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PHGY 209 > nerve/synapse lectures 5-6 > Flashcards

nerve/synapse lectures 5-6 Flashcards

1
Q

what is presynaptic terminal

A

swelling at end of axon
includes active zone

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2
Q

what is active zone

A

specialized region
vesicles parked here in active zone
held in place
faces postsynaptic spine

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3
Q

what are presynaptic vesicles

A

presynaptic terminals filled with presynaptic vesicles
made out of plasma membrane
packages neurotransmitter - chemical released by presynaptic terminal

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4
Q

what is synaptic cleft

A

name of gap between presynaptic terminal and postsynaptic spine

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5
Q

what is postsynaptic density

A

in post synaptic membrane
looks dark - many proteins
high density of proteins involved in process of transmitting info from presynaptic terminal to postsynaptic spine

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6
Q

what triggers neurotransmitter release in presynaptic terminal

A

activation of voltage gated calcium channels
ion channels are next to docked synaptic vesicles

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7
Q

what are ligand gated ion channels

A

postsynaptic receptors for transmission at brain synapses

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8
Q

describe ligand gated ion channels

A

ion channels open up pore when binds a small messenger molecules
released by presynaptic terminal and activates ion channel in postsynaptic spine

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9
Q

what are ligand gated ion channels AKA

A

neurotransmitter receptors
ionotropic receptors (since they are ion channels)

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10
Q

what does calcium do

A

biochemical signal and causes cell to do things
can cause cells to contract (biochemical signal in skeletal muscle)
triggers sequence of biochemical events in presynaptic terminal

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11
Q

describe calcium levels inside and outside cell

A

outside cell = low concentration
inside cells and presynaptic terminal = veryyyyy low, so calcium wants to flow in down concentration gradient

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12
Q

do neurons want to keep calcium levels high inside the cell

A

wants to keep calcium levels in cell low because calcium is a signalling molecule

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13
Q

describe the types of signal transformations during synapse

A

ap = electrical signal then gets to presynaptic terminal and is converted to chemical signal = neurotransmitter and then converted back to electrical signal in postsynaptic cell

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14
Q

name the 3 main steps of chemical synaptic transmission

A

1 = ap invades presynaptic terminal, calcium channels open and result in calcium influx into terminal
2 = synaptic vesicles fuse with presynaptic membrane releasing transmitter into synaptic cleft
3 = transmitter diffuses across the cleft and activates receptors in postsynaptic membrane

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15
Q

describe step 1 of chemical synaptic transmission

A

wave of depolarization depolarizes presynaptic terminal and gets more positive
causes voltage gated calcium channels to open
calcium levels increase, small amount flowing in changes the concentration significantly
calcium binds to proteins found in presynaptic terminal and activates them and sequence of biochemical events, so a few vesicles docked in active zone will fuse to PM and open and dump contents (neurotransmitter) into cleft

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16
Q

describe step 2 of chemical synaptic transmission

A

neurotransmitter in cleft
binds to ligand gated ionotropic neurotransmitter receptors and causes ion channels to open and changes electrical properties of postsynaptic cell

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17
Q

what is the fusion of a synaptic vesicle at an active zone dependent on

A

calcium

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18
Q

the postsynaptic response to neurotransmitter is either what (name and describe - 2)

A

EPSP = excitatory postsynaptic potential, depolarizes postsynaptic membrane
IPSP = inhibitory postsynaptic potential, hyperpolarizes postsynaptic membrane

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19
Q

describe excitatory synapses (EPSP)

A

on spines
makes postsynaptic cell more likely to fire an ap
closer to ap threshold, depolarizes

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20
Q

describe inhibitory synapses (IPSP)

A

on dendritic shaft
makes postsynaptic cell less likely to fire an ap, hyperpolarizes postsynaptic cell and pushes away from ap threshold

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21
Q

what is the main excitatory neurotransmisster in brain

A

glutmate (an amino acid)

