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Brain And Behaviour > Lecture 4- Chemical Signaling And Neuromodulation > Flashcards

Lecture 4- Chemical Signaling And Neuromodulation Flashcards

1
Q

What is neuromodulation

A

It modulates the activity of the neuron, alters the speed of the neurone

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2
Q

Neuropeptides are

A

Endorphins

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3
Q

Amino acid transmitters are responsible for

A

Fast transmission

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4
Q

What is glutamate responsible for

A

Excitatory causing next neurone to fire

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5
Q

What are GABA and Glycine responsible for

A

Inhibitory

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6
Q

Glutamate synthesised from

A

Glucose or glutamine

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7
Q

Glutamate is released by

A

Exocytosis (Ca+ dependent mechanism)

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8
Q

Too much glutamate can cause

A

Hyperexcitability (epilepsy)

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9
Q

Too little GABA can cause

A

Hyperexcitability (epilepsy)

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10
Q

What is cerebral ischemia

A
  • Insufficient blood flow due to plaque
  • Due to High glutamate
  • Reversal of the Na+ K+ gradient
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11
Q

Receptors vary in

A

Pharmacology (what transmitter binds and how drugs interact)

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12
Q

What are agonist drugs

A

Produce a cellular reaction when bound to receptor

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13
Q

What is an antagonist drug

A
  • Reduces or completely blocks the activity of an agonist

- No cellular effect

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14
Q

Receptors vary in their

A
  • Kinetics (rate of binding)
  • Selectivity (what binds)
  • Conductance (rate of flux)
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15
Q

Glutamate receptors allow

A

Sodium ions influx

Excitatory

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16
Q

GABA receptors cause

A

Chloride (Cl-) influx

Inhibitory

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17
Q

What are the three types of glutamate receptors

A
  • AMPA
  • NMDA
  • Kainate
  • Named on the agonist that binds with glutamate
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18
Q

AMPA receptor is

A
  • Iontropic receptor
  • Leads to opening of Na+ channel
  • Causes depolarisation
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19
Q

NMDA receptor features

A
  • iontropic receptor
  • it’s Non-competitive antagonist is PCP
  • Needs glutamate and glycine to bind
  • Permeable to Na+, K+ and Ca+
  • Voltage gated
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20
Q

Which has slower kinetics, NMDA or AMPA

A

NMDA

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21
Q

AMPA and Kainate are permeable to

A

Na+ and K+

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22
Q

NMDA receptors are only activated in

A

An already depolarised membrane in the presence of glutamate.
This allows the magnesium blocking NMDA to be dispelled

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23
Q

What are NMDA receptors blocked by

A
  • Magnesium

- PCP (the drug)

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24
Q

Certain antipsychotic drugs enhance current flow through

A

NMDA channels

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25
Q

Glutamate excitotoxicity caused by

A

Excessive Ca+ influx which activate things that damage the cell
Occurs after stroke

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26
Q

NMDA receptors associated with what illness

A

Schizophrenia

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27
Q

Too much GABA can cause

A

Sedation, coma

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28
Q

GHB (date rape drug) causes

A

Increases amount of available GABA

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29
Q

Alcohol acts at what receptor

A

GABA a

30
Q

GABAa receptor

A
  • Iontropic
  • Ligand gated Cl- channel
  • Fast IPSP
  • Inhibitory
  • Multiple binding sites
31
Q

GABAb receptors

A
  • Metabotropic receptor
  • G protein coupled receptor
  • Indirectly coupled to K+ (opens) or Ca2+ (closes) channels
  • Slow IPSPs
  • Inhibitory
32
Q

GABAa increases

A

Chloride permeability and hypolarises the neuron

33
Q

What’s GABA agonist and antagonist

A

Agonist- muscimol (a mushroom)

Antagonist- bicuculine, picrotoxin

34
Q

Drugs increasing GABA activity reduce anxiety

A

Agonist- Alcohol, barbiturates

Indirect antagonist- Benzodiazepines

35
Q

Drugs decreasing GABA activity increase anxiety

A

Antagonist- Flumazenil (reverses effects of benzodiazepines)

