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Neuro Biology > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

What is trepanation?

A

a surgical intervention where a hole is drilled into the skull exposing the duramatter
- aka a craniotomy

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2
Q

What is a trepanation where the bone isn’t replaced?

A

craniectomy

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3
Q

What is a trepanation/craniotomy used for?

A
  • used to relieve pressure and treat health problems -surgical access for intracranial pressure monitoring
  • to treat epidural and subdural hematomas
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4
Q

What is a hematoma?

A
  • a solid swelling of clotted blood
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5
Q

What is the brain made of?

A

network of neurons and glia

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6
Q

How do neurons communicate?

A

-electrical and chemical signals

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7
Q

What is the neuronal pulse called?

A

AP

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8
Q

What is aphasia?

A

partial or complete loss of language abilities

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9
Q

Which aphasia is known as fluent or sensory aphasia?

A

Wernicke’s Aphasia

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10
Q

What are the symptoms of Wernicke’s aphasia?

A
  • fluent speech that makes no sense
  • poor comprehension
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11
Q

Which aphasia is known as motor aphasia, non-fluent aphasia, or production aphasia?

A

Broca’s Aphasia

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12
Q

What are the symptoms of Broca’s aphasia?

A
  • non-fluent speech, struggle to produce words
    -telegraphic (agrammatical)
  • speech makes sense
  • good comprehension
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13
Q

What do the different types of aphasia prove?

A

localization of function

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14
Q

What is localization of function?

A
  • different areas of the brain control different functions
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15
Q

How does aphasia prove localization of function?

A
  • damage in the different areas of the brain have different results
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16
Q

Where does wernicke’s aphasia occur?

A
  • temporal lobe
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17
Q

Where does broca’s aphasia occur?

A
  • frontal lobe
    -cerebral cortex
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18
Q

What is a stroke?

A
  • a rapid loss of brain functions due to a loss of blood supply
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19
Q

What are the types of strokes?

A

-ischemic
-hemorrhagic

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20
Q

What is an ischemic stroke?

A
  • a blockage of blood supply
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21
Q

What is a hemorrhagic stroke?

A

blow out to blood supply

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22
Q

What are transient ischemic attacks (TIAs)

A
  • mini strokes
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23
Q

What are the symptoms of a stroke?

A

-depends on the area of the brain it effects

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24
Q

What did Camillo Golgi do?

A
  • developed the Golgi stain
  • reticular theory
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25
Q

What did Ramon y Cajal do?

A
  • grandfather of neuroscience
  • neuron doctrine
  • discovered the synaptic cleft
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26
Q

How wide is the synaptic cleft?

A

20 mm wide

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27
Q

What is the site of synaptic contacts?

A

dendritic spines

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28
Q

Are all axons milenated?

A

no, but most are

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29
Q

What does myelin do?

A
  • increases speed at which AP travels down the axon
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30
Q

What are the non-neuronal cell types?

A

-mast cells
- microglia
-macroglia (everything below= micro)
- astrocytes
-oligodendrocytes
-radial glia
-Schwann cells
-satelite glial cells

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31
Q

What are astrocytes?

A
  • chemical environment regulation
  • buffer extracellular K+ levels
  • modulate and control blood flow in the brain
  • CNS
    -sucks up K+
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32
Q

What are Mast cells?

A
  • Immunoactive cells in the CNS
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33
Q

What are microglia?

A
  • specialized macrophages
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34
Q

What are oligodendrocytes?

A

myelin
CNS

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35
Q

What are radial glia

A

-neuron progenators
-stem cells
- scaffolds
-highways
-CNS

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36
Q

What are Schwann cells?

A

-myelin in the PNS

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37
Q

What are neuronal circuts?

A
  • a population of neurons interconnected by synapses and supported by non-neuron cells
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38
Q

What do neuronal circuits do?

A
  • carry out specific functions when activated
    -underlies all functions of the nervous system
    -simple or complex
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39
Q

How do neuronal circuits work?

A
  • input- processing- output
    -afferent to efferent
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40
Q

What are examples of simple circuits?

A
  • stretch reflex (knee jerk)
  • leg withdrawal reflex
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41
Q

What do efferent signals do?

A
  • carry nerve impulses away from the CNS
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42
Q

What do afferent signals do?

A
  • carry nerve impulses from receptors/sense organs towards the CNS
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43
Q

What is a seizure?

A

-abnormal neuronal activity

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44
Q

What is epilepsy?

A
  • chronic condition of repeated seizures
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45
Q

What is an EEG and what does it do?

A

-electroencephalography
- measures brain electrical signals

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46
Q

How does an EEG work?

A
  • shows voltage fluctuations from ionic current flows by large groups of neurons
  • displaying synchronous activity by many neurons in similar spatial orientation
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47
Q

What is an EMG and what does it do?

A
  • electromyography
    -measures muscle signals
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48
Q

What is an EKG and what does it do?

A
  • electrocardiography
    -measures heart signals
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49
Q

What is a current?

A

energy flow between one area and another

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50
Q

What are seizures caused by?

A

chronically overexcited neurons
- you can see them on an EEG even when they aren’t happening

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51
Q

What are the surgical treatments for epilepsy?

A
  • remove the focal point
  • remove the corpus callosum
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52
Q

What does removing the corpus callosum do for seizures?

A
  • limits how seizures spread because the two sides can’t communicate
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53
Q

What do drugs do for epilepsy?

A
  • cause a use-dependent increase in the inactivation time of voltage-dependent Na+ channels
    -Enhance GABAergic inhibition
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54
Q

Does an axon’s membrane have a charge?

A

yes

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55
Q

What does a membrane’s charge do?

A
  • allows for AP to be induced and for APs to travel down the axon without a loss of signal
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56
Q

What has to happen for signals to be transmitted across the axon’s membrane

A

-ions must cross the membrane
- membranes are too thick for ions to flow through so Ion channels are neccessary?

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57
Q

Do all ions flow in the same direction?

A
  • no
    -Different ions flow in different directions
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58
Q

What are the key characteristics of ion channels?

A
  • they are specific for particular ions (element, not just charge)
    -integral membrane potentials
  • they can open and close
  • don’t physically ions, they move down a gradient
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59
Q

How do ions move through the ion channels?

A
  • Move passively down a gradient
    -Electrical and chemical gradients
    -Different ions move in different directions across the membrane
    -ions travel in the direction of the electrochemical gradients
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60
Q

What is membrane potential?

A
  • the difference in electric potential between interior and exterior of the cell
    -what you measure
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61
Q

What dictates the direction an ion flows?

A
  • the driving force and the concentration/electrical gradients
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62
Q

If an ion is positively charged and the gates are open what would happen to the membrane potential?

A
  • membrane potential would be more positive
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63
Q

If an ion is negatively charged and the gates are open what would happen to the membrane potential?

A
  • would become more negative
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64
Q

What is Vm

A

membrane potential

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65
Q

What does more ions do to the driving force?

A

-more ions= stronger driving force

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66
Q

What is equilibrium potential?

A
  • membrane potential where the ion is at electrochemical equilibrium
  • for a single ion
    -when concentration and electrical driving forces are equal and opposite
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67
Q

What is wrong with the Nerst equation?

A
  • it doesn’t equate forpermeability
  • Most neurons are permeable to more than 1 ion so Vm doesn’t normally match Eion
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68
Q

What is the typical mammalian membrane potential?

A

-40 - -90

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69
Q

How many ions move to generate membrane potential?

A
  • very few ions move to generate membrane potential
  • no immediate effect on the concentration gradient
  • over a long time (especially in active neurons) Na+ and K+ can run down
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70
Q

Does the NaK+ Pump actively drive AP?

A

no

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71
Q

What drives AP

A

ion channels

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72
Q

What does the NaK+ pump do?

A

plays an important role in maintaining concentration gradients OVER TIME

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73
Q

What are ion transporters?

A
  • integral membrane proteins
    -selective for specific ions
    -actively moves ions across the membrane
  • moves ions opposite to the concentration gradient
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74
Q

What cells regulate K+

A
  • astrocytes buffer extracellular K+ levels
  • they link together to widely regulate K+
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75
Q

How does astrocyte-neuron communication through Calcium and gliotransmitter signaling in the tripartite synapse work?

