Neurotransmitters & Pharmacology Flashcards

1
Q

4 features of Synaptic Transmission

A

Rapid timescale
Diversity
Plasticity
Learning and memory

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2
Q

what are protien molecules called on dendrites

A

spine

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3
Q

function of cell body/soma

A

Information reception
then integration of the information
lastly
Rapid transfer (action potential)

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4
Q

function of spine

A

increase the surface area of recipet of information recipt

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5
Q

what sort of trasmition happen in an action potential

A

electrical (AP)
chemical(nuerotrasmiter)
Electrical (AP)

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6
Q

can nuerotrasmition happen anywhere else other than synapse

A

nope

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7
Q

what are the post synaptic clefts

A

dendrite or soma

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8
Q

Synaptic transmission: 3 stages

A
  1. Biosynthesis, packaging and release of neurotransmitter (●)
  2. Receptor action( bind to receptor on postsynaptic receptor)
  3. Inactivation(happens on the postsynaptic region)
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9
Q

3 types of nuerotrasnmitter

A

Amino acids
Amines
Neuropeptides

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10
Q

Recap: synaptic transmission – essential features

A

Restricted to specialised structures - the synapses

Calcium is essential - transmitter release requires an increase in intracellular Ca2+ (200 M)

Transmission is fast - within ms

Synaptic vesicles (SVs) provide the source of neurotransmitter (4,000-10,000 molecules per SV)

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11
Q

transduction

A

is the transmission of molecular signals from a cell’s exterior to its interior

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12
Q

where are the synaptic vesciles docked

A

synaptic zone

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13
Q

how do nuerotransmitter enter vescicles

A

they have protien pumps

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14
Q

after being docked onto the pre synaptic membrane what happens

A

theyre primed
to release the nt
then fuse

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15
Q

what do the Special proteins on the vesicle and presynaptic membrane enable

A

enable fusion & exocytosis

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16
Q

what are they called on vesicles

A

vesicular protien
mediate the action of exocytosis of nt
improtnant in docking

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17
Q

Vesicular proteins are targets for

A

neurotoxins

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18
Q

what is Alpha latrotoxin

A

from black widow spider

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19
Q

function

A

stimulates transmitter release to depletion of presynaptic termial

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20
Q

what do the victims suffer from

A

muscular paralysis

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21
Q

function of Zn2+-dependent endopeptidases

A

inhibit transmitter release

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22
Q

example using tetanus toxin

A

causes spasms & paralysis

by inhibiting GABA and glycine release

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23
Q

another example using BOTULINUM TOXIN

A

causes flaccid paralysis

paralyisis due to muscle relaxation

24
Q

structure of BOTULINUM TOXIN

A

bi chain (2 chain)

25
Q

how does it work

A

first part binds to nerve terminal (cholernergic)

2nd chain penetrates the cholonergic nerve terminal and intercats with vesicular proteins
cleaves peptide bond thus inactivating them
so you no longer get docking
fusion or relase of transmiter

26
Q

how is vesicle docking and a rapid response to Ca2+ entry leading to membrane fusion and exocytosis enabled

A

Protein complex formation between vesicle, membrane and cytoplasmic proteins

27
Q

is the transmitter release require energy

A

yes

28
Q

Ion channel-linked receptors

mediate what sort of trasnmittion

A
FAST response (msecs)
Mediate all fast excitatory and inhibitory transmission
29
Q

exitotory signal is produced by what

A

opening of sodium ion channel (glutamate receptors)

leads to depolarisation of post synaptic terminal

30
Q

and ihnibitory

A

chlorine( GABA) leads to hyperpolarisation of postsynaptic terminal

31
Q

G-protein-coupled receptors

mediate what action

A

SLOW response (secs/mins)

32
Q

what are the effectors

A

enzymes or channels

33
Q

what happens upon binding to the gpc receptor

A

g protien binds to a receptor inside the cell (adenyl cyclase) produces sencond messenger like cAMP ehich causes effect to enzymes or channel

34
Q

examples of Ion channel-linked receptors

A

CNS- Glutamate,GABA

NMJ-ACh at nicotinic receptors (nuermo muscular junction)

35
Q

G-protein-coupled receptors

examples

A

CNS and PNS: ACh at muscarinic receptors
dopamine
noradrenaline
serotonin

36
Q

Ion channel-linked receptors have how many subunits

and what do they allow

A

5

→ distinct functional properties

37
Q

what does a excitatory nurotranssmitter receptor cause

A

an excitory postsynaptic potential

EPSP

38
Q

what does an Inhibitory neurotransmitter receptor

cause

A

inhibitory postsynaptic potential (IPSP)

39
Q

what is the main Excitatory trasmitter in brain

A

Glutamate

40
Q

and Inhibitory t in brain

A

GABA

41
Q

2 examples of Glutamate receptors

A

AMPA RECEPTORS

NMDA RECEPTORS

42
Q

AMPA RECEPTORS mediate

A

Majority of FAST excitatory synapses

Rapid onset, offset and desensitisation

permeable to na

43
Q

NMDA RECEPTORS

mediate

A

Slow component of excitatory transmission

Serve as coincidence detectors which underlie learning mechanisms

44
Q

NMDA RECEPTORS permeable to

A

na and ca

45
Q

how is glutamate synthesised

A

from glucose via TCA cycle & transamination

46
Q

what happens once glutamate is exocyotsed

A

Glutamate reversibly binds postsynaptic receptors

47
Q

how is it inactivated

A

Rapid uptake of glutamate

reloaded in vesicles and used again

48
Q

how are they uptaken in glial cell and where are they

A

glial cell surround synapses

3. Rapid uptake of glutamate by excitatory amino acid transporters (EAATs)

49
Q

what happens in the glial cell

A
  1. Glutamate enzymatically modified by glutamine synthetase to glutamine in glial cells
50
Q

by what enzyme

A

glutamine sythesase

51
Q

what happens to the glutamine

A

in is pumped into presynaptic teminal and used to make more glutamate

52
Q

what is the process called

A

glutamate glutimine cycle

53
Q

what happens when too (uncintrolled) much glutamate release

A

spiking in the Electroencephalography (EEG) (measures electrical activity in the brain)

54
Q

what happens if too much glutumate in synapse

A

Abnormal cell firing leads to seizures associated with excess GLUTAMATE in the synapse

55
Q

what happens as the glutamate is comming bac =k down to normal level

A

converted to glutamine but takes lomger to come back down to normal level