Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuroscience > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

who proved the basis of chemical transmission?

describe his experiment

A

Otto Lewi in 1992

he took an isolated frogs’s heart with its vagus nerve connected

if he electrically stimulated the vague nerve
-> could alter the contraction of the heart

made a cut through the vague nerve to break the electrical connectivity to the heart muscle

removed the bathing solution surrounding the original
-> showed that the solution could mimic the electrical excitability seen when the nerve was connected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what was Loewi postulating?

what was the soluble molecule in the solution surrounding the heart in Loewi’s experiment?

A

the electrical stimulation of the heart was releasing some sort of messenger that was driving the contraction

acetylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are neurotransmitters?

what are the 2 fundamentally important synapses?

A

endogenous chemicals
which transmit signals from a neurone to a target cell
across a synapse

axodendritic
neuromuscular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the 3 stages leading to post-synaptic signal?

A
  1. presynaptic action potential
  2. depolarisation of synaptic terminal
  3. release of chemical transmitter
  4. postsynaptic signal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the major neurotransmitters of the mammalian brain?

what are the synapses that use these called?

A

glutamate
(glutamatergic)

GABA
(GABAergic)

ACh
(Cholinergic)

Noradrenaline
(Noradrenergic)

Dopamine
(Dopaminergic)

5HT (serotonin)
(Serotonergic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the composition of ACh?

what is required for this to form?

A

an ester of acetic acid and choline

blood supply to brain, brings choline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the 3 amino acid neurotransmitters?

are they inhibitory or excitatory?

which NT is a glutamate derivative?

which purine is a NT?

A

glutamate
(excitatory)

aspartate
(excitatory)

glycine
(inhibitory)

GABA

ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which amino acid are catecholamine NTs synthesised from?

what are these NTs?

A

tyrosine

dopamine

noradrenaline

adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

which indoleamine is an NT?

which amino acid is this synthesised from?

which imidazoleamine is an NT?

A

serotonin

tryptophan

histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what criteria define a ‘classical’ NT?

A
  1. synthesis
    - regulated synthetic machinery in the nerve terminal
  2. storage
    - in secretory vesicles
  3. release
    - regulated release into the synaptic space
  4. reception
    - presence of receptors
  5. removal
    - a means for terminating the action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe the life cycle of a typical NT

A
  1. synthesis of NT at nerve terminal
  2. packing of NT into small vesicles
  3. action potential depolarises membrane -> Ca2+ influx
    - > triggers fusion and release of vesicles
  4. NT interacts with postsynaptic receptors
  5. clearance system
    e. g. uptake via transport system into a glial cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are autoreceptors?

A

receptors in the presynaptic membrane of the nerve terminal

bind the release signal molecule

to regulate further NT release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

describe the synthesis and vesicular packaging of glutamate

what type of gradient does this require?

A

glutamine
-> glutamate
using glutaminase

VGluT
(vesicular glutamate transporter)
actively transports glutamate into the vesicles

proton gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how is ACh synthesised?

A

from acetic acid and choline

via choline acetyl transferase (ChAT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe what happens at a cholinergic synapse

A

ACh is synthesised + packaged into vesicles

vesicles fuse with membrane + release ACh into synapse

binds to nicotinic or muscarinic postsynaptic receptors

signal is propagated until ACh is terminated via enzymatic degradation by AChE
(acetylcholinesterase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does AChE produce?

where is it located?

what happens to choline?

why?

A

acetate and choline

lipid-anchored to presynaptic membrane

taken back up by a transporter

it is a limiting resource

  • relies on delivery via blood from diet
  • so makes sense to recycle it
17
Q

what is AChE a primary drug target for?

A

treating Alzheimer’s disease

inhibition of AChE

  • > maintains ACh levels
  • > prolongs cholinergic signalling
18
Q

what cognitive process are glutamatergic synapses responsible for?

A

memory

19
Q

describe glutamate synthesis

how is this packaged into vesicles?

when do these vesicles fuse with the membrane?

A

glutaminase converts glutamine into glutamate

via the VGluT

when the membrane is depolarised

20
Q

which post-synaptic receptor sub-types does glutamate interact with?

A

AMPA receptors
NMDA receptors
mGlu receptors

21
Q

what are AMPAR and NMDAR both classed as?

which ions interact with the receptors?

