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Nervous tissue > neurotransmitters (week 11) > Flashcards

neurotransmitters (week 11) Flashcards

1
Q

what are the 4 criteria which a neurotransmitter must satisfy to be defined as a neurotransmitter?

A
  1. Synthesis of the NT must be in the pre-synaptic neurone
  2. stored presynaptically
  3. the NT must be released on demand
  4. the NT must be inactivated
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2
Q

what are the three ways a neurotransmitter can be inactivated?

A

diffusion, enzymes inactivation, re-uptake

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3
Q

what are co-agonists and constitutively active receptors?

A

types of receptors which are activated by more than one type of neurotransmitter

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4
Q

what are the three types of amino acid neurotransmitter?

A

glutamate, GABA (gamma-aminobutyric acid) and glycine

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5
Q

what is the primary excitatory neurotransmitter of the central nervous system?

A

glutamate (amino acid neurotransmitter)

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6
Q

How does glutamate (the neurotransmitter) primarily excite neurons?

A

by opening cation channels (e.g. sodium channels) (NMDA receptors also sometimes permeable to calcium ions)

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7
Q

how is the neurotransmitter glutamate inactivated?

A

by re-uptake, it is recycled to either glutamate or GABA

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8
Q

which neurotransmitter is widespread in the brain and connects hemispheres of the brain?

A

glutamate

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9
Q

which neurotransmitter is involved in synaptic plasticity?

A

glutamate (kainate glutamate receptors)

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10
Q

which type of glutamate receptor is involved in slow transmission and can be over stimulated causing a large influx of calcium ions?

A

NMDA glutamate receptors

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11
Q

what is excitotoxicity?

A

process of cell death resulting from overstimulation and excitation of glutamate NMDA receptors

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12
Q

what is thought to be the primary cause of migraines?

A

a massive transient depolarisation through the visual cortex and a massive glutamate efflux

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13
Q

what happens in the brain in epilepsy?

A

there is excess excitation which can cause uncontrolled waves of excitation over expanding areas in the brain

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14
Q

what are partial complex seizures?

A

an excess excitation in an isolated area of the brain and result in an alteration of consciousness

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15
Q

what are grand mal seizures?

A

seizures which involve the whole brain

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16
Q

which drug is used to treat epileptic seizures which acts to increase the action of GABA?

A

benzodiazepines

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17
Q

which drug is used to treat seizures which acts by increasing the refractory period in voltage gated sodium channels?

A

phenytoin

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18
Q

what is the general mechanism of the drug benzodiazepines?

A

they act on a separate receptor binding site to the GABA receptor and act by increasing the ability of GABA to open chloride channels

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19
Q

what neurotransmitter is the principle inhibitory neurotransmitter of the CNS?

A

GABA (which is made from glutamate)

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20
Q

where is GABA found?

A

predominantly in the CNS but also in the striatum and globes pallid us where it refines motor information

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21
Q

how does GABA act?

A

at ligand gated chloride channels

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22
Q

how is GABA inactivated?

A

by presynaptic reuptake

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23
Q

what happens in huntington’s disease?

A

GABAergic neurons degenerate, leading to uncontrolled movement(can be treated with GABA mimetic)

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24
Q

what changes can alcoholism result in (involving GABA)?

A

alcoholism can cause a change in the transmission of GABA resulting in withdrawal results causing convulsive movements and seizure. (treated with benzodiazapines (diazepam, temazepam) and phenytoin)

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25
Q

what is a treatment sometimes used for anxiety and sleeplessness (as well as epilepsy and as anaesthetics)?

A

GABA agonists

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26
Q

what is the second most common inhibitory neurotransmitter of the CNS and is synthesised from serine?

A

glycine

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27
Q

where is glycine mainly found as a neurotransmitter?

A

in the interneurones of the spinal cord and brainstem but is also present in the brain

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28
Q

what is thought to be the primary cause of inherited mammalian Myoclonus? (muscle twitching)

A

glycinergic dysfunction

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29
Q

what is tetanus caused by?

A

a toxin from the bacteria clostridium tetani

30
Q

what does the toxin released from clostridium tetani in tetanus do?

A

inhibits the release of glycine which disrupts the excitation/inhibition balance (this can lead to loss of inhibition in the cerebra leading to epileptiform fits)

31
Q

what is the treatment for tetanus?

A

injection of antitoxin which binds the toxin and benzodiazepines which boost the GABAergic pathways

32
Q

what are the two main groups the biogenic amine neurotransmitters are composed of?

A

catecholamines and indolamines

33
Q

what are the neurotransmitters defined as catecholamines?

A

noradrenaline, adrenaline and dopamine

34
Q

which catecholamine NT is a sympathetic NT, the inhibition of which is used in the treatment of parkinson’s ADHD?

A

noradrenaline (agonists are cocaine and tricyclic antidepressants)

35
Q

which catecholamine NT is a peripheral hormone from adrenal medulla and is a pharmacological target for cardiac and circulatory problems?

A

adrenaline

36
Q

which catecholamine NT is a NT and neuromodulator involved with pleasure, addiction and movement?

A

dopamine

37
Q

where are catecholamine NTs synthesised?

A

in the bouton

38
Q

how are catecholamine NTs inactivated?

A

principally by re-uptake

39
Q

which catecholamine NTs are involved in the ‘fight or flight’ response (in the gut, heart, respiration etc)

A

adrenaline and noradrenaline

40
Q

what is the structure f adrenoceptors like?

A

G-protein linked metabotropic receptors

41
Q

what behaviours are controlled by noradrenaline in the brainstem?

A

sleep, wakefulness, attention and feeding behaviour

42
Q

which disorder is noradrenaline involved in?

A

bipolar disorder

43
Q

what is the locus coeruleus?

A

the area of the brainstem whose neurons project noradrenalin axons

44
Q

what type of receptors receive dopamine?

A

G-protein linked metabotropic receptors (dopaminergic axons project to majority of the CNS, excluding the cerebellum)

45
Q

what are the three primary actions dopamine is involved in?

A

control of movement, certain symptoms of psychiatric disease and regulation of the release of certain hormones

46
Q

where does dopamine exert control of hormone release?

A

in the anterior pituitary

47
Q

how is dopamine involved in parkinsons disease?

A

parkinson sufferers who experience tremor, muscle rigidity and bradykinesia (slowness of movement) have depleted dopamine in the motor co-ordination circuits (treatment is with antipsychotics)

48
Q

what types of addiction is dopamine involved in which works through the pleasure centres of the CNS located in the mesolimbic dopamine system?

A

abusive drugs, exercise and certain behaviours including sex

49
Q

what is the primary type of indoleamine? (type of biogenic amine NT)

A

serotonin

50
Q

where do serotonin neurons originate and project to?

A

originate in the Raphe nuclei in the brain stem and project to the majority of the brain and brain stem

51
Q

where are the large family of serotonin excitatory and inhibitory receptors found?

A

in the CNS and PNS

52
Q

what are some examples of neurotransmitters serotonin modulates?

A

glutamate GABA and dopamine

53
Q

what is serotonin dysfunction (reduction) associated with?

A

depression and OCD (both can be treated with fluoxetine)

54
Q

what are some serotonin receptor agonists exploited by drug abusers?

A

LSD, psilocybin and mescaline

55
Q

where are peptide NTs made?

A

in the neurone cell body and transported to the bouton

56
Q

what are two examples of peptide NTs involved in the perception of pain?

A

Encephalins and dynorphin

57
Q

what is substance P involved in?

A

the transmission of pain

58
Q

which condition are neuropeptide Y, neurotension and cholecystokinin involved in?

A

schizophrenia

59
Q

which receptors do endorphins and encephalins act as the endogenous ligand?

A

they act at opiate receptors in the brain and spinal cord

60
Q

what does taking opiates (e.g. heroin) lead to?

A

down regulation of opiate receptors throughout the CNS, which causes opioid tolerance and increased intake

61
Q

what sort of effects do opiates have?

A

emotional effects as well as pain

62
Q

which drug can be given to heroin addicts to reduce symptoms?

A

naloxone

63
Q

what NT is the principle peripheral excitatory neurotransmitter?

A

Acetylcholine (found mainly in PNS but also in CