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Year Two - Brain and Behaviour > Chemical Signalling > Flashcards

Chemical Signalling Flashcards

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1
Q

outline synaptic transmission.

A
  • AP reaches synaptic terminal
  • NTs released and diffuse across synaptic cleft
  • receptors recognise NTs and initiate a response
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2
Q

define neuromodulation

A

alters presynaptic cells ability to release more NT or post-synaptic cells ability to respond

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3
Q

name categories of NT.

A
  • amino acids
  • monamines
  • acetylchlorine
  • neuropeptides
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4
Q

where are classical NTs synthesised and where are neuropeptides synthesised?

A

classical NTs are synthesised locally in pre-syn terminal whereas neuropeptides are synthesised in the cell soma and transport to the terminal.

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5
Q

what type of transmitter is responsible for fast transmission?

A
  • amino acids
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6
Q

name the difference between excitatory and inhibitory.

A

excitatory causes the next neurone to fire an impulse whereas inhibitory blocks the next neurone from firing an impulse.

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7
Q

state criteria for NTs

A
  • chemical synthesised pre-synatically
  • electrical stimulation leads to the release of the chemical
  • chemical produces physiological effect
  • terminate activity
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8
Q

outline glutamate synthesis, storage, release and reuptake.

A
  1. synthesised in nerve terminals from glucose or glutamine
  2. loaded and stored in vesicles by vesicular glutamate transporters
  3. released by exocytosis
  4. acts at glutamate receptors on post-synaptic membrane
  5. reuptake by excitatory amino acids transporters in the plasma membrane of pre-synaptic cell and surrounding glia
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9
Q

what can too much glutamate and too little GABA lead to…

A

hyperexcitatory - epilepsy, excitotoxicity

cereal ischemia - insufficient blood flow

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10
Q

receptors can vary in their pharmacology, define pharmacology.

A

what transmitter binds to receptor and how drugs interacts varies

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11
Q

describe the difference between agonist and antagonist.

A

agonist are drugs that can combine with a receptor on a cell to produce a cellular reaction, whereas antagonists are a drug that reduces or completely blocks the activity of the agonist.

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12
Q

define kinetics.

A

rate of transmitter binding and channel gating determine the duration of effects.

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13
Q

define selectivity and conductance.

A
  • what ions are fluxed

- rate of flow

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14
Q

outline fast synaptic transmission.

A
  • glutamate inotropic receptors in general flux Na+ which causes an EPSP depolarising the post-syn neurone.
  • GABA ionotropic receptors flux CI- which causes an IPSP hyper-polarising the post-synaptic neurone
  • integration of all changes in membrane potential will decide whether a post-synaptic neurone will fire an AP or not.
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15
Q

state ionotropic receptors that respond to glutamate.

A

NMDA
AMPA
Kainate

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16
Q

defien AMPA.

A

binding of glutamate leads to the opening of Na+ channels and hence depolarisation.

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17
Q

in NMDA, what happens during the RMP and depolarised membrane?

A

RMP - glutamate binds, channel opens, blocked by Mg+

depolarised membrane - Mg+ pushed out of pore, channel is open, ion movement, further depolarisation.

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18
Q

which receptor has slower kinetics?

A

NMDA - channel stays open longer

  • requires glycine as a cofactor
  • and gated by membrane voltage
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19
Q

describe the association between NMDA and schizophrenia.

A

NMDA receptors blocked by phencyclidine and MK801 which both bind in one space, producing symptoms that resemble the hallucinations in schizophrenia (reduced NMDAR function).

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20
Q

what causes glutamate excitatoxiticty?

A
  • excessive Ca+ influx into cell which activates calcium dependent proteases and phospholipase that damage cell, can lead to stroke.
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21
Q

outline GABA synthesis, storage, release and reuptake.

A
  1. GABA is synthesised from glutamate
  2. GABA is loaded and stored into synapse by a vesicular GABA transporter
  3. GABA released by exocytosis
  4. acts at ionotropic GABAa and metabotropic GABAb receptors o post-synaptic membrane
  5. cleared from synapse by reuptake using transporters on glia and neurones including non-GABAergic neurones.
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22
Q

what can too much GABA cause?

A
  • sedation/coma
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23
Q

what drug increases the amount of available GABA?

A

GHB - moderate dose like alcohol

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24
Q

name differences between GABAa receptors and GABAb receptors.

A

GABAa are ligand gated C- channel, whereas GABAb are G-protein coupled, GABAa are fast IPSPs, GABAb are slow IPSPs.

25
Q

how many submits does the heteropentamic structure have?

A

2 - 3 more submits

6 possible submits

26
Q

which out of muscimol and bicycling, picrotoxin is an agonist?

A
  • muscimol

- bicucline, picrotoxin are antagonists.

27
Q

what can drugs increasing GABA lead to?

A

reduced anxiety.

28
Q

name drugs that increase GABA.

A
  • alcohol, barbiturates, BDZ
29
Q

name drugs that increase anxiety.

A

antagonists e.g. fluazenil, decreases GABA.

30
Q

give evidence for GABAergic dysfunction in anxiety disorders.

A

PD patients have less BZD binding sites and lack sufficient inhibitory control in cortical and limbic regions to suppress inappropriate fear responses and subsequent panic attacks.
frontal cortex shows hyperactive responsiveness during periods of anxiety.

31
Q

state problems to barbiturates (amplifies GABA).

A
  • depression of neuronal activity
  • poor therapeutic ratio - small difference between therapeutic dose and overdose
  • lead to dependence
  • only used for severe insomnia, seizures
32
Q

what do BZDs act as…

A
  • anxiolytic
  • anticonvulsant
  • sedative
  • muscle relaxant
  • amnesic
33
Q

state advantages and disadvantages to BZDs.

A

advs - fast acting

dis - dependance

34
Q

define neuromodulators.

A

affect response properties of neurone, some NMs act as NTs, and some NTs acts as NMs,

35
Q

describe the dopaminergic system.

A
  • cell bodies in the midbrain

- project into forebrain

36
Q

describe the nigrostraital system.

A

role in movement

- dysfunction: parkinsons, huntingtons

37
Q

describe the mesolimbic system

A

role in reinforcement

- dysfunction: addiction

38
Q

describe the mesocorticol system.

A

role in functions such as WM and planning.

- dysfunction - schz and addiction

39
Q

outline the dopamine synthesis.

A

tyrosine - L-dopa - dopamine

40
Q

outline regulation of TH.

A
  • feedback inhibition by endoproducts, lowers TH activity
  • pre-synpatic activity leads to phosphorylation of tH which increases activity
  • prolonged activity in pre-synaptic neurone leads to an increase in transcription of the TH gene leading to more enzyme synthesised.
41
Q

state drugs that affect dopamine synthesis and storage modulate behaviour.

A
  • reserve impairs storage of monoamines in synaptic vesicles
  • L-DOPA, precursor of dopamine, is used as a treatment for Parkinson’s.
  • AMPT inactivates TH
42
Q

what occurs during dopamine release.

A
  • depolarisation of pre-synaptic membrane
  • influx of Ca+ through voltage gated Ca+ channels
  • Ca+ dependant vesicle docking and release
43
Q

what happens during dopamine reuptake/ metabolism.

A
  • signal terminated by reuptake into axon terminal by transporters powered by electrochemical gradien.
44
Q

in the cytoplasm dopamine is…

A

… reloaded back into vesicles

… enzymatically degraded by monoamine oxidases or COMT.

45
Q

state drugs that effect dopamine release and reuptake modulate behaviour.

A
  • cocaine, amphétamine, methylphenidate (psychostimulants)

- block reupatke

46
Q

which drugs prevent breakdown of catecholamines?

A
  • selegiline (MOA inhibitor)

- entacapone (COMT inhibitor)

47
Q

describe the noradrenergic system.

A
  • projections form the locus coeruleus throughout the brain, role in arousal and attention
  • dysfunction: anxiety and depression
48
Q

describe the serotenergic system.

A
  • nine raphe nuclei with diffuse projections
  • descending projections to cerebellum and spinal cord
  • ascending
  • dorsal and medial raphe project throughout cerebal correct
49
Q

what are raphe neurones function?

A
  • fire tonically during wakefulness, quiet during sleep

- function in: mood, sleep, pain, appetite

50
Q

outline serotonin synthesis.

A

tryptophan, 5 - HTP, serotonin

51
Q

state stages to serotonin.

A
  1. serotonin synthesis
  2. serotonin storage
  3. serotonin release
  4. serotonin reuptake/ metabolism
52
Q

state drugs that effect serotonin release and reuptake modulate behaviour.

A
  • fuxetine blocks reuptake (SSRISs)
  • MDMA
  • MAOs inhibitors
53
Q

describe the cholinergic system in the periphery.

A

acetylcholine at neuromuscular junction and synapses in the automatic ganglia

54
Q

describe the cholinergic system in the brain.

A

basal forebrain complex

pontomesencephalotegmental complex

55
Q

each cholinergic interneurone innervates 1000s of…

A

local principal neurones and modulates their activity.

56
Q

describe acetycholine system.

A
  1. synthesis
  2. storage
  3. release
  4. metabolism
57
Q

state drugs affecting acetylcholine release, storage and degradation modulate behaviour.

A
  • acetylcholinesterase inhibitors
58
Q

state drugs affecting vesicle docking and release.

A
  • botulinum and tetanus at synapse in NMJ
  • botox acts directly at synapse in NMJ
  • tetanus toxin is transported up at NMJ and works inhibitory synapses on cholinergic neurones of spinal cord .
59
Q

state disorders of cholinergic system.

A
  • peripheral: myasthenia growth
  • Brain: alzheimers
  • addiction
  • epilepsy

Year Two - Brain and Behaviour (6 decks)

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