36
Q

Patients with panic disorders have less

A

Benzodiazepine binding dites

37
Q

If you have GABA and the barbiturate it results in

A

Bigger hyperpolerisation

38
Q

When be benzodiazepines are applied on their own it results in

A
  • No effect

- GABA and benzodiazepines results in an effect

39
Q

Problems with barbiturates

A
  • General depression of neuronal activity, can result in not breathing
  • Poor therapeutic ratio (small difference between dose and overdose)
  • Long term treatment leads to dependence
40
Q

Why are benzodiazepines better for calming anxieties

A
  • Indirect antagonist on its own
  • Fast acting
  • Large therapeutic window
41
Q

Disadvantages of benzodiazepines

A
  • May cause dependence

- Effects potentiated by alcohol

42
Q

Dopamine neurons are where

A
  • Cell bodies in the midbrain

- Project into the forebrain

43
Q

3 key dopamine pathways

A
  • Role in movement
  • Role in reinforcement
  • Role in working memory and planning
44
Q

Damage to movement system (nigrostiatal system)

A
  • Parkinson’s disease

- Huntington’s disease

45
Q

Damage to reward system (mesolimbic system)

A

Addiction to drugs

46
Q

Damage to working memory system (mesocortical system)

A

Schizophrenia

47
Q

Dopamine synthesis

A
  • Tyrosine to
  • L-Dopa to
  • Dopamine
48
Q

What drugs affect dopamine synthesis

A
  • Reserpine, impairs storage of dopamine

- L-DOPA, precursor of dopamine, used to treatment for Parkinson’s disease, increases dopamine

49
Q

AMPT inactivates

A

TH

50
Q

Dopamine release causes

A
  • Depolarisation of presynaptic membrane

- Influx of Ca2+ through voltage gated Ca2+ channels

51
Q

After release, cytoplasm dopamine is

A

Reloaded back into vesicles and enzymatically degraded

52
Q

Drugs that affect dopamine release and reuptake

A
  • Cocaine, amphetamine and methylphenidate
  • Selegiline
  • Entacapone
53
Q

What do psychostimulants (cocaine) do to dopamine release

A
  • Block reuptake of monamines

- Extended action of dopamine on postsynaptic neuron

54
Q

What can drugs that affect dopamine release and reuptake also do

A
  • Have antidepressant activity

- Can treat Parkinson’s

55
Q

What does the noradrenergic system do

A
  • Role in arousal and attention

- Role in anxiety, heroin withdrawal, depression

56
Q

Where does the serotonergic system project

A

Throughout the cerebral cortex

57
Q

What does the serotonergic system function in

A
  • Mood
  • Sleep
  • Pain
  • Appetite
58
Q

Process of serotonin synthesis

A
  • Tryptophan
  • 5-hydroxytryptophan
  • Serotonin
59
Q

More tryptophan might help

A

Improve your mood

60
Q

Serotonin released through

A

Ca2+ dependent mechanism

61
Q

What degrades dopamine and serotonin

A

MAOs

62
Q

Drugs that affect serotonin

A
  • Fluoxetine (Prozac)
  • Fenfluramine
  • MDMA
63
Q

What does fluoxetine do

A

Blocks reuptake of serotonin

Antidepressant

64
Q

What does fenfluramine do

A

Causes release of serotonin and inhibits it’s reuptake.

Appetite suppressant

65
Q

What does MDMA do

A
  • Causes noradrenaline and serotonin transporters to run backwards.
  • Neurotransmitters into synapse
66
Q

What is acetylcholine synthesised from

A

Choline

67
Q

What can acetylcholinesterase inhibitors do

A
  • Treat Alzheimer’s
  • Myasthenia gravis
  • Autoimmune disorders
68
Q

Drugs that affect vesicle docking and release

A
  • Botox
  • Botulinum
  • tetanus toxins
69
Q

Tetanus prevents

A

Glycine release

70
Q

Tetanus toxin causes

A

Disinhibits the cholinergic neurons so they continually fire resulting in permanent muscle contraction

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