A

glutamate-gated ion channels

AMPA = sodium 
NMDA = sodium + calcium
22
Q

where did the AMPA and NMDA nomenclature come from?

A

NMDA and AMPA are chemical analogs of glutamate

  • they don’t exist in the mammalian nervous system
  • but are synthetic chemicals that can distinguish between the 2 receptor sub-types
23
Q

what is the basic structure of mGlu?

what is is responsible for?

A

7 transmembrane spanning receptor

slower signalling
- metabolic processes

24
Q

how is glutamate taken up by astrocytes (glial cells)?

what happens to glutamate in the glial cell?

A

EAATs
(excitatory amino acid transporters)

glutamate converted to glutamine
via glutamine synthatase

25
Q

what happens to glutamine in the astrocyte?

what is this process known as?

A

glutamine exported out of astrocyte through SN transporter
- retaken up into nerve terminal via SA

glutamine broken down by glutaminase
-> glutamate

glutamate-glutamine shuffle

26
Q

why is the glutamate-glutamine shuffle required?

what can over-excitation result in?

A

to detoxify the glutamate
+ prevent over-excitation

damage
-> associated with disorders e.g. epilepsy

or even post-ischemic stroke

27
Q

what is the metabolic link between glutamate and GABA?

how does this effect the neurone?

A

glutamate can be produced downstream from basic metabolism

glutamate can be converted to GABA via GAD (glutamate decarboxylase)

goes from being an excitatory neurone to an inhibitory one

28
Q

what tri-peptide does glutamate give rise to?

what is its function?

A

glutathione

major protective antioxidant in the mammalian nervous system
- scavenges free oxygen radicals

29
Q

describe what happens at a GABAergic synapse

A

glucose -> glutamate -> GABA (via GAD)

  • > packaged into vesicles
  • > exocytosis of GABA into synapse

GABA binds to receptors on post-synaptic membrane

30
Q

what are the GABA receptors on the post-synaptic membrane?

how is GABA removed from the synapse?

why is GABA not shuttled back to the nerve terminal?

A

GABA-A receptors
= ion channels

GABA-B receptors
= GPCRs

via GAT on glial cells or nerve terminals

GABA can be synthesised from glucose via basic metabolism
+ GABA is less toxic so doesn’t need an elaborate control system

31
Q

describe what happens at a dopaminergic synapse

A

tyrosine enters nerve terminal

  • > converted into DOPA
  • > dopamine
  • > packaged into vesicles
  • > exocytosis into synapse
  • > dopamine binds to post-synaptic receptors
32
Q

what receptors does dopamine bind to?

how is dopamine removed?

how is this dopamine than metabolised?

A

D1R and D2R
= GPCRs

via (DAT) dopamine transporter

via MAO (monoamine oxidase) + COMT (catechol-O-methyl transferase)

33
Q

describe the biosynthesis of catecholamines

A

tyrosine
-> DOPA
via tyrosine hydroxylase (adds hydroxyl group)

DOPA
-> dopamine
via DOPA decarboxylase
(removes carboxyl group)

dopamine
-> noradrenaline
via dopamine-beta hydroxylase

noradrenaline
-> adrenaline
via phenylethanolamine N-methyl transferase

34
Q

what is the presence of tyrosine hydroxylase defining of?

A

a catecholinergic synapse

e.g. dopamine, noradrenaline or adrenaline

35
Q

a neurone can only produce what?

A

one type of neurotransmitter

36
Q

describe the synthesis of serotonin (5HT)

A

tryptophan
-> 5-hydroxytryptophan
via tryptophan-5-hydroxylase

5-hydroxytryptophan
-> serotonin
via aromatic L-amino acid decarboxylase

37
Q

which part of the brain uses dopamine as an NT?

which part of the brain uses serotonin as an NT?

which part of the brain uses glutamate as an NT?

A

substantia nigra
in the basal ganglia

Raphe nuclei
= sleep centre of the mammalian NS

hard to know
- can’t stain for the synthetic enzymes as they’re involved in central metabolism

BUT can stain for VGluT
(>60% of synapses stain)

38
Q

what do all drugs in humans target to treat all neurological disease?

A

synthesis,
breakdown,
or mimics the signalling
…of NTs

Neuroscience (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions