Exam 1 - PNS (Everything not Brain & Spinal Cord) Flashcards
(229 cards)
1
Q
What are the 2 main nerves in the PNS?
A
Cranial nerves and Spinal nerves.
Cranial nerves (12) come directly off the brain Spinal nerves come directly off the spine
2
Q
What is the list of Cranial nerves? List the correct numbers and whether they are sensory, motor, both, and/or Parasympathetic.
A
- Olfactory Nerve (S)
- Optic Nerve (S)
- Occulomotor Nerve (M) (Para)
- Trochlear Nerve (M)
- Trigeminal Nerve (B)
- Abducens Nerve (M)
- Facial Nerve (B)
- Auditory Nerve (S)
- Glossopharyngeal Nerve (B) (Para)
- Vagus (B) (Para)
- Spinal Accesory Nerve (M)
- Hypoglossal Nerve (M)
Oh Oh Oh To Touch And Feel A Great Vagina Seems Hot
Some Say Marry Money But My Brother Says Big Books Matter More
3
Q
Which are the 3 nerves that participate in the Parasympathetic system?
A
- Occulomotor nerve
- Glossopharyngeal nerve
- Vagus nerve
OGV!
4
Q
What are the functions of each of the 12 Cranial Nerves?
A
- Olfactory Nerve (S) - Smell
- Optic Nerve (S) - Vision
- Occulomotor Nerve (M) (Para) - Eye Movement, tears, pupil constriction
- Trochlear Nerve (M) - Often attached to dorsal surface of Trigeminal
- Trigeminal Nerve (B) - Large, sends Motor info that moves jaw and brings in sensory info from Tongue.
- Abducens Nerve (M) - External rectus muscles of eyeball
- Facial Nerve (B)
- Auditory Nerve (S)
- Glossopharyngeal Nerve (B) (Para) -Mouth and tongue
- Vagus - Controls smooth muscles of the gut, lungs, and brings information from those muscles.
- Spinal Accesory Nerve (M) - Muscles of head, neck, shoulder
- Hypoglossal Nerve (M) - Tongue and neck
5
Q
What are the 2 different ways to distinguish functions of PNS?
A
Anatomical (cranial and spinal nerves) and Functional (autonomic and somatic).
6
Q
Where in the body does the somatic nervous system (of the PNS) affect functionally?
Is it voluntary or involuntary?
Where does it receive sensory information from?
A
The output of the Somatic Nervous system (voluntary) innervates the skeletal muscles.
It’s voluntary because these muscles move only when we plan on it.
It receives information from the skin senses and the striated muscles.
7
Q
Where in the body does the autonomic nervous system (of the PNS) affect functionally?
Is it voluntary or involuntary?
Where does it receive sensory information from?
A
The muscle component is smooth (organs) and cardiac (heart).
It’s involuntary.
It brings in information from all of my senses: ears, eyes, tastes, smells.
8
Q
What are the subdivisions of the PNS?
What is the subdivision of the Autonomic Nervous System?
Explain what activation to each component will do.
How do they differ anatomically in where they exit the CNS?
How do they differ in terms of first and second stage neurons?
A
Somatic and Autonomic.
Autonomic subdivides into Sympathetic and Parasympathetic.
-Both systems innervate the same target organs, BUT, they have opposing affects on the same organs.
ex.
Activation to the Parasympathetic (slows heart, independent activation of neurons)- Pupil Constriction
Sympathetic (speed heart, coordinated and quick activation of neurons)- Pupil Dilation
-They differ anatomically in where they exit the CNS:
Parasympathetic exits through Cranial or Sacral of spine
Sympathetic NS exits spine from Thoracic and Lumbar portion
——————————————————————————-
-The first stage neurons that come out of the the CNS in the Parasympathetic is relatively LONG and second stage that makes contact with the target organs is SHORT
The first stage neurons that come out of the the CNS in the Sympathetic is SHORT and second stage that makes contact with the target organs is LONG
> The point of contact between first and second stage ganglia are all lined up adjacent to the spinal cord and all in contact (string of beads) with each other.
9
Q
Why is there a different Anatomical set-up between the systems in the Autonomic Nervous System?
hint: which one has a coordinated activation, and why is that important?
A
Fight or Flight.
For the Sympathetic NS, the response must be coordinated and happen AT THE SAME TIME. We will have to speed up our heart rate to pump oxygen and glucose into our blood, so that it can feed the muscles that will let us RUN!
10
Q
When we are in a relaxed state listening to a bio psych lecture, which one of the systems is more dominant:
Sympathetic or Parasympathetic?
A
Parasympathetic.
Mnemonics: Paramedics will tell you to chill… relax…
11
Q
Which part of the Autonomic nervous system are the ganglia, or the point of connection between the first and second stage neurons, connected?
A
In the Sympathetic nervous system, connected and lined up as a string of beads outside the spinal cords - when you activate 1 ganglion, you activate all of them.
12
Q
What’s the difference between a nerve and a tract?
A
Tract = CNS Nerve = PNS
13
Q
What bilayer is the neural membrane cell comprised of?
What is the process that created these cells called?
What’s the benefits of this type of cell structure?
A
Neural membrane of a cell is comprised of a Phospholipid bilayer. It’s made by head and tails of a phosphate group… Since the heads are hydrophilic (water lover) and tails are hydrophobic (water hater)- the pressure between them caused them to fold in on each other in a process called Invagination.
The benefit of this type of cell is that it’s fluid. It is semi-permeable because SOME things can go through this layer and some cannot. It is also ‘fluid mosaic’ so that ions and proteins can travel freely without wasting energy.
14
Q
What are the 2 pores that go through the cell membranes?
A
Ion channels which allow specific ions to go into and out of cells.
Ion pumps look the same but use energy to “pump” where ion channels don’t.
15
Q
Explain the internal structures of the cell body starting from:
Nucleus DNA Cytoplasm Endoplasmic Reticulum ---> Ribosomes (2) Golgi Apparatus ----> Enzymes Mitochondria Lysosomes Cytoskeleton ---> Microtubials and Microfilaments ---> Kinesin
A
> The nucleus, encased in it’s own phospholipid bi-layer, and unlike the cell bodies, it has holes in it to allow for the ion channels.
> The DNA for every single cell is INSIDE the nucleus.
> Cytoplasm fills the cell to give shape and allow travel throughout the cell.
> Endoplasmic reticulum surrounds the Nucleus because it is considered the factory of the cell. It makes the product that the cells themselves need AND what the cells need to export.
There are 2 types of Endoplasmic reticulum:
1) Smooth - No Ribosomes, manufactures Lipids
2) Rough - Ribosomes (why it’s rough texture).
Ribosomes (factory) are protein based molecules that MAKE protein and attach to the Endoplasmic reticulum as well as float freely in the Cytoplasm.
> Once the protein and lipids are made, it needs to be exported outside of the cells and must be packaged - Golgi Apparatus is lipid based packagers that transport around and export out of cell. Packaging the cell is important because there are Enzymes in the cytoplasm that will tear things apart and recycle them.
> Mitochondria produces the cells energy. It has it’s own DNA separate from the nuclear DNA… is Mitochondria alien?? It IS providing us energy while we provide it nutrients and protection…
> Lysosomes are produced by the Golgi Apparatus, inside of the Cytoplasm. They are vesicles filled with enzymes that are used for cell maintenance. They destroy portions of the cell itself (apoptosis).
> Within the Cytoplasm and throughout the cell, the Cytoskeleton resides - Microtubials (extends across space within cell) and Microfilaments (attach to structures within the cell). Microtubials are the roads of the cell. It’s found along Axons to give structure and allow for transportation of the proteins. Vesicles move along the Microtubials by binding to Kinesin (strands of twisted protein and their free ends on both top and bottom attach to a vessicle and walk up and down a microtubial). This is a nano-machine!
If a substance (neurotransmitter) is moved from cell body down to axon terminal - Anterograde transport
If a substance (neurotransmitter) is moved from the axon terminal to cell body - Retrograde transport
Through a chemical signal, Microfilaments can detach and push parts within the cell.
16
Q
When a cell is signaling that it’s ready to die, which component within the cell body will help it on it’s way?
A
Lysosomes are produced by the Golgi Apparatus, inside of the Cytoplasm. Lysosomes are vesicles filled with enzymes that are used for cell maintenance. For injured cells that are beyond the point of repair, Lysosomes will split themselves open to release the enzymes into the cytoplasm and the cells are consumed completely in response to a chemical signal produced by the dying cell… aka Apoptosis (cell suicide).
Basically, Lysosomes help to “euthanize” cells and assist in their suicide by using their own enzymes (they shoot up the cell). They guard the cell by recycling the cells.
Mnemonics: LYSOL-somes - LYSOL kills bacteria.
17
Q
Describe the 4 main parts of a Neuron.
A
- Soma - Houses Nucleus
- Dendrites - Receptors of information either directly from sensory (skin), or through other Neurons.
- Axons - Electrical signal (Action Potential)
- Axon Terminals - Communicates with the other neurons, muscles, or glands.
18
Q
Where is the Action Potential generated?
A
At the Axon Hillock
19
Q
What’s the difference between Unipolar, Bipolar, and Multipolar Neuron?
Where are they found?
A
Unipolar - Has 1 process that leaves the Soma. It splits into 2 portions, 1 dendrite and 1 terminal. Found in Sensory, Motor, PNS.
Bipolar - 2 processes that leaves the Soma. 1 has Dendrites on one end and terminals on the other end. Found in Sensory (retina, cochlea).
Multipolar - Multiple processes that leaves the Soma. 1 single Axon with multiple dendrites. The Axon itself can split into multiples.
20
Q
What is it called when an Axon splits?
A
Collateral
21
Q
What are the 3 types of functional variations of Neurons?
hint: how do neurons transmit information??
A
- Sensory (Afferent) neurons transmit info INTO the CNS from sensations
- Motor (Efferent) neurons transmit into AWAY from CNS into muscles and glands
- Interneurons that act as a bridge between sensory and motor neurons. They don’t directly work with sensory or motor. This is the most common.
22
Q
How are Glial cells different from neurons?
A
Glial cells make up about 10 to 1.
They don’t conduct electrical signals like neurons do.
23
Q
What are the 2 divisions of the Glial Cells?
A
Microglia
Macroglia - Astrocytes, Oligodendrocytes, Schwann
24
Q
What is Microglia’s main 2 functions?
hint: phagocytes
A
Main function is in the immune support of the brain - inflammatory response.
> They are phagocytes which engulf and destroy things in the extracellular fluid.
Pretty much the “police” and check to make sure the cell belongs there (do you have a brain tag?) - if not, it eats it up and then spits up the cell’s amino acids and carbo chains back into the extracellular fluid for recycling or waste.
> Within the extracellular fluid, Microglia regulates and stabilizes concentration of ions which allows us to use chemical signaling.
Mnemonics: (P)hagocytes - (P)olice
Micro-(PH)one - Micro - (PH)ag… sounds catchy?
25
What are the functions of Astrocytes? hint: communicates, recycles, balances glucose, BBB.
Astrocytes wrap around blood vessels within the brain and neurons - forms connection between the blood and the neuron and it wraps around the points of connection bw 2 neurons to isolate the individual synapses so things remain private...
Recycles: Pulls neurotransmitters out of synapses and send it back to the neurons as well as hold onto them and release them at will.
Astrocytes keep blood sugar balanced: Astrocytes pre-process glucose and oxygen from the blood to deliver to the neuron so it's in an instantly usable form. It also stores the glucose (energy) to give it to the neuron!
Blood brain barrier: Layer of protection like the pia mater to keep bad things away from neurons.
26
Are astrocytes capable of communicating?
Yes, astrocytes can pull and release chemicals from synapses. They can affect the communication. For example, if the neuron releases too much chemical signal, the astrocyte can make the signal weaker and vice versa.
27
What is the epithelial cells referring to in connection to Blood Brain Barrier?
Epithelial cells make up blood vessels. These cells have gaps between them which allow things like glucose to freely flow in and out of the blood.
However, cells in the brain does not have the gaps, so large protein cells cannot penetrate through the epithelial cells.
Another layer coming from the astrocyte regulates what can get out of the brain tissue.
28
Give an example of an area with a "weak" blood brain barrier with less astrocyte covering blood vessels in the area. Why would we have a system like this?
The Area Postrema is there to accurately evaluate what is in my blood. It is near the 3rd ventricle and area that induces vomiting when toxins are detected. It's important to get rid of the poisons before it gets worse.
29
Glial cell Oligodendrocytes function, structure, and appearance.
Produces Myelin for CNS neurons.
Paddle-like.
Function: Myelinates multiple axons.
30
Glial cell Schwann Cell function and appearance.
Produces Myelin for PNS.
Flat, pancake-like.
Function: Myelinates 1 axon at a time.
31
Explain Mitochondria's role within the cell.
>Mitochondria produces the cells energy. It has it's own DNA separate from the nuclear DNA... is Mitochondria alien?? It IS providing us energy while we provide it nutrients and protection...
Mnemonics: MIGHTY-chondria - It's mighty, full of energy!
32
Explain the Endoplasmic Reticulum and what it's considered within the cell structure. What do they produce?
>Endoplasmic reticulum surrounds the Nucleus because it is considered the factory of the cell. It is PRODUCER and makes the product that the cells themselves need AND what the cells need to export.
There are 2 types of Endoplasmic reticulum:
1) Smooth - No Ribosomes, manufactures Lipids
2) Rough - Ribosomes (why it's rough texture).
Ribosomes (factory) are protein based molecules that MAKE protein and attach to the Endoplasmic reticulum as well as float freely in the Cytoplasm.
Mnemonics: Endo PRODUCER (R)eticulum - EndoPLASMIC (R)IBOSOMES.
33
Explain what the Cytoskeleton does and it's 2 parts. Be specific about each role.
If a substance is moved from cell body down to axon terminal - it is considered what type of transport?
If a substance is moved from the axon terminal to cell body - it is considered what type of transport?
hint: nano-machines
>Within the Cytoplasm and throughout the cell, the Cytoskeleton resides - Microtubials (extends across space within cell) and Microfilaments (attach to structures within the cell). Microtubials are the roads of the cell. It's found along Axons to give structure and allow for transportation of the proteins. Vesicles move along the Microtubials by binding to Kinesin (strands of twisted protein and their free ends on both top and bottom attach to a vessicle and walk up and down a microtubial). This is a nano-machine!
If a substance is moved from cell body down to axon terminal - Anterograde transport
If a substance is moved from the axon terminal to cell body - Retrograde transport
Through a chemical signal, Microfilaments can detach and push parts within the cell.
34
How does MS occur?
Immune system attacks Myelin.
MS can resolve itself if the immune system stops attacking myelin, the myelin can grow itself back with immune suppressors.
Apoptosis can send signals to lysosomes to totally kill off the neurons-permanent apoptosis.
35
What is Myelin?
What is it made of?
Allows electrical signals move faster, saves neurons energy by keeping ionic concentration stable.
Made of lipids and small protein.
36
What are the 2 different Neural Communications?
What is Neural communication considered?
Between neurons - Chemical (neurotransmitter, signal goes TO neurons)
Within neurons - Electrical (signal goes THROUGH the neuron)
Neural communication is Electrochemical.
37
Define 'ion'. How does ion affect the way cells move?
A charged particle that is either positive or negative.
Depending on whether the cell is positive or negative, it will move differently.
38
What makes intercellular and extracellular fluid different from one another?
The concentrations of ions!
39
Describe Resting Membrane Potential. What does it mean i
Define depolarization and hyper-polarization.
What does it mean if the RMP is -65mV?
Measurement of the electrical potential INSIDE of the cell relative to the OUTSIDE of the cell. Just a measurement of difference, not an absolute value.
>Depolarization - what happens to the RMP if you apply positive charge to membrane, making the difference between in and out more same.
Hyperpolarization - the membrane becomes more negative during hyperpolarization so the diff. bw inside and out is GREATER.
>ie; If the RMP is -65mV, it just means that the difference of electrical potential on the inside of the cell is -65mV LESS than the outside.
40
What type of transport is it when a substance is removed from the cell body down to the axon terminals?
Terminal to the cell body?
Anterograde transport is when a substance is removed from the cell body to the axon terminal.
Retrograde transport is when a substance is removed from the axon terminal to the cell body.
41
Describe the structure of a sensory neuron. Explain where this neuron might reside in and how it would transmit information.
Sensory neurons are the most simple - they are bipolar neurons and found in the retina of the eye for example.
It has a single dendrite and single short axon.
The bipolar neurons transmit afferent sensory info from the retina's light receptors to the neurons that carry the information to the visual centers of the brain.
42
Describe the structure of an interneuron. Explain where this neuron might reside in and how it would transmit information.
They are also called association cells because they have an association between the sensory and motor neurons.
The pyramidal cell has 2 sets of dendrites - one from the apex of the cell body and one from its sides. These interneurons carry information from the cortex to the rest of the brain and spinal cord.
43
Describe the structure of a unipolar neuron.
What type of process do they have?
Where would you find these neurons?
There's only 1 process that leaves the soma, but splits into one portion (dendrites) and one portion (axons).
Found in sensory and motor neurons - so the dorsal horn's dendrites extend out to the skin, the cell bodies are in the dorsal horn, and the terminals are in the spine.
44
Describe the structure of a multi-polar neuron.
What type of process do they have?
Where would you find these neurons?
Multi-polar neurons have multiple processes coming off the soma - all but one is dendrites. The single one is axon (the axon itself can split into multiple axons or axon collateral).
45
What is happening with neurons during someone who suffers from MS?
Neurons are dying because they are not getting a "talk back" signal due to lack of myelin (since the system is attacking it's own myelin due to odd immune system issue). They die without communication. They are hella social.
46
How does Dr. Trevitt define neurocommunication?
What allows us to move our muscles and to respond to our environment.
47
True or false: Neural communication flows anterograde or retrograde.
False - that applies to neurotransmitters, but NOT neurons. Electrical communication flows just 1 way.
48
How are neurons unique in the way they transmit their signal?
They have the ability to transmit electrical signals which most cells can't.
49
Why is the potential of the extracellular fluid different from the potential of the intracellular fluid?
Because the ion concentrations (and electrical charges) are different!
50
What are the 2 ways to anatomically categorize neurons?
Shapes: Unipolar, Bipolar, Multipolar
Function: Afferent and Efferent
51
Why is the inside of the cell more negative than the outside?
The charged particles (ions) concentrations found between the 2 different fluids.
52
What is more negative, the intracellular or extracellular fluid?
The intracellular fluid is more negative.
53
What are the ion charges of the following ions:
Sodium
Potassium
Chloride
Sodium - Positive
Potassium - Positive
Chloride - Negative
54
How is the extracellular fluid similar to sea water?
Since we were made from seawater, our extracellular fluid is composed mostly of positive ion Sodium and negative ion Chloride.
55
If Potassium is positively charged, why does it hang out inside of the intracellular fluid? How come it doesn't hang with it's homie Sodium?
There are protein molecules which are in the cell which are negatively charged.
56
What does movement of ions in the membranes create?
Electrical signals.
57
Describe the forces that make Ions move.
Diffusion AND Electrostatic Pressure.
58
Describe diffusion and which ion participates in this action.
Ions like elbow room and spreads out from like ions.
Move from HIGH concentration to LOW concentration.
Ex) Sodium does NOT like it's own kind. Does not care about Chloride.
Diffusion is about CONCENTRATION (gradient).
59
Describe electrostatic pressure and which ion participates.
Seeks out Opposite charges. Repelled by the same charged ions.
Ex) Neg. charged ions are attracted to Pos. charge.
Electrostatic is about CHARGE.
60
Use sodium as an example and describe its diffusion and electrostatic behavior.
Sodium does not want to be with other Sodium (diffusion - get away from its own) but also doesn't want to be with Potassium (electrostatic - repelled by same charge)
Attracted to Chloride (negative charge).
61
What happens to the negatively charged proteins when the ion channels open?
Nothing, they're too large to go through the channel - they keep the intracellular NEGATIVE.
62
If we open a Potassium channel when the membrane is at resting potential? Explain what the diffusion and electrostatic forces do.
Due to Electrostatic pressure, K+ will stay inside since opposite attracts.
Makes sense that the force of diffusion will push the potassium out since the concentration of K+ is so high inside, and there IS A LEAK, but overall not much movement.
63
If we open a Chloride channel, where does it go? Explain what the diffusion and electrostatic forces do.
Diffusion forces pushes it INTO the cell (too many on the outside) while Electrostatic pressure pushes it out (Chloride is negative like the inside)
Not a lot of movement with Chloride.
64
If we open a Sodium channel, where does it go? Explain what the diffusion and electrostatic forces do.
Diffusion pushes the sodium INTO the cell to spread itself out.
Electrostatic forces also push the sodium INTO the cell because it's positive charge is attracted to the negativity.
65
What is the only channel when open, makes a difference in the RMP? Why?
Sodium channels. Because, it's actually moving due to diffusion and electrostatic pressure.
66
What are the 3 types of channels?
Describe them all.
Voltage-gated channels: Will open or close when membrane it's embedded in reaches a specific voltage.
>Depends on the membrane potential
Transmitter-gated: This gate only opens if there is a neurotransmitter bound to it.
Some channels have BOTH gates (ie; the membrane has to be at a certain potential AND it has to have a neurotransmitter bound to it for it to open).
67
What are ion channels comprised of?
Ion channels are comprised of protein subunits, and span the membrane.
68
How specific are ion channels?
Very specific. Only let 1 ion per channel.
69
What is Depolarization also known as?
Excitatory Post-Synaptic Potential
70
What is Hyperpolarization also known as?
Inhibitory Post-Synaptic Potential.
71
How are the names EPSP and IPSP derived?
Derived from the effects of these changes in the membrane potential in the next cell in the chain and how likely the next membrane will have an action potential.
72
Which potential makes it more likely for the next neuron in the chain to have an action potential?
Depolarization (EPSP) makes it more likely for the next neuron to have an action potential, while hyperpolarization (IPSP) makes it less likely.
73
What does it mean when a cell is depolarizing?
What does it mean when a cell is hyperpolarizing?
Ie: what's the inside of the cell relative to the outside?
Depolarization aka EPSP (excitatory post synaptic potential) describes when the inside of the cell is becoming more positive. (and more similar because it’s closer to the extracellular fluid).
Hyperpolarization aka IPSP (inhibitory post-synaptic potential) describes when the RMP becomes more negative inside relative to outside.
74
What does threshhold mean? What happens during threshold?
When a cell is depolarized to threshold, an action potential is produced. This is when the sodium and potassium channels open up.
75
-65 -> -70 , depolarized or hyperpolarized?
Hyperpolarization of the cell membrane. The resting potential goes down!
76
-65 -> -60 , depolarized or hyperpolarized?
Depolarization of the cell membrane. The resting potential goes up!
77
What accounts for the rise and fall of an action potential?
The opening of sodium channels and potassium channels in the neural membrane accounts for the rise and fall seen in a recording of an action potential.
78
What does it mean when the sodium and potassium channels open up?
Threshold has been reached
79
Which area, if threshold is met, will trigger an action potential?
What happens with the ions?
If change in Membrane Potential exceeds threshold at the axon hillock, there will be an AP.
This is when the sodium channels open.
80
What is a refractory period?
Limits cells firing during this time.
81
How does the axon hillock evaluate whether to trigger an AP or not?
Calculator:
Each synapse will signal the synapse right next to it, changing the membrane potential.
Evaluates (sums) all input to the neuron over a given time period (~msec) and determines if overall change in membrane charge exceeds threshold.
82
What is passive conduction?
What does this have to do with the axon hillock?
When energy shot from the action potential is super fast but disappears quickly.
The axon hillock sums up all the passive conductions and sums them up to see overall change in the membrane potential.
Therefore, synapses closer to the axon hillock have more of a say than the ones out in the boondocks since their signals are weaker.
83
What does it mean when synapses are strengthened due to practice or learning?
The synapse connection in certain neurons become stronger because the synapses migrate closer to the axon hillock.
84
Why is AP considered a transient reversal?
Transient - doesn't last forever, quick
Reversal - the cell membranes change concentration of ions
85
What's happening with ions during AP?
Na+ rushes into cell via voltage-gated channels (diffusion + electrostatic pressure)
Influx of Na+ (100 million ions/sec) raises membrane potential to ~40mV
Voltage-gated K+ channels open
K+ rushes out of cell (diffusion + electrostatic pressure)
At peak of AP, Na+ channels become refractory
K+ continues to leave cell, driving MP down
Membrane becomes hyperpolarized, K+ channels close, Na+ channels reset
Extra K+ outside diffuses away, Na+/K+ pump works to restore MP back to RPM
86
What does active and passive conduction mean for a myelinated axon?
What are it's advantages and disadvantages?
What does it mean when there's a mix of active and passive conduction?
Active AND passive conduction = saltutory conduction.
Myelin (fast) and Nodes of Ranvier (passive)
advantages and disadvantages temporal and spacial summation
Passive conduction: Fast and cheap; Energy Dissipates
Active conduction: Never lose signal; Slow and expensive.
87
What does the sodium-potassium pump do?
It restores the ion concentrations so that the next time an AP is to start again, sodium can be drawn into the cell by both diffusion and electrostatic pressure. Before the sodium-potassium pump cleans up the mess, there's too much sodium inside of the cell already, so diffusion would not allow sodium to enter again.
88
What is going on during absolute and relative refractory period?
During absolute refractory periods, it limits action potentials. The absolute refractory period is when a neuron cannot produce another action potential during this period, since an action potential is already occurring at this time.
During the relative refractory period, the resting membrane is in a hyperpolarized state. Starting an action potential at this state will require a larger depolarization, or a greater stimulus than usual.
89
Define synapse.
A synapse is a point of communication between two neurons.
90
What's the difference between electrical synapse and chemical synapse?
Electrical synapses are characterized by very tiny synaptic gaps crossed by ion channels from the pre- and postsynaptic neurons.
Chemical synapses involve the release of neurotransmitter by the presynaptic cell.
91
How does calcium act when calcium channels open? Why is this important for the process of changing from an electrical signal to chemical?
When calcium channels open, it acts like sodium since Calcium is in higher concentration outside of the cell and is positively charged (both diffusion and eletrostatic pushes it into the cell)
It causes the vesicles hanging out in the axon terminals to dock /attach to the inner surface of the terminal membrane, once attached it cleaves them open to spill their contents into the space in the synapse between the pre and post- synaptic cell...
The vesicle membrane is continuous with the terminal membrane (made of same stuff).
92
What is a physical limitation of an electrical synapse?
The pre-synapse has to be larger than the post. So the absolute change will depend on the volume.
93
What's good about chemical synapses?
More flexible
| Most prevalent type of synapse
94
What is pinocytosis? Where does it happen?
It happens in the upper portion of the terminals.
The cell membrane is pinched in for new vesicles to form which is then filled to either be transported to the soma to be filled up there or just in the terminals depending on the neuron.
This is the process where the electrical signal becomes chemical.
95
What's the difference bw an EPSP and IPSP?
EPSP will depolarize and IPSP will hyperpolarize if the cell is at RMP.
96
Why should you not eat fugu?
The neurotoxins BLOCK sodium channels which prevent AP,
97
At approx. +40mV, what happens to the sodium channels?
It becomes refractory.
The AP is at it's peak - the sodium channels trap door shuts (but it's still open). Potassium rushes in.
98
What brings the AP down?
The potassium starts to exit the cell.
99
Why is the undershoot so important in the AP?
It resets the sodium channel. During hyperpolarization, the sodium channel closes all the way, and the "trap door" won't swing down again until below the RMP.
100
What is the Na+/K+ pump? What does it do?
Restores the initial ionic concentration.
101
What is the difference between and electrical synapse and a chemical synapse?
The electrical synapse between the cells is much smaller and it's very LIMITED in what type of information it can exchange (basically just ionic concentration changing the membrane potential. SIZE RESTRAINTS (pre must be bigger than post). They are VERY FAST.
Chemical synapse is SLOWER because of the greater distance between synapses.
It's much more FLEXIBLE in communication with the post-synapses.
102
Why is calcium so important for synaptic communication?
Neurotransmitters can't release unless calcium attaches to the vesicle to open it up.
103
How does action potentials actually START in regards to summation?
The inputs from adjacent synapses will either produce EPSPs or IPSPs in that specific area of the membrane adjacent to the synapse-that change in membrane conducts the signal through passive conduction
104
How do NT reactivate?
Re-uptake
Enzymes
Diffusion
Astrocytes - sucks up NT and releases them at will
105
Describe the 3 types of synapses and which is most powerful.
Axo-exonic - Axon terminal to axon terminal most powerful
Axo-somatic - axon terminal to soma
Axo-dendritic - axon terminal to dendrite
106
How does drugs affect Neurotransmitters? (5)
```
Neurotransmitter synthesis
Neurotransmitter storage
Neurotransmitter release
Receptors and Channels
Reuptake and enzymatic deactivation
```
107
Where does EPSPs and IPSPs sum to be determined whether the overall sum is enough to trigger an AP?
The site of the axon hillock. This is where it will determine if the sodium channels should open.
108
How can a single pre-synaptic neuron produce a change in a post-synaptic neuron (produce AP)?
Through temporal summation - one neuron fires repeatedly, and the potentials that are created each time is summed up with the potentials of others to make a larger change in potential.
109
How does EPSPs and IPSPs cancel each other out?
As they are summed up at the axon hillock site, they can be even, thereby canceling out.
110
What's the main difference between an IPSP/EPSP and an AP?
EPSP and IPSPs can be graded potentials while APs are all or nothing.
You can have a large or smaller change in a membrane potential depending on how large or small an EPSP was.
111
What is the difference between presynaptic facilitation and presynaptic inhibition in relation to axo-exonic synapse?
Presynaptic facilitation and inhibition refers to how much NT is released at the synapse.
An Inhibitory input will increase the amount of NT released, while the Excitatory input (depolarization) will decrease the amount of NT on a specific synapse because of the "jump" from the already depolarized axon which is losing it's power...
This influences how much calcium gets in... so smaller jump = smaller calcium entry = less NT released.
112
What are the 2 different postsynaptic receptors?
Ionotropic receptors = physically located ON an ion channel
Metabotropic receptor = stand-alone, not physically coupled to an ion channel
113
Explain metabotropic receptors and it's couple-system.
Coupled through an ion channel through the messenger system called G protein, which happens inside of the postsynaptic receptor.
114
Will you be more able to produce an AP during a EPSP or IPSP?
Explain using example of sensory to motor neuron.
EPSP - stimulating a sensory fiber for example will produce a depolarization on the motor neuron to which the fibers connect.
IPSPs will increase the charge on a membrane away from the threshold level
115
What question does Summation of graded potentials answer?
How do both the EPSP and IPSP interact? What if there are 2 EPSPs in succession? Does it matter if the time bw them is increased or decreased? What happens if an EPSP and IPSP arrive together?
116
Acethylcholine ___________ heartbeat.
Where is this found?
Inhibits heartbeat when activated - it is in the neuromuscular junction.
117
How does ACh work in the somatic and autonomic system?
ACh activates the skeletal muscles in the somatic system, which in turn either excites or inhibits the autonomic system
118
What is epinephrines function and what is it produced by?
It is adrenaline and is produced by the adrenal glands - raises heart beat.
119
What is dopamine's role in Parkinsons' Disease?
When levels of dopamine is reduced of normal levels, it can cause parkinsons.
120
How does ionotropic receptors respond when a NT binds to it?
The ion channels open.
121
What is an advantage of an ionotropic receptor?
The change in the channel (to allow ions to flow) happens as soon as the NT binds to the receptor.
122
How is metabotropic receptors set-up?
The protein which has the receptor site on it is actually inside of the synapse and works in a 2-step process with a G protein system.
When a NT binds to the metabotropic receptor, it triggers the G protein. A part of the G protein segment breaks off into the intracellular side of the post-synaptic cell then it binds to an ion channel which will then open or close the ion channels.
123
What are all of the advantages of metabotropic receptor?
Amplification of signal -instead of opening up 1 ion channel, it can open up 10.
Sustained, ion channels will be open longer due to the G protein hanging onto the channels. Effects will last longer.
3. The G protein systems can do more than just open ion channels- can also activate: protein synthesis, gene transformation, calcium release from internal vesicles.
124
What is a disadvantage of metabotropic receptor?
It costs a lot of energy.
125
Describe diffusion and it's effects.
Diffusion usually occurs with neuromodulators and neurohormones
126
Describe deactivations of NT.
Deactivation by enzymes within the synapse
Reuptake - Presynaptic terminal membranes have TRANSPORTERS that suck up the NT to put it back into the vesicles in the presynaptic terminals.
127
When a NT is bound to a receptor on a membrane, what are 1 of 2 things that happens?
Either depolarize (EPSP - opens Na+ channels) or hyperpolarize (IPSP - opens Cl- or K+ channels)
128
What are the 3 broadest signaling chemicals?
NT
Neuromodulators
Neurohormones
129
How do we distinguish the 3 different signaling chemicals?
The distance between the point of release and it's target receptor site.
130
What distance do the 3 signaling chemicals travel?
NT travel length of synapse
NM travel further and binds to receptors on surrounding area
NH travel farthest, into the bloodstream until they meet their receptors
131
What is the oldest NT amino acid proteins?
Glutamate and GABA
132
What is the major excitatory NT in the CNS?
Glutamate!
133
True or false? Glutamate is an EPSP, therefore produces depolarization all by itself.
False. It's not the NT molecule but the receptor which determines the effect.
Every time Glutamate binds to it's receptor, it produces a depolarization (EPSP) - but doesn't have ANYTHING to do with Glutamate. It just happens that the receptors get stimulated by Glutamate and produce an EPSP.
134
What is the NMDA receptor involved in?
It is involved in learning.
135
What type of NT is GABA in the CNS?
It is an inhibitory NT. When stimulated, it produces IPSPs.
136
How many receptor areas does GABA have? What are they?
How long have they been around?
4
1. Alcohol
2. Benzodiazepine (valium, xanax)
3. GABA
4. Barbiturate
THEY HAVE BEEN AROUND FOREVER SINCE WE HAVE RECEPTOR SITES FOR THESE DRUGS!
137
How can GABA receptors have areas for drugs that appear to be modern?
We make all the products within our own bodies (endogenous). Alcohol, benzodiazepine, Barbiturate; etc.
138
Why is Inhibition important?
What happens when infected with Tetanus?
Sensory gating?
Muscular: When you are infected with tetenus, it binds to GABA receptors and inactivates them PERMANENTLY. This causes muscles to go into spasms that can kill you.
Non-muscular: Sensory gating (schizoprehenia, autism) - lack of inhibitions of other neurons...
139
Which NS does Acethylcholine affect?
Where is it made in?
Where does it project to?
What type of disease is it involved in?
Made in the cholinergic nuclei of the pons (hindbrain) and midbrain.
Project to: hippo, amygdala, basal forebrain, neocortex, thalamus.
Involved in huntington's and alzheimers.
Mostly the CNS, and Somatic to Autonomic NS.
140
Does ACh solely affect muscular system?
What systems does ACh affect?
