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Neuroscience > Synapses and Neurotransmitters 1 - 3 > Flashcards

Synapses and Neurotransmitters 1 - 3 Flashcards

1
Q

synapse is

A 
junction between 2 neurons allowing signals to pass
evidence for neurons: 
golgi stain
study of reflexes
electron microscopy
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2
Q

electrical synapse

A

formed of gap junction that allows current to pass directly between neurones
directly connects cytoplasms
made of connexin proteins that join to make connexons then gap junctions

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3
Q

how to tell if neurons are connected by gap junctions

A

small molecules e.g. dyes diffuse from one neuron to other
researchers filled green neuron with red dye and saw another neuron fill with red dye
both hyper and depolarising stimuli passed from one neuron to other - blocked by deleting a connexin gene

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4
Q

electrical synapses are good for …

A

fast communication, synchronising neurons

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5
Q

first evidence of a chemical synapse

A 
2 isolated frog hearts
stimualte vagus nerve
heart rate slows
remove fluid
add to other heart
heart rate slows
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6
Q

prototypical chemical synapse

A

post synapse can be another neuron or non neuronal
e.g.
motor neuron — skeletal muscle
autonomic neuron —- hormonal gland, smooth muscle or heart

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7
Q

steps in chemical synaptic transmission

A

1 - package neurot in vesicle, put at pre synaptic terminal
2 - action potenital arrives —-> voltage gated Ca channels opens
3 - Ca influx —–> vesicles fuse to membrane, neurot released
4 - neurot diffuses across cleft, activate receptors on post syn membrane —-> further signalling
5 - neurot removed from cleft

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8
Q

synaptic vesicles vs secretory granules

A

‘clear’, small (40-50nm) —– ‘dense’, large (100nm)
small molecule neurot —– peptide neurot
filled by transporter proteins at pre-syn terminals —– created and filled by ER/ Golgi secretory apparatus
recycled by endocytosis —– ‘one and done’

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9
Q

fusion of vesicles

A

via SNAREs
Vesicle SNAREs or Target SNAREs
when vesicle is ready to fuse, SNAREs join together to anchor it down
synaptotagmin forms complex with SNAREs, it has Ca binding sites so when Ca enters it binds and changes synaptotagmins shape = makes SNARE ‘zip’ together forcing vesicle to fuse to plasma membrane
SNAREs are targets for toxins e.g. botulinum / tetanus toxin

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10
Q

bidning at post synaptic receptors

A

ligand gated ion channels (ionotropic) - directly depolarise or hyperpolarise post-syn cell
GPCR (metabotropic) - more complex effects

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11
Q

removal of neurotransmitter

A

different methods:
1 - diffuse away
2 - actively took up by transporters for recycling (into pre syn or glia)
3 - destroyed in synaptic cleft by enzymes

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12
Q

electrical vs chemical synapses

A

signals pass in both directions —– one direction
passed directly, cna only be attenuated —– can be radically transformed
fast —– slower
both are ‘plastic’ - can be modified, but chemical more so allowing summing up of inputs by post neuron
most synapses = chemical

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13
Q

neuromuscular junction

A

fast and reliable transmission
mtotor neuron action potenitals always cause muscle cell action potential
uses ACh
one of largest synapses
presyn - large no of active zones
postsyn - motor end plate, contains juncitonal folds that precisely align with active zones, densely filled with neurot receptors

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14
Q

how did we find that neurots come from vesicles?

A

stimulate motor nerve and record from muscle

  • evoked response were all integer multiple of spontaneous potenitals
  • statistical distribution showed neurot come in quantal packets
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15
Q

CNS synapses

A

axodendritic
axoaxonic
axosomatic

dendrosomatic
dendrodendritic

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16
Q

neurotransmitters should be …

A

in pre synaptic terminals
released in respnse to stimulation
acting on post syn

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17
Q

experiments for determining neurot molecules -

is it there?

A

immunohistochemistry e.g. antibody testing

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18
Q

experiments for determining neurot molecules -

does the cell express enzymes to synthesise it or transporter proteins to store it?

A

immunostaining - in situ hybridisation

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19
Q

experiments for determining neurot molecules -

is it released?

A

collect fluid around neruons after stimulating (difficult)

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20
Q

experiments for determining neurot molecules -

does it affect post syn cell?

A

test if molecule mimics effect of stimulating pre syn cell

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21
Q

experiments for determining neurot molecules -

does it block neurotransmitters?

A

apply drugs, delete genes encoding enzyme/transporters/receptors

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22
Q

types of neurotransmitters

A

amino acids
amines
peptides
neurons usually release only one kind of neurot , but can release more
often peptide releasing neurons also release small mol transmitter = co transmitter

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23
Q

amino acid and amine neurot

A

small molecules
stored in vesicles
bind to ligand gated ion channels or GPCR

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24
Q

peptide neurot

A

large molecules
stored in secretory granules
only bind to GPCRs

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25
types of neurot receptors
lignag gated ion channel - ionotropic directly depolarise/hyperpolarise post syn cell GPCR - metabotropic multiple possible 2nd messengers - allow amplification
26
convergence and divergence
allow flexibility each transmitter can activate multiple receptors = divergence each receptor can have different downstream effectors different transmitters/receptors can activate same downstream effectors = convergence
27
glutamate
most common excitatory transmitter in CNS amino acid found in all neurons 3 ionotropic glutamate receptor subtypes selective agonists action is terminated by selective uptake into presyn terminal and glia
28
3 subtypes of glutamate receptors
AMPA NMDA kainate
29
AMPA receptors
mediate fast exitatory transmission Ca cant pass through channel opens and lets Na/K in results in excitatory post syn potential - EPSP at rest cell is mostly permeable to K so cells mem pot lies quite close to Nernst pot for K, when channel opens it allows permeablility to both so mem pot becomes more positive
30
NMDA receptors
often co exist with AMPA receptors voltage dependant Mg block only open when neuron is already depolarised let Ca in ---> downstream signalling function as coincidence detectors: at rest Mg is attracted by -ve voltage in cell which blocks opening of pore, if cell was previously depolarised Mg wont block so glutamate binds and it opens which lets Na, K and Ca in
31
glutamate also activates metabotropic glutamate receptors
mGluRs - allows glutamate to sometimes by inhibitory
32
ionotropic vs metabotropic glutamate receptors - receptor - example - mechanism - speed
4 subunits forming gated ion channel ----- GPCR AMPA, NMDA ----- mGluR1/2 open ion channel ----- activiate G proteins, trigger cascade fast (msec) ----- slow (sec/min)
33
GABA ( gamma amino butyric acid)
not an amino acid used to syntheisise proteins made from glutamate by glutamic acid decarboxylase action is terminated by selective uptake in presyn terminal or glia normally an inhibitory neurot , most common one in CNS produces IPSPs via GABA-gated chloride channels (GABAa receptors), if membrane potenital is above Nernst pot for Cl- too much inhibition = coma/loss of conciousness (silencing too many neurons) too little = seizures (over excited neurons)
34
modulation of GABAa receptors
other chemicals can bind to this receptor and modulate response to GABA binding have no effect without GABA binding (allosteric binding) ethanol benzodiazepines neurosteroids barbiturates
35
GABA also acts via metabotropic GABAb receptors
GPCRs act in diverse ways in different cells but may: open K channels, close Ca channels, trigger other 2nd messengers like cAMP often presynaptic or autoinhibitory - feedback loop
36
glycine
inhibits neurons via glycine gated chloride channels - opens channel Cl enters cekk which suppresses post syn from firing or binds to NMDA glutamate receptors, sometimes binding of glycine and glutamate needed for receptor to open
37
dendritic integration
multiple EPSPs in dendrites, current travels passively | spike initiation zone at cell body makes action potential and travels along axon
38
spatial arrangement
