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physiology and pharma > L1 - neurotransmitter release > Flashcards

L1 - neurotransmitter release Flashcards

1
Q

what is SSRRRD

A 
Synthesis 
Storage 
Release 
Receptors 
Reuptake 
Degradation
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2
Q

list the types of NT release

A

spontaneous
asynchronous
calcium independant
synchronous

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3
Q

what is spontaneous NT release

A

small amounts of NT release that is calcium dependant but doesnt trigger action potential

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4
Q

what is asynchronous NT release

A

AP may be triggered but not in time with NT release.

Ca dependant also

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5
Q

describe calcium independent NT release

A

NT release via revere transportation of a transporter

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6
Q

what is synchronous NT release

A

calcium dependant release of NT triggers AP

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7
Q

describe process of synchronous NT release

A
  1. depolarisation of presynaptic neurone (beginning in axon travelling to presynaptic terminal)
  2. triggers opening of VGCCs - Ca influx
  3. causes vesicular movement and priming
  4. vesicles dock via snare proteins
  5. vesicle fusion with presynaptic membrane
  6. NT released and vesicle recycled
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8
Q

describe process of presynaptic neurone depolarisations

A
  1. EPSPs and IPSPs from dendrites further upstream summate at the cell body
  2. if the EPSPs are sufficient and reach the threshold -55mv an AP is generated in the axon hillock (spike initiation zone)
  3. AP travels down axon jumping between nodes of ranvier
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9
Q

why are APs initaited in the Axon hillock / spike initiation zone?

A

high concentration of VG Na and K channels

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10
Q

why do nodes of ranvier conduct AP well?

A

high concentration of VG Na and K channels

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11
Q

how does the AP change from the presynaptic axon to terminal and why

A

width in axon -> 2ms
width in presynaptic terminal -> 350ms

the presence of Ca channels increases the width of the AP

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12
Q

why does Ca infulx?

A

Conc trandient and voltage gradient

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13
Q

list the names of the subfamilies of calcium channels

A

Cav1 (L)
Cav2 (N)
Cav3 (T)

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14
Q

describe opening of Cav1 channels

A

stay open for long time, dont inactivate quickly

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15
Q

describe opening of Cav2 channels

A

open and inactivate at a speed between Cav1 and Cav3

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16
Q

describe opening of Cav3 channels

A

stay open for very short period (fastly inactivating)

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17
Q

explain the difference between C channel opening times

A

the faster inactivating, briefly open Cav2&3 are involved in NT release
the longer open, slower inactivating Cav 1 is involved in muslce contraction

18
Q

describe general negative feedback pathway of NTs

A

NT binds to GPCR coupled receptors (Go) which interacts with and blocks VGCC reducing the amount of Ca entering the terminal

19
Q

describe the general positive feetback mechanism of NTs

A

NTs bind to Ligand gated ion channels on presynaptic membrane, allowing more Ca entry

20
Q

what receptor is involved in long term potentiation, describe it

A 
NMDA glutamate 
(presynaptic, LGIC, allows Ca entry)
21
Q

name a calcium independant type of NT release

A

reverse transportation of a transporter

22
Q

what is the difference between ion channels at the NOR and presynaptic terminals

A

NOR -> Na and K

terminal -> Na, K and Ca

23
Q

which G protein subtype regulates NT release? where is it found

A

Go

presynaptic membrane

24
Q

what is priming?

A

vesicular movement and molecular changes that allow vesicle fusion to occur

25
Q

what are SNARES

A

proteins found on vesicles and cell membranes

65 residue domains`

26
Q

name the 3 snare proteins

A

synaptobrevin
syntaxin-1
SNAP25

27
Q

where is synaptobrevin found?
does it have TMDs
how many SNARE motifs

A

vesicle membrane
yes 1
1

28
Q

where is syntaxin-1 found
how many TMDs
how many SNARE motifs

A

cell membrane, on top of SNAP25
0
1

29
Q

where is SNAP 25 found
does it have TMDs
how many SNARE motifs

A

cell membrane
yes
2

30
Q

describe synaptotagmin components

where is it found ?

A

+ve amino acids (+ve charged)
Ca binding motifs
PIP2 binding motifs

within snare complex

31
Q

describe function of synaptotagmin

A
  1. Ca binds to synaptotagmin
  2. triggers binding of synaptotagmin to PIP2
  3. leads to structural change opening up snare complex and membranes, releasing NT
32
Q

describe process of vesicle fusion

A
  1. Ca binds to synaptotagmin
  2. triggers binding of synaptotagmin to PIP2
  3. leads to structural change opening up snare complex and membranes, releasing NT (exocytosis)
33
Q

what happens during vesicle recycling

A

readdition of synaptobrevin and transporters to vesicle membrane

34
Q

describe co release

A

when two different NTs are released from the same terminal

the NTs can either be in the same vesicle, or separate vesciles for each NT

35
Q

what is segregation

A

where one axon has two different presynaptic terminals releasing different NTs`

36
Q

example of two NTs that are co released? and where from

A

ATP and NA in sympathetic vas deferens

37
Q

what controls Ca2+ release from ER / SR

A

ryanodine receptors (ca2+ mediated Ca2+ release)

IP3 receptors

38
Q

define EPSP

A

excitatory post synaptic potential. This is a subthreshold positive change in
potential derived from an excitatory neuronal input through changes in Na+
conductance. These can summate to initiate the action potential at the axon hillock

39
Q

define IPSP

A

inhibitory post synaptic potential. This is a subthreshold negative change in
potential derived from and inhibitory neuronal input, usually thorough increase Cl- or
K
+ conductance. These can also summate to make the potential more negative, and
thus an action potential less likely to occur.

40
Q

what occurs at the axon hillock>

A

summation of EPSPs and IPSPs

41
Q

what features of the axon hillock that allow AP to be generated here

A

located very close to axon so is able to summate inputs from soma

has high density of Na+ and K+ channels, so if the threshold for AP is reached many can open at once triggering an AP

physiology and pharma (18 decks)

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