No, it affects the parts of the brains that are related to muscles.
Also affects learning and memory.
141
What are the 2 main receptors families of acetylcholine?
Are they ionotropic or metabotropic?
Where are they mostly found?
What happens when they are stimulated?
Nicotinic Receptors (all activated by DRUG nicotine)-
- Ionotropic (control Sodium)
- Found in: Muscle cells AND CNS in the axoaxonic synapses.
- When stimulated, people smoke after they eat because it increases gut movement (smooth muscles) to aid in digestion.
Muscarinic Receptors -metabotropic - G protein system coupled to a K+ channel
-Found in CNS (Basal ganglia and hippocampus)
142
What are monoamines?
How are they subdivided?
Family of NT which all share a single AMINE group (ie; dopAMINE)
Monoamines =
1. Catacholamines
2. Indolamines
143
What type of monoamine is Dopamine?
Where is it produced in?
DOPAMINE = CATACHOLAMINE
Dopamine - produced in Ventral tegmentum and projects to Frontal, Hippocampus/Amygdala, Nucleus Accumbens.
144
1. Catacholamines
2. Indolamines
NT categorized depends on what?
Which amino acid you start with in their metabolic pathways.
145
What NT is involved in the Nucleus Accumbens?
What does this area do?
Dopamine.
Not a pleasure center like media suggests - think of drug addicts who are NOT experiencing pleasure... They still get activity in the nucleus acumbens, SO this area is most likely for learning and predicting correctly.
>Dopamine input while learning something new.
>"Where do I FIND drugs? Food?"
146
What are the things Dopamine is involved in?
Movement (substancia nigra and basal ganglia)
Learning/Attention (frontal and nucleus acumbens)
Reinforcement (Nucleus acumbens)
Planning
147
Drea has a hard time planning something ahead paying attention. She is also a gambler and doesn't seem to think about risks involved. What NT can affect this?
Lack of dopamine.
148
What is the biosynthesis of the Catecholamines?
All of this converts in the following order:
Caracholamine-->Tyrosine --> L -DOPA --> Dopamine --> Norepinephrine --> Epinephrine
149
True or false: Dopamine and Epinephrine stimulates the same receptors.
Why or why not?
True. They are all from the same structure within the Catacholamine family- And the closer one is to another, the stronger the activation.
150
What does enzymes have to do with NT structure?
We look at ENZYMES that MAKE NT to see what NT's composed of and how they affect each other.
151
What are the 2 subdivisions of Dopamine?
Are they ionotropic or metabotropic?
What happens when you stimulate them? (Be specific about the "family")
What is the big picture about dopamine's specific families?
D1 Family - D1 & D5
>Positively coupled to G-protein system - when stimulated, produces EPSP
D2 Family - D2, D3, D4
>Negatively coupled to G-protein system - when stimulated, produces IPSPs
* Dopamine can produce EPSP OR IPSP depending on which receptor is stimulated.
- All are metabotropic.
152
Where is Norepinephrine produced?
Where does it extend to?
Which part of the NS does it participate in?
What is it involved in?
Produced in the locus coeruleus (blue place) in the tegmentum - extends all over cortex, cerebellum, and spinal cord
Participates in Autonomic system. Need the Norepinephrine to wake all of the ganglion cells up!
Involved in arousal and vigilance.
153
Jenn is very vigilant and very alert and receptive to stimuli in the environment... what type of NT is being produced?
Norepinephrine.
154
What NT do we get a shot of right when we wake up?
Norepinephrine.
155
How does Norepinephrine released?
How are they unique in the way they release themselves?
It's released from swellings called axonal varicosities all along the axons, AND the terminals.
Norepinephrine neuron can release norepinephrine in a much larger area over only releasing it from terminals like other NTs.
Makes sense bc we need to wake up the brain - signal other neurons to pay attention! More likely to depolarize.
156
What is the norepinephrine subdivided from?
What are it's 2 families? Which produce EPSP and IPSP?
*not on test
Catacholamine.
It's 2 families are metabotropic:
Alpha:
a1 - EPSP
a2 - IPSP
Beta:
Found in cortex - important for arousal
157
Which category of NT is Seratonin(5-HT) in?
It is an Indolamine.
158
What type of functions (specific about brain) is Seratonin involved in?
Through connection with hippocampus and limbic system involved in basic functions: appetite, sleep, mood disorders
159
Higher suicide risks can be due to a lack of what NT?
Seratonin
160
Serotonin starts with which amino acid family?
Indolamine--> Tryptophan --> 5-HTP--> 5-HT (seratonin)
161
How many sub-receptors does seratonin have?
Is it on Pre- and postsynaptic?
metabotropic or ionotropic?
Currently aware of about 17 different sub-receptors
Pre- and postsynaptic
All are metabotropic, except 5-HT3 (ionotropic) which controls Na+ and/or Cl- channels
162
Neuropeptides
Often coexist with?
How many known neuropeptides?
Longer with several amino acids.
Function as NTs, neurmodulators and neurohormones- they can travel diff. lengths.
Often coexist with a small-molecule NT and modulate its effects
40 known neuropeptides:
Endogenous Opioids - analgesia
Substance P – pain perception
Insulin – digestion, energy storage
163
What is presynaptic facilitation?
Axo-Axonal synapse hyperpolarizes the terminals of the membrane which is about to get hit with the action potential – it creates a greater change in potential which opens more calcium channels… it facilitates the volume of neurotransmitters for the post-synapse.
164
Are glutamate receptors ionotropic? Or metabotropic?
Both. At some receptors they can produce IPSP or EPSP. The transmitters is just the “switch” and whatever the switch is attached to will determine.
165
What does it mean that GABA is the “universal inhibitor”?
Every GABA receptors found produces IPSP
166
Why is washing down valium with a glass a wine a *very* bad idea?
Both bind to GABA and similar actions – potentiate each other… greater sedative effect.
167
What are the 4 criteria to be a NT?
1. Endogenous
2. Calcium dependent
3. Enzymic deactivation
4. Produce observable affect in low dose
1. Produced by the body (i.e. endogenous) [rules out drugs which are exogenous]
2. Released due to an action potential (Ca2+ dependent release) – due to entrance of Calcium (unless you’re a neuromoderator whose release isn’t dependent on Calcium)
3. Removed from the synapse by an active process (enzymatic deactivation (Acethylcholine) or reuptake)
4. Produce an observable effect at relatively small concentrations (if it binds to a receptor and nothing happens with the post-synaptic cell, it’s not neurotrans.. Unless there’s things that are not observable)
168
What type of "neuro" is the following?
Canabinoids
Adenosine
Nitric Oxide
Neuromodulators.
169
Nitric Oxide is thought to contribute to what between neurons?
Communication - talk back signal
170
What are the 3 criteria for drugs?
1. Exogneous
2. Not required for normal cellular function
3. Observable effect at low dose
171
How do drugs affect neural communication?
Agonists BOOST activity of NT
Antagonist INTERFERE with NT
172
What are the 5 ways drugs can affect NTs?
1. synthesis
2. storage
3. release
4. Receptors and Channels
5. Reuptake and enzymatic deactivation
173
If Choline was added to our diet, our memory will get better right?
No, there isn't enough Acethyl CoA
174
Black widow venom is an ACh agonist or antagonist?
It is an agonist - it leads to greater production of ACh.
175
Botulin toxin is an ACh agonist or antagonist?
Antagonist.
176
ACh is specifically an agonist for what?
Nicotinic receptors.
177
Drugs that effect Acetylcholine? Agonist or antagonist?
Black Widow spider venom (AGONIST)– increases release; can be fatal
Nicotine AGONIST (IONOTRIPIC RECEPTORS) – stimulates nicotinic receptors
Muscarine (AGONIST) METABOTROPIC – stimulates muscarinic receptors
**The black widow spider smokes nicotine and flexes it's muscles, and all the other spiders are in agony!**
Botulinum toxin (ANTAGONIST)– blocks release of ACh; extremely toxic; used as a biological weapon
Curare (OPP. OF NICOTINE AND IS AN ANTAGONIST)– blocks nicotinic receptors; causes paralysis and decreased respiration to the point of death; used in surgeries to paralyze muscles, but does not block pain – nicotinic receptors are located at the neuro-muscular junction (for hunters to use on their arrows)
Atropine
(ANTAGONIST)– blocks muscarinic receptors; a belladonna alkaloid.
**Atropine don't CURARE about botox, he's an antagonist!**
178
Why do we give people with parkington's disease l-dopa instead of dopamine?
How will this affect them in the long run?
L-dopa can survive the BI tract but dopamine can't - however, L- Dopa produces free radicals which will eventually make it worse...
179
How does reserpine affect dopamine?
It interferes with storage for all MONOAMINES- causing vesicles to become leaky. There will be less dopamine transported.
180
How does amphetamine affect dopamine?
increases dopamine , binding of vesicles to pre-synaptic membrane… more dopamine released into the post-synapse.
181
Apopmorphine stimulates or blocks dopamine receptors?
Apomorphine – acts like dopamine and stimulates dopamine (D2) receptors D2 agonist.
182
How do the following drugs affect dopamine, and are they agonist or antagonist?:
```
Deprenyl
Reserpine
Chlorpromazine
Cocaine
Amphetamine
Ritalin
```
Deprenyl (AGONIST) – antidepressant; destroys MAO (oxides monoamines)
Cocaine (AGONIST)– blocks DAT (sits are receptor longer)
Amphetamine (AGONIST) – blocks DAT and stimulates release (sits are receptor longer)
Ritalin (AGONIST)– blocks DAT, stimulates release, stimulates receptors, acts like dopamine on the receptors
Reserpine (ANTAG) – causes VMAT to run “backwards”; inhibits storage of monoamines in vesicles
Chlorpromazine (ANTAG)– antipsychotic; blocks D2 receptors, pushes positive symptoms
183
Drugs that affect Norepinephrine (agonist or antagonist):
Desipramine
MDMA
Amphetamine
All are agonist:
Desipramine – inhibits reuptake of NE (; anti-depressant – blocks the NET, much more than the DAT (dopamine transport)
MDMA (Ecstasy) – Reverses flow of NETransport (re-uptake), in effect increasing release (causes the Epinephrine hanging out in terminals to be plot into a receptor) and decreasing uptake of NE…
Amphetamine – stimulates release of NE
184
Drugs that affect 5-HT (seratonin) and if they are AG or ANTAG.
Fenfluramine (AGONIST)– stimulates release and blocks reuptake; appetite suppressant
Fluoxetine (Prozac) (AGONIST)– SSRI, blocks reuptake; antidepressant and anxiolytic
LSD (AGONIST)– stimulates 5-HT2a receptors (thought to be involved in dreaming); hallucinogen
MDMA (Ecstasy) (AGONIST)– causes SERT to run backwards, increasing release and blocking reuptake (thought to be responsible for hallucinatory effects of MDMA)
- does not directly stimulate the 5-HT2 receptors
185
What's the difference between competitive vs. Noncompetitive binding?
-Competitive Binding
Drug occupies the same binding site on the receptor that the NT occupies
-Noncompetitive Binding
Drug occupies a different binding site on the receptor than the NT
186
How are small molecule NTs derived?
They come from the food we eat! (ACh example)
187
Auto-receptors are located wherE?
In the pre-synapse
188
What is the presynaptic heteroreceptors involved in?
Presynaptic facilitation and inhibition
189
Dendritic autoreceptors (post-synapse ; these NT are neuromodulators) participate in what?
feedback mechanism (tells the pre- and regulates the NT to stop sending signal – serves to hyperpolarize the membrane).
When a dendrite of postsynaptic nueron is depolarized, it will release NT from the dendrite.
This NT will bind to autoreceptors located in the dendritic membrane, and produce an IPSP
This is the way it says "message received!"
190
Self-recognizing receptors (auto-receptors) do what when NT binds to these?
It tells the presynapse to stop producing. Talks back.
191
Facilitation vs. Blocking – so if a drug stimulates auto-receptors, it’s an antagonist or agonist? Why?
Facilitation vs. Blocking – so if a drug stimulates auto-receptors, it’s an antagonist because in the big pic, there’s less NT transmission…
192
What are all the different methods of taking drugs?
What are the benefits and disadvantages of each method?
Intravenous (IV); drug immediately enters blood stream and reaches the brain in seconds (INTO THE CIRCULATORY SYSTEM- Not Artery because we want the drug to mix with other blood – air bubble in artery bad…
Increase and decrease- adjust… reaches target tissue faster and huge volumes.
Danger – too fast, overdose; rapid effects and disappear rapid
Intraperitoneal (IP); rapid (not as fast as IV), most common ROA for lab animals
Peritonium (space around the internal organs through the abs) and picked up by the blood stream
Rapid, not as fast as IV
Not usually used in humans
Dangers – putting drug into an organ; if on human, uses CT scan
Intramuscular (IM); drug absorbed into bs via capillaries in muscle
Bad: Slow and painful ( so need small volumes)
Good: Sustained effect. Slow leaching into the circular system.
Subutaneous (SC); slow, fat beneath skin, only for small volumes
Good: Slow leach
Bad: Small amounts
Oral; drug must be able to survive GI tract (enzymes, acid), absorbed from GI into blood
Bad: Longer wait time, not immediate and only a small percentage will end up in the blood stream
Food lowers the transit time but lowers the PH of the stomach
Sublingual; under the tongue, drug absorbed into blood stream through capillaries in mucous membranes, fairly fast
Some does get absorbed through saliva, but goes through the bloodstream of the mouth
Inhalation; fastest route of administration
Rapid and strong
Blood goes from lungs (if the target tissue is the brain since blood from lungs go straight to the brain)
Topical; drug applied to skin, usually in a cream or ointment
Absorbed through epidermis and dermis
Slow but sustained effects; selectively administer drug to just 1 part of body
193
-Positive correlation of how fast a drug gets into a target tissue and how it’s eliminated… What is this a reference to?
Addiction and withdrawal time-line - the faster it peaks, the faster the withdrawal.
194
What is the difference between a tract and a nerve?
Tract is a collection of nerve fibers in the CNS, and nerve is in the PNS
195
What is the difference between a nucleus and a ganglion?