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22
Q

what is monosodium glutmate

A

MSG
can have effects if too much since glutamate is a biologically active neurotransmitter

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23
Q

what is rapid excitatory transmission at synapses due to

A

actions of glutamate on 2 types of ionotropic glutamate receptors = AMPA and NMDA receptors

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24
Q

describe NMDA and AMPA receptors

A

both in postsynaptic spine
ion channels that open in response to binding of small molecules (like neurotransmitters) to receptor sites on their external surfaces

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25
Q

what are AMPA receptors responsible for

A

fast EPSP at excitatory synapses

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26
Q

describe AMPA receptors creating EPSP

A

calcium flows into presynaptic terminal
docked glutamate vesicles will fuse and dump glu into cleft and binds to AMPA receptor in postsynaptic cell and opens ion channel
pore is permeable to sodium, so sodium flows in and depolarizes

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27
Q

what is EPSP

A

small transient depolarization of the postsynaptic spine
depolarization is super short, a few milivolts and lasts around 20msec (long compared to ap)
just brings it a bit closer to threshold

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28
Q

in typical brain synapses

A

depolarization causes by a single EPSP is > (or equal to) a few milivolts and lasts around 20msec

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29
Q

is the depolarization caused by a single EPSP large enough to depolarize initial segment to threshold

A

NOOOO too small
need around 50-100 epsps
neuron usually has many synapses, most are excitatory EPSP and many of these happen at same time
they add to each other and drives postsynaptic cell to ap threshold

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30
Q

does ap happen in dendrites

A

nooo
depolarization spreads passively and can add together = depolarizes initial segement

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31
Q

how many epsps must sum at initial segment to initiate ap

A

50 to 100

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32
Q

what can the near simultaneous epsps come from

A

multiple synapses acting in synchrony
individual synapses activated at high frequencies

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33
Q

what are the 2 key properties of NMDA receptors

A

at resting membrane potential the pore is blocked by magnesium, depolarization expels magnesium and enables pore to conduct
open pore is highly permeable to calcium and monovalent cations

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34
Q

describe NMDA receptors at resting potential

A

pore plugged by mg
so will not react when glu arrives
also need glycine (along with glu)

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35
Q

describe NMDA receptors at threshold potential

A

if membrane is depolarized = mg comes out since the inside is not as negative, and magnesium is attracted to the negatives, unplugs and allows calcium to flow
opens and makes pore for calcium and flows into presynaptic cell and triggers biochemical events in spine

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36
Q

what does NMDA receptor act as

A

Coincidence receptor

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37
Q

what is a coincidence receptor

A

detects 2 things happening at same time
detects presynaptic neuron released glutamate and postsynaptic cell is already depolarized
if these 2 things happen at same time = NMDA receptor can conduct calcium into cell

38
Q

what happens at -70mv and if postsynaptic membrane is depolarized

A

at -70mv, almost all synaptic current at an excitatory glutamate synapse is carried by Na+ through AMPA receptors
if postsynaptic membrane is depolarized a substantial calcium current flows through NMDA receptors

39
Q

what is synaptic plasticity

A

high active excitatory synapses become stronger
epsps become larger
involves NMDA receptors

40
Q

how do you learn things

A

synapses which get stringer
ex = learn a new word, connections between the word and meaning become stronger by specific synapses becoming stronger, pathways become stronger

41
Q

what is LTP (long term potentiation)

A

Experimental protocol
records epsps in postsynaptic neuron and puts electrode to simulate presynaptic neuron
send an ap = 1 test pulse and then stimulate presynaptic membrane a bunch

42
Q

what happens when burst of aps (LTP)

A

high frequency activity depolarizes postsynaptic spine, removes magnesium block of NMDA receptor and enables them to conduct calcium
lots of glutamate released, induction phase

43
Q

what happens hours after induction of LTP

A

epsps are larger
send a single test pulse = will be larger than initial
synapse will have greater influence on if cell fires ap
many effects can happen

