulate ion channels or other signaling proteins.
o These downstream effects result in cellular responses, such as changes in enzyme
activity, gene expression, or ion channel opening.
6. Inactivation and Reset:
o The Gα subunit has intrinsic GTPase activity, meaning it can hydrolyze GTP back to
GDP. This process inactivates the Gα subunit, turning it back into its GDP-bound
form.
o Once the Gα subunit is bound to GDP again, it reassociates with the Gβγ dimer and
returns the G-protein to its inactive state.
o The GPCR can be reset for future signaling events after the ligand unbinds
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Adenylyl Cyclase Pathway
G-protein activation → G-proteins can either be stimulatory (Gs) or inhibitory (Gi)
for adenylyl cyclase.
i. Gs protein → when a ligand binds to a receptor coupled with a Gs protein, it
activates adenylyl cyclase.
1. Effect on adenylyl cyclase → increases its activity.
2. Second messenger → cAMP (cyclic adenosine monophosphate) is
produced.
3. Downstream effect → cAMP activates protein kinase A (PKA), which
then phosphorylates various target proteins to regulate functions
like metabolism, gene transcription, and cell proliferation.
ii. Gi protein → when a Gi-coupled receptor is activated, adenylyl cyclase is
inhibited.
1. Effect on adenylyl cyclase → decreases its activity.
2. Second messenger → less cAMP is produced, leading to decreased
activation of PKA.
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Phospholipase C Pathway (via Gq protein)
G-protein activation → the Gq protein activates phospholipase C (PLC).
i. Gq protein → upon activation, Gq stimulates PLC.
1. Effect on phospholipase C → PLC cleaves a membrane phospholipid
into two second messengers: IP3 (inositol triphosphate) and DAG
(diacylglycerol).
2. Second messengers →
a. IP3 → binds to receptors on the endoplasmic reticulum to
release calcium ions into the cytosol.
b. DAG → along with calcium, activates protein kinase C (PKC)
3. Downstream effect → calcium and PKC regulate numerous cellular
processes, including muscle contraction, secretion, and cell growth.