Clusters of cell bodies. Nucleus is in the CNS, ganglion in the PNS
196
What is the difference between black widow spider venom and nicotine?
Both agonists – ACh is not a specific agonist, while nicotine is very specific
197
What is addiction?
Compulsive administration of a drug
| Behaviorally defined
198
What are the advantages of i.m. administration? The disadvantages?
Advantages are that drugs are sustained – longer it takes to peak, longer it takes to eliminate
Disadvantage – painful, small volume
199
Which route of administration gets drugs into the brain the fastest?
Inhilation
200
What is the difference between pharmacokinetics and pharmacodynamics?
How we get drugs into our system and how they move, where they go, rate of the way they reach target, eliminations (routes of administration) vs. what do the drugs do in the body?
201
What is tolerance?
Physiological reaction of the body when repeatedly presented with substance that disrupts homeostatis.
202
Reserpine prevents monoamines from being stored in vesicles. What is it?
Monoamine antagonist (drug)
A drug blocks the reuptake of serotonin. What is it?
Agonist – across the board for all seratonin receptors
203
A drug binds to the same site as NE and stimulates the receptor. What is it?
Agonist for NE receptors
204
A drug binds to pre-synaptic DA receptors and stimulates them. What is it?
Dopamine Antagonist – Auto-receptors when stimulated turn off release… ALL across the board (pre-synaptic)
205
What is withdrawal?
More enzymes, less receptors!
206
What is the difference between competitive binding and non-competitive binding?
Drug occupies same receptor binding site that the natural NT is on… Non-competitive – Both bind to receptor on diff. receptor sites at the same time even when producing diff. effects.
207
A drug increases the production of AChE.
What is it?
| Antagonist – increases production of AChE it is eliminating ACh at a faster rate
208
Why does Tolerance occur?
changes in enzymes (up or down regulation, up for deactivating the drug… like orally, the enzymes in the gut will do up regulation; the brain. )
changes at the level of the synapse (yanking of receptors)
Learning – both of these up there can be conditioned to certain situations… why? Because the enzymes had been conditioned in same place, people, time… the enzymes are ready!!! No cues? No up-regulations…
209
How are Oligodentracytes and Schwann cells different in the way they react to neural damage?
Oli – if a node of ranvier in the CNS is damaged, Oli secretes chemicals to prevent the regrowth of the axon.
Hinders re-establishment of this neuron.
Schwann – Secretes chemicals to re-establish it’s previous axons - PNS
210
Why do we think Oligodendrocytes function the way they do?
It has to do with learning – connections don’t work or create right associations and if we don’t use them, they die… so if we couldn’t forget we could never learn something new!
211
What are the functions of the Ependymal cells?
Macro - Ependymal cells – line the ventricles
-Cilia keeps the CSF flowing
- Makes CSF with choroid plexus
- Some evidence it participates in immune system in regulating what can get in the brain through the fluid.
212
Explain Radial Glia cells and their roles.
What do they do for other neurons?
Why are they considered plura-potent?
It looks like they play a role in Brain development.
- Provides scaffolding that newly generated neurons use to find it’s target resting place in the brain
- kind of like stairs for neurons to follow up…
-Brain stem cells (new neuron cells are made from the radial glial, which is in the neural tube)
They are considered Plura-potent- They can be anything! It splits to be come a neuron and one glia cell.
213
The Therapeutic index for Lithium is 2. What does this mean? How did they calculate this?
What should be higher and lower?
2 = taken more than 2 times, you will die.
It's LD50 (lethal dose 50%/effective dose 50%)
Anything less than 10 is dangerous. We want lethal dose high and effective dose low.
214
PsychopharmacologyWhy do drugs differ in their effectiveness?
Different drugs have different mechanisms (aspirin and morphine do the same thing, but aspiring works at site of injury while morphine actually blocks the pain signals from the PNS.
Lipid solubility - fat will get into brain faster
Affinity for site of action; the higher the affinity, the lower the dose needed to produce an effect - stronger the drug, more able to boot off natural NT off the receptor.
215
What do all stimulants do to which NS?
Increase the Sympathetic NS - increased heartrate, decrease salivation; etc.
216
What NT are the following drugs attached to?
```
Caffeine
Nicotine
Cocaine
Amphetamine
Methamphetamine
Ecstasy (MDMA)
```
```
Caffeine - Adenosine
Nicotine - ACh
Cocaine- Dopamine
Amphetamine - Dopamine
Methamphetamine - Dopamine
Ecstasy (MDMA) -Dopamine & Seratonin
```
217
Why is quitting opiates so hard?
Because the pain you get after you quit is so hard to deal with.
218
What is alcohol and agonist/antagonist of?
Alcohol is a GABA agonist.
219
Agonist of Norepinephrine.
- Desipramine - inhibits reuptake of NE (antidepressant)
- MDMA (Ecstacy) - reverses flow NET, in effect increases release and decrease uptake.
- Amphetamine - stimulates release of NE
-DESIpramine nore-playing when he's amped (amphetamine) up on MDMA.
220
Adenosine contributes to what type of function?
What is a direct antagonist of caffeine?
Adenosine contributes to: Motor function, attention, paid modulation
Caffeine is a direct antagonist of Adenosine
221
What are the neuromodulators discussed in class? (3)
Cannabinoids
Adenosine
Nitric Oxide
222
Agonists of Acethylcholine:
Black Widow spider - increases release
Nicototine - stimulates nicotinic receptors
Muscarine - stimulates muscarine receptors
Other BW spiders are in AGONY and seethe (aSEETHEacholyne) when Buff "Muscurine" Black Widow Spiders puff on "Nicotine
223
Antagonists of Acethylcholine:
- Botulinum toxin -Blocks ACH release
- Curare - Blocks nicotinic receptors, causing paralysis
- Atropine - Blocks muscarinic receptors
"My aunt (antagonist) seethes (aseethacholine) when her kid can't CURARE less about winning ATROPhy, so she wants to kick her BOTULINUM (butt).
224
Antagonist of seratonin
-Reserpine - interferes with storage (all monoamines)
225
Agonist of seratonin
- Fenfluramine - stimulates release and blocks reuptake
- Fluoxetine (prozac) - SSRI - blocks re-uptake
- LSD - stimulates 5-HT2 receptors
- MDMA - Causes SET to run backwards
226
Antagonist of Dopamine
- Reserpine - Causes VMAT to run backwards and inhibits storage of monoamines
- Chlorpromazine - Blocks D2 receptors
227
Agonist of Dopamine
- Cocaine - Blocks DAT
- Amphetamine - Blocks DAT and stimulates release
- Ritalin - Blocks DAT, stimulates release AND receptors.
- Deprenyl - Destroys MAO
Dopamine Agonist = C.A.R.D ...MOST OF THESE AMP SOMEONE UP! Schizophrenics have hyper-imagination...
228
A drug that affects dopamines auto receptor (pre synaptic involved in reuptake). Describe a situation where blocking (essay 6)
D2 is pre and pro synaptic and chlorophromaine blocks d2 recetors(it's blocking the reuptake process)
229
Outside and Inside of the cell membrane at RMP?
Outside: Lots of Chloride and sodium, little bit of potassium
Inside: Lots of negatively charged proteins, LOTS of potassium, and little Chloride