44
Q

what are the 3 steps/summary of LTP

A

control
induction
LTP

45
Q

what is excitotoxicity

A

high concentrations of glutamate is toxic to neurons
Phenomenon thought to involve calcium influx through NMDA receptors

46
Q

what is glutamate

A

also a neurotoxin
brain must regulate carefully

47
Q

what happens if too much glu

A

neurons get way too depolarized and lots of calcium flows into and if calcium is super high cell with die

48
Q

describe effect of msg

A

adults have blood brain barrier so glutamate will not get into brain
but in babies = not developed and more susceptible to excitotoxicity
(in olden days, msg would be in baby food since moms would taste and be like yum, so good for baby)

49
Q

describe effect of stroke

A

no oxygen to regions of brain and neurons die (1st phase of neurodegeneration) and release much glu and diffuses to other neurons and diffuses out of localized region where stroke happened into surrounding areas (penumbra) and too much depolarization and cells die too (2nd phase of neurodegeneration)

50
Q

what is excitotoxicity likely to contribute to

A

neuronal degeneration after stroke and in some neurodegenerative diseases
important in epilepsy

51
Q

what is main inhibitory neurotransmitter in brain

A

gamma-aminobutyric acid (GABA)

52
Q

what receptor is responsible for IPSPS

A

postsynaptic receptor GABA a receptor

53
Q

describe GABA a receptors

A

GABA is in vesicles and is released and binds to post synaptic ligand gated ion channels GABA a receptors
open and form pore and changes electrical properties of post synaptic cell

54
Q

what is GABA

A

neurotransmitter derived from amino acid
smal molecule

55
Q

what type of receptor is GABA a

A

ionotropic

56
Q

what does activation of GABA a receptor cause

A

influx of chlorine and hyperpolarizes postsynaptic membrane
inhibits post synaptic cell

57
Q

what can GABA a receptors be acted on by

A

pharmacological agents

58
Q

describe effects of benzodiazepines on GABA a

A

xanax and valium
mild tranquillizers
feel relaxed and sleepy
drugs bind to GABA a and potentiate, make receptor more sensitive to GABA enhances transmission to inhibitory synapses and causes more inhibition in brain and increased efficacy of inhibitory synapses

59
Q

describe effects of barbiturates on GABA a

A

phenobarbital and pentobarbital
do same thing and act on GABA and makes inhibitory synapses stronger
stronger than benzodiazepines
has bigger effect on receptors and will just put you to sleep

60
Q

describe effects of ethanol - alcohol on GABA a

A

makes you sleepy
acts on GABA a receptors
partly due to potentiating GABA a

61
Q

do neurons receive both excitatory and inhibitory synapses

A

yesssss
some of each type

62
Q

where are excitatory and inhibitory synapses located

A

excitatory = located on dendritic spines
Inhibitory = clustered on or near the cell soma, where inhibitory effect is maximal

63
Q

whether or not neuron fires ap depends on…

A

relative balance of EPSPs and IPSPs
depends on relative amounts of excitatory vs inhibitory, shapes firing power of neuron and how it communicates

64
Q

what is output of neuron

A

all or none firing of action potentials down axon

65
Q

can a neuron be both excitatory and inhibitory

A

NOOO
excitatory or inhibitory
will only released GABA or glu from terminal, will not switch back and forth

66
Q

give an ex of an inhibitory and excitatory neuron

A

pyramidal neurons = excitatory, release glu
perkinje = inhibitory, release GABA

67
Q

describe how inhibitory neurons are stimulated to release GABA

A

must fire ap and to fire ap must have excitatory synapses on dendrites
drives ap to inhibit other neurons

68
Q

what happens if there is no inhibition and just excitation

A

excitation takes over and feeds on itself = epileptic seizure, electrical storm in brain
inhibitory sculpts activity in nervous system and acts as break to control excitation
drugs that block GABA receptors can also cause seizures