A

-gliotransmitters leave astrocyte through transporter and bond to their receptor on the neuron
- neurotransmitters leave the neuron and bind to gq proteins on astrocyte
- Inside the astrocyte PLC is coming through GQ protein
- pLC to PIP2 to IP3 to ER to Calcium
-glial cells can regulate extracellular milieu and buffer K+

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76
Q

What is AP controlled by?

A

-voltage-gated ion channels
-ion permeability and conductance
- current flow
-inactivation of voltage gated channels

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77
Q

What is ap conduction influenced by?

A
  • passive and active components
    -myelin
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78
Q

When does undershoot occur?

A

after repolarization

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79
Q

What is hyperpolarization?

A

-when the membrane doesn’t immediately return to resting potential bc voltage-gated channels are open
- K+ is flowing out through leak channels and since K+ is flowing out the positive ion is leaving the membrane becomes more negative

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80
Q

How does the membrane go back to normal after the undershoot?

A

leak channels

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81
Q

What is overshoot?

A
  • When membrane potential reaches the positives
    -doesn’t quite reach Na+ potential bc K+ channels kick in and the voltage channels overlap
  • Na channels close and K+ starts leaving
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82
Q

What is the rising phase?

A
  • when Na+ and K+ channels are open
    -Na+ flowing in is what makes the membrane less negative, depolarizing it
    -once rising for a little while before it can start again
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83
Q

What is the falling phase?

A
  • where re-polarization is happening
  • K+ is flowing out of the cell
  • K+ pumps have been on the entire time just too slow to cause a response until now
  • Since K+ is slower it helps control AP and allows cell to be open longer
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84
Q

What are the phases of AP?

A
  • Threshold: K+ going in and out at an equal rate
  • Rising: K+ going out, Na+ going in
  • Falling: K+ going out only
  • Threshold
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85
Q

What mediates the rising phase?

A
  • voltage-gated Na+ channels
  • these are different from leak channels open at rest
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86
Q

What are the advantages of the voltage-gated channels?

A

-can open and close very fast
- has an ion-selective pore, a voltage-gated sensor that opens the pore via an activation gate in the pore and an inactivation gate separate from the voltage gate
- once it opens it can’t open again until it repolarizes to a negative voltage

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87
Q

What mediates the falling phase?

A

-voltage gated K+ channels

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88
Q

What are the ways to graph the changes during AP?

A

-membrane potential (vm)
- ionic permeability or conductance’s
V=IR
V=I(1/g)
1/g=R

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89
Q

What does depolarization do to K+ channels?

A
  • Voltage-gated K+ channels are activated by depolarization but are much slower to open than Na+-gated channels
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90
Q

How many different types of voltage-gated K+ channels?

A

lots

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91
Q

Does K+ have an activation gate?

A
  • yes activation gate
    -some have deactivation gate
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92
Q

What is the AP positive feedback loop?

A
  • AP is all or none
  • depolarization
    -opens voltage-gated Na+ channels
  • Na+ influx is greater than K+ efflux
    -more depolarization
    -threshold
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93
Q

What is threshold?

A
  • membrane potential at which Na+ influx overcomes K+ efflux resulting in at least 1 AP
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94
Q

How does the brain slice technique work?

A
  • take a thin slice out of a rats brain
  • keep it as alive as possible in the petri dish
    -typically studies caudut/putman area and nucleus accumbens
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95
Q

What does Putman area control?

A
  • motor control
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96
Q

What does the nucleus accumbens control?

A

reward and motivation

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97
Q

What are the types of patch recordings?

A

-voltage clamp
-current clamp
- dynamic clamp

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98
Q

What does a voltage clamp measure?

A

current changes

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99
Q

What does a voltage clamp manipulate

A

voltage

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100
Q

What is the clamp formula?

A

V=IR

101
Q

What does a current clamp measure?

A

voltage changes

102
Q

What does a current clamp change?

A

current

103
Q

What does more depolarization lead to?

A

more AP

104
Q

Do all neurons respond the same to depolarizatoin?

A

no
-they have different types and densities of ion channels

105
Q

What does an inward current mean?

A
  • a positive current is going into the neuron or a negative one is coming out
106
Q

What does resistance measure?

A

-if things are open

107
Q

What is resistance measured in?

A

conductance

108
Q

What is an absolute refractory period?

A

when an AP cannot be generated

109
Q

What does the absolute refractory period look like on the ionic basis?

A
  • inactivated V-gated channels
110
Q

What is the relative refractory period?

A

harder to generate AP, but still possible

111
Q

What does the relative refractory period look like on?

A

some voltage-gated K channels tend to keep the membrane closer to Ex and farther from the threshold, maybe a few Na channels are still inactivated

112
Q

What does one class of epilepsy drugs do?

A

-causes a use-dependent increase in the inactivation time of the voltage-dependent Na+ channels
-extends refractory time
-means its closed for longer and can’t hyperfire
-harder to generate AP

113
Q

What is the drawback to epilepsy drugs?

A
  • slower movements and reaction time
114
Q

What is AP propogation?

A
  • AP must travel from azon hillock to terminals
115
Q

Do APs cross the chemical synapse?

A

no only chemicals do

116
Q

How do APs regenerate?

A
  • Depolarization causes AP on one side of the membrane, which causes another Ap depolarization nearby…
  • this is a high fidelity process that can almost perfectly copy and go over and over
117
Q

Is AP generation a passive, or active current flow?

A

a passive current flow that decays with distance

118
Q

Do Aps move in both directions?

A

not often

119
Q

Why don’t APs move in both directons?

A
  • because voltage-gated Na+ channel inactivation, takes time to regenerate
    -if an AP has already happened, even if you injected a current it wouldn’t flow in both directions
120
Q

What happens if you inject a current before an AP happens?

A

it would open Na+ channels and cause AP to fire
- in this case it would go bothways

121
Q

What does myelin do (what is saltatory conduction)?

A

makes ap go faster because it lets them jump to other parts of the axon and skip regenerating AP

122
Q

What are the nodes of ranvier

A

unmyelinated, specialized region of the axonal membrane
-includes the highest density of voltage-gated ion channels on axon

123
Q

What is MS?

A
  • neurodegenerative disease of oligodendrocytes in CNS
    -autoimmune disease
124
Q

Why do signs and symptoms of MS differ?

A

-localization of function
-degeneration

125
Q

Is there a cure to MS?

A

no

126
Q

What are the movement symptoms of MS?

A

-numbness/weakness in 1+ limbs
-Typically 1 side at a time (l,r,u,d)
-electric shock with certain neck movements (especially bending foward)
- tremor
- lack of coordination/unsteady gait

127
Q

What are the vision symptoms of MS?

A
  • partial/complete loss of vision
  • usually one eye at a time
  • pain during eye movement
  • prolonged double vision
  • blurry vision
128
Q

What are the misc. symptoms of MS?

A

-slurred speech
-fatigue
- dizziness
-tingling/pain in the body
- problems with sexual, bowel, bladder functions

129
Q

How does passive current move across the axon?

A

-moves down the axon
-less current loss across the membrane and capacitance is increased

130
Q

What are the three regions that are defined by axial glial interactions at the nodes of Ranvier?

A
  • adjacent paranode (PN)
  • juxta perinodal region (JP)
    (contains delayed rectifier K+ channels)
  • Internode
131
Q

Do the nodes of Ranvier have Na+

A

yes, Na+ rich

132
Q

How is the axon domain regulated?

A
  • by soluble signals from myelinating glia and direct contact and interactions between proteins expressed on the surface of axons and glia
133
Q

Does the myelin sheath have plasma?

A
  • very little cytoplasm between the plasma membrane that makes up the sheath
  • this creates a thicker membrane especially with regard to its electrical properties
134
Q

Do glial cells influence AP?

A

yes, through myelination
-can direct localization of membrane proteins in neurons including ion channels

135
Q

How do AP and calcium affect NT realeas?

A
  • AP depolarizes terminal which leads to an influx of Ca leading to vesicular fusion and NT release
136
Q

How do we know vesicular fusion is a thing?

A
  • we can measure vesicular fusion, NT release on the presynaptic neuron, and NT binding on the post synaptic neuron
137
Q

What do SNARE proteins do?

A
  • help dock vesicles in place
138
Q

Where are V-Snares?

A

-vesicular membrane

139
Q

What is an example of a V-snare?

A

synaptobrevin

140
Q

Where are t-snares?

A

terminal membrane

141
Q

What is an example of t-snares?

A
  • syntaxin
    -SNAP 25
142
Q

How can you stop NT action?

A
  • diffusion
    -enzymatic degradation
  • reuptake
143
Q

When is enzymatic degradation common?

A
  • protein NTs (neuropeptides)
    -ACH
144
Q

When is reuptake common?

A
  • small molecule NTs that are actively taken back from the synaptic cleft by the presynaptic terminal or peri synaptic glial cells?
145
Q

What do electrical synapses allow for?

A
  • direct ion flow
    -fast but dumb
    -direct current flow from one neuron to another
    -bidirectional ion flow
    -synchronization of many neurons
146
Q

How do electrical synapses allow for direct ion flow?

A
  • through gap junctions formed by connexions
  • allows for moderately sized compounds through
147
Q

Where are electrical synapses found?

A
  • coordinates movements of gut, respiration, brainstem
148
Q

What are drawbacks to electrical transmission?

A
  • bidirectional, less versatile, signal not amplified, polarity can’t change,
    less potential for modulation
149
Q

Do chemical synapses have a physical gap?

A
  • yes
    -synaptic cleft
150
Q

Where is the synaptic cleft?

A
  • in chemical synapses, between presynaptic and postynaptic cell
151
Q

How can you tell the difference between pre-synaptic and post-synaptic cleft?

A
  • presynaptic is denser than post synaptic
152
Q

Where does the info for chemical synapse come from?

A
  • neurotransmitters that cycle in the synaptic cleft
153
Q

What is a drawback to a chemical synapses?

A
  • slower than electrical
    -smart but slow
154
Q

Where are astroglia found?

A

CNS

155
Q

Where are schwann cells found?

A

PNS

156
Q

How many chemical signals can a single synapse release?

A

multiple

157
Q

What are the types of chemical signaling in order of slowest to fastest?

A
  • classical endocrine
    -paracrine signaling
  • autocrine signaling
    -synaptic transmission
158
Q

What is classical endocrine signaling?

A
  • hormones in blood stream to reach target
159
Q

What does paracrine signaling target?

A

nearby things

159
Q

What does autocrine signaling target?

A
  • the thing that secreted it
160
Q

What is the NT cycle in the synaptic cleft?

A

reserve
ready pool
release
refill

161
Q

What does synaptic transmission target?

A

NT at synapse, very close range things

162
Q

What are neuropeptides?

A
  • NT
    -some act as hormones in 1 context, NTs elsewhere
163
Q

How long are neuropeptides?

A

3-36 amino acids

164
Q

What are examples of neuropeptides?

A
  • enkephalines,
    -substance P
    -somatostatin
    -CART
165
Q

Where are neuropeptides synthesized and packaged?

A
  • dense core vesicles
166
Q

What are the types of small molecules?

A

-monoamines
-ACH
-amino acids
-purines

167
Q

What are examples of monamines?

A
  • serotonin, histamine, octopamine, catecholamines
168
Q

What are examples of catecholamines?

A
  • dopamine
  • epinephrine
    -norepinephrine
169
Q

What are examples of amino acids?

A
  • glutamate
    -GABA
    -glycine
    -asparate
170
Q

What are examples of purines?

A

-ATP
-Adenosine

171
Q

Describe NTs?

A

-packaged synaptic vesicles
- NTs

172
Q

How are neuropeptides made?

A
  • synthesized like all other proteins in the cell then transported to terminal
173
Q

How are small molecules made?

A
  • only made if necessary, packaged in the terminal and some in the vesicle
174
Q

What is anterograde transport?

A
  • from soma to axon terminal
    -depends on kinesin
175
Q

What is retrograde transport?

A

-axon terminal - soma
-depends on dynesin

176
Q

How is ACH packaged?

A

-packed in vesicles
-proton pump generates a proton gradient and across a vesicle membrane
-ach transporter uses energy from proton gradient to move ACH into the vesicle

177
Q

How is ACH stopped?

A
  • degraded in synaptic cleft by ACHE
178
Q

How is ACH recycled

A

-choline is transported into the terminal
-choline is used to make more ACH

179
Q

What does too much choline cause?

A
  • hypotension and liver damage
180
Q

What is serotonin uptook by?

A

serotonin transporter

181
Q

Where is serotonin repackaged or degraded?

A

presynaptic terminal by MAO

182
Q

What is GABA uptook by?

A
  • selective uptake by GABA transporters and glutamate transporters
183
Q

Do GABA and glutamate require synthesis in the neuron?

A

no
-usually packaged outside using Na+ as the energy source

184
Q

How do GABA and glutamate transporters get their energy?

A
  • proton gradient
185
Q

What type of transporters are GABA and glutamate?

A
  • vesicular
186
Q

What is excitation?

A
  • post-synaptic neuron is more likely to fire
    -depolarizes
187
Q

What is inhibition?

A

makes postsynaptic neuron less likely to reach threshold (voltage) in the postsynaptic nueron

188
Q

What is postsynaptic potential?

A
  • change in membrane potential in the postsynaptic neuron
189
Q

What clamp is postsynaptic potential?

A
  • current clamp
190
Q

What is Excitatory Postsynaptic Potential?

A

-input makes the postsynaptic neuron more likely to reach threshold

191
Q

What is an inhibitory postsynaptic potential?

A

-input makws the postsynaptic neuron less likely to reach threshold

192
Q

What are postsynaptic currents?

A
  • change in membrane current in the postsynaptic current (recorded in voltage clamp)
193
Q

What do potentials and currents look like on a graph?

A

-curves

194
Q

What does a downward deflection on a current mean?

A

-positive ions in or negative out

195
Q

how can you test which ions carry current?

A
  • removing the ion from extracellular fluid
196
Q

How is ACH broken down?

A

ACHE

197
Q

What happens if you switch from current to voltage clamp?

A

-depiction flips

198
Q

Is ENa excitatory or inhibitory?

A

-typically excitatory because it is above threshold
- the potential is depolarizing bc membrane potential is hyperpolarized

199
Q

If CL had its way which way would membrane potential move?

A
  • towards hyperpolarization bc it has a negative equilibrium potential
200
Q

What is the reversal potential for a synapse?

A
  • membrane potential of a post-synaptic neuron (or another target cell) at which an NT causes no net current flow
  • equilibrium potential, but for a synapse
201
Q

What determines postsynaptic excitation and inhibiiton?

A
  • reversal potentials
    -threshold potentials
202
Q

What determines reversal potential?

A
  • what ions can flow
203
Q

What happens if the reversal potential is more positive than threshold?

A
  • excitation occurs
204
Q

What happens if the reversal potential is more negative than threshold?

A
  • inhibiton occurs
205
Q

What is an excitatory synapse?

A
  • a synapse in which the current resulting from activation of a ligand-gated ion channel has a reversal potential that is depolarized compared to threshold
206
Q

What is an inhibitory synapse?

A
  • a synapse in which the current resulting from activation of a ligand-gated ion channel has a reversal potential that is hyperpolarized compared to threshold
207
Q

How does synaptic integration work?

A
  • a neuron receives input from hundreds of thousands of synapses
  • All active inputs and intrinsic properties are taken into account at the axon hillock
  • if threshold is reached, an AP is fired
208
Q

Where does voltage of the membrane need to hit threshold?

A
  • axon hillock
209
Q

Is the immediate effect of synaptic integration on the membrane at each synapse local or far-extending?

A

local

210
Q

Does synaptic integration amplitude decrease with distance?

A

yes

211
Q

Does AP decrease with distance?

A

no

212
Q

What does synaptic integration amplitude depend on?

A

internal and membrane resistance

213
Q

How is AP generated before the axon hillock?

A

-mostly passive current

214
Q

What is spatial summation?

A
  • inputs combined across nearby spaces
215
Q

What is temporal summation?

A
  • inputs combined bs they occurred close in time
216
Q

How does driving force change?

A
  • ions, membrane potentials
217
Q

What is neuromodulation?

A
  • the physiological process by a given neuron uses one or more neurotransmitters to regulate large and divers populations of neurons
218
Q

How is neuromodulation different from classical synaptic transmission?

A
  • in classical a presynaptic neuron directly influences a single postsynaptic partner and in modulation a large and diverse population is controlled
219
Q

What are examples of neuromodulators?

A

-dopamine
-serotonin
- ACH
- histamine

220
Q

Can neuromodulators bind to ionotropic receptors?

A

yes but they don’t have to

221
Q

Describe NT receptors?

A
  • highly specific for a given NT
    -each NT has many different receptors
    -receptor determines the effect of the NT
    -ionotropic or metabotropic
    -localized to different areas
222
Q

Where are NT receptors localized to?

A
  • postsynaptic membrane (always)
  • presynaptic membrane (sometimes)
  • peri synaptic glial membrane (usually, maybe always)
223
Q

Describe ionotropic receptors?

A
  • ligand (NT) gated receptors
  • open within 1/2 a msec
  • usually 4-5 protein subunits each with 4 transmembrane domains
    -ion channels
    -different combos of subunits lead to different subtypes of that receptor
224
Q

What subunits bind to the AMPA receptor?

A

-GLUTAMATE
-glu 1-4

225
Q

What subunits bind to the NMDA receptor?

A
  • NR1, NR2A-D
226
Q

What subunits bind to the Kainate receptor?

A
  • glu R5-7
    -ka1+ka2
227
Q

What subunits bind to the GABA receptor?

A

a 1-7
b 1-4
Y- 1-4
8 looking thing
epsilon
P1-3

228
Q

What subunits bind to the glycine receptor?

A

a1-4
b-4
Y
8 looking thing

229
Q

What subunits bind to the serotonin receptor?

A

5HT3

230
Q

What subunits bind to the purine receptor?

A

P2x1-7

231
Q

What are agonists?

A

drugs that bind to a receptor and mimmick the effect of the natural NT

232
Q

What are examples of agonists?

A
  • NMDA, AMPA, Muscarine, Nicotine
233
Q

What are glutamate receptor agonists?

A
  • NMDA receptors
    -AMPA receptors
234
Q

What are the ACHR receptor agonists?

A

-muscarine
-nicotine

235
Q

What are antagonists?

A
  • bind to the receptor and block the normal activity of the ligand
236
Q

What are examples of glutamate receptor antagonists for the NMDA and AMPA receptors?

A

-AP5 and CNQX

237
Q

Whatis atropine?

A

MACHR antagonist

238
Q

What is curare?

A
  • NACHR antagonist
239
Q

What does glutamate do?

A

depends on the receptor it activates

240
Q

What are the three glutamate receptors?

A

-kinate
-AMPA
-NMDA

241
Q

What is the ampa receptor?

A

-gated by glutamate
-allows cations to flow in and out of the neuron
- principal gated ions are NA and K+ in the typical ampa receptor

242
Q

What is the NMDA receptor?

A
  • ion channel that is gated by voltage and glutamate and low levels of glycine
    -very useful for ion channel causing long term changes inside of the postysynaptic neuron
243
Q

What must happen for NMDA to bind?

A

-glutamate and glycine must bind
- strong depolarization of the postynaptic membrane

244
Q

Describe the effects of AMPA and NMDA together?

A

Glutamate binds to AMPA and NMDA
- N+ and Ca2+ now also flow through NMDA receptors. This further depolarizes the membrane and triggers signal transduction pathways
which recruits other ion channels and changes the ene expression inside the postynaptic neuron

245
Q

Describe gaba?

A
  • usually inhibitory
    -a variety of drugs alter the effect of GABA when binding to its receptor
  • some neurosteroids do the same thing naturally (paracrine signaling)
246
Q

What is a neurosterioid?

A
  • hormone produced inside the brain by neurons or glia
247
Q

Describe metabotropic receptors?

A

-monomeric
-pharmacology defines receptor subtypes
- no ion channels
-g-proteins couple effector systems
- slower (30ms-1s)
-one or more change leads to changes in mebrane permeability and or altered cellular metabolism through secondary messengers
-each gene codes a specific receptor that will dictate what happens

248
Q

Describe cholinergic receptors?

A

-agonist: nicotine and muscarine
-antagonist: curare and atropine
- nicotine ACHR typically allows N+ and K+ ions to flow
- curare is a Nachr antagonist and paralytic bc neuromuscular junction is being blocked by Curare which is an antagonist blocking its functions

Neuro Biology (4 decks)

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