an inhibitory signal can block propagation of an EPSP towards soma GABAa receptor dont always produce IPSP e.g if Vm is near Cl nernst potential in this case they act by shunting inhibition opening Cl conductance decreases membrane resistance - current leaks out of membrane if arranged differently inhibitory signal would have no effect on action potential
39
presynaptic inhibition
GABA blocks output of another neurons presynaptically GABA causes inactivation of Ca channels so less Ca enters and less neurots are released which causes a reduced effect on post syn membrane
40
acetylcholine
made by ChAT - from acetyl CoA and choline = good marker for cholinergic neurons ACh broken down in cleft by acetylcholinesterase into acetic acid and choline choline is re taken up by choline transporter to make more ACh acts on nicotinic and muscarininc receptors
41
ACh and nicotinic receptors
ACh gated Na/Ca channel, found at NMJ in CNS
42
ACg and muscarininc receptors
5 types if GPCRs, found in CNS and ANS - vagustoff from experiment was ACh
43
how do different molecules affect ACh?
block release block aceytlcholinesterase activate ACh receptors block ACh receptors
44
blocking release of ACh
botulinum toxin - by destroying SNAREs to stop fusion of vesicles therefore diapraghm doesnt work = die black widow venom - causes large Ca influx = release ACh but stops further release
45
blocking ACh enzyme
nerve gas - ACh isnt broken down so activation of muscles is messed up organophosphate pesticides - ACh stays in cleft too long alzheimers treatment - cholinergic neurons die, so stop exsisting ACh from being taken up may help
46
activating ACh receptors
nicotine and muscarine | neonicotinoid pesticides
47
blocking ACh receptors
nicotinic - curare, alpha-bungarotoxin (snake venom) | muscarin - atropine
48
monoamines
synthesised from amino acids catecholamines: dopamine, norepinephrine, epinephrine seratonin: made from tryptophan
49
storage and removal of monoamines
packed into vesicles by vesicular monoamine transporters removed from cleft by reuptake transporters - specific for each monoamine destroyed by monoamine oxidase (MAO) and catechol-o-methyltranferase (COMT) on post syn cell - only for catechols not serotonin
50
monoamine receptors
mostly GPCR | different receptors activate different G protein effectors
51
neurotransmitter and its receptor
dopamine ----- D1 like receptors: D1, D5 and D2 like receptors: D2,3,4 nor/epinpehrine ----- adrenergic: alpha and beta types seratonin ----- 7 receptors - 6 GPCRs and 1 ligand gated Na/K channel
52
dopamine in motor control
dopaminergic neurons are in the nucleus substantia nigra and project to striatum nigrostriatal pathway facilitates initiation of voluntary movement these neurons die in parkinsons disease
53
treating parkinsons
by increasing dopamine tyrosine --(tyrosine hydorxylase - rate limiting step)-- L dopa ---- dopamine so can give L dopa to patients as it crosses blood brain barrier MOA-B inhibitors MOA-B is an enzyme that destroys dopamine so can enhance remaining dopamines actions
54
dopamine in reward
these neurons live in ventral tegmental area and project into cortex and limbic system mesolimbic pathway mediates reward/motivation
55
noradrenergic neurons
regulate arousal small number in locus coeruleus innervate whole brain sleep/wake, attention, arousal, mood
56
serotonergic neurons
regulate sleep/wake, mood | live in Raphe nuclei, project all over brain
57
drugs affecting monoamines
cocaine, amphetamines - block reuptake of dopamine (increase of dopamine in cleft = rewarding) and norepinephrine antipsychotics - block dopamine receptors (possible side effect: Parkinson-like effects) antidepressants: tricyclics - block reuptake of NE, seratonin SSRIs - selective, only block seratonin receptors MOA-A inhibitors - stops seratonin being destroyed
58
other important neurotransmitters
opioid peptides ATP endocannabinoids nitric oxide
59
opioid peptides
bind to opioid receptors - GPCRS regulate pain perception, emotion etc regulate coughing, GI tract opioid receptors = target of morphine and heroin
60
ATP
often a co transmitter P2X2 - ATP gated ion channels P2Y2 - GPCRs
61
endocannabinoids
lipid soluble, not in vesicles Ca triggers synthesis, not vesicle fusion retrograde signalling ( postsyn--->pressyn) bind to GPCRs - target of THC
62
nitric oxide
gas - membrane permeable | acts on soluble guanylate cyclase, not membrane receptor

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