69
Q

what are. Metabotropic receptors (G-protein coupled receptors, GPCRs)

A

different family of neurotransmitter receptors
not ion channels

70
Q

what do glutamate synapses have

A

ionotropic receptors = AMPA and NMDA
metabotropic glutamate receptors (mGluRs)

71
Q

describe mGluRs

A

not ion channels
activated by glutamate
relays chemical signal to inside of postsynaptic neuron

72
Q

what does activation of mGluRs generate

A

chemical signal called second messenger inside postsynaptic spine
changes conformation and becomes activated and initiates synthesis of 2nd messengers
receptor initiates biochemical events on inside of cell

73
Q

what are 2nd messengers

A

transmit messages, build up in cell and can diffuse
concentrations build up and then can activate proteins inside of cell, ex like bind to ion channel and open it up and change electrical properties of post synaptic cell

74
Q

what can 2nd messengers activate

A

ion channels
protein kinases
transcription factors

75
Q

are metabotropic receptors fast

A

nooooooooo
slow to turn on and off
generation, diffusion and effects of small molecules can last long

76
Q

describe 2nd messengers activating protein kinases

A

activate proteins
attaches phosphate groups to proteins
stick proteins to enzymes
changes biochemistry of cells

77
Q

describe 2nd messengers activating transcription factor

A

activated transcription factor migrates into nucleus and regulates transcription/expression of new genes (regulation of genes)

78
Q

what do glutamate and GABA activate

A

both ionotropoic and metabotropic receptors
glu = NMDA, AMPA and mGluRs
GABA = GABA b and GABA b

79
Q

what is difference between GABA a and GABA b

A

a = ionotropic
b = metabotropic
both activated by GABA

80
Q

what are neuromodulators

A

dopamine
serotonin
Norepinephrine
neuropeptides like endorphins
interact mainly or entirely with metabotropic receptors

81
Q

describe purpose of neuromodulators

A

not directly involved in fast flow of info, modulate global neural states like attention, mood, alertness
shapes overall properties (global) of neuron systems
overall functional states of nervous system

82
Q

describe effects of norepinephrine

A

involves in sleep wake cycles and attention
when asleep = neurons that release norepi are off
when awake = neurons that release norepi fire at steady rate
if suddenly pay attention = fires bursts of ap and release more norepi

83
Q

describe effects of serotonin

A

given for depression
specific serotonin reuptake inhibitors = increases amount of serotonin in brain
correlation between serotonin and mood
more serotonin is better than not enough

84
Q

describe effects of dopamine

A

involved in behaviour associated with reward
like casino and gambling, win = brain releases dopamine then neurons will release dopamine when gamble and you become a gambler
also cigarettes = cause increase in dopamine and indirectly affects other receptors, if an addict went into a room with people smoking = neuron will release dopamine

85
Q

where do neurons that release neuromodulators originate

A

small brainstem or mid brain nuclei
axons project diffusely throughout the brain

86
Q

describe neurons that release neuromodulators

A

small amount of neurons
small clusters of them
axons spread and branch all over brain and cerebral cortex

87
Q

neurons that release neuromodulators are usually…

A

targets for pharmacological agents = treat psychological disorders
main targets for substance abuse

88
Q

describe effect of cocaine

A

cocaine up nose = face turns numb
cocaine = local anesthetic like lidocaine and benzocaine
inhibits voltage gated sodium channels
but people still use it since it increases amount of dopamine and has stimulant and reinforcing effects, makes ppl wanna do it again

89
Q

name the 2 specific areas where neurons that release neuromodulators are

A

SN = substantial nigra
VTA = ventral tegmental area

90
Q

describe effects of antidepressants

A

affect serotonin transmission

91
Q

describe effects of amphetamines and cocaine and other stimulants

A

affect dopamine and norepinephrine (speeds you up, causes norepi neurons to release a lot of it) transmission

PHGY 209 (19 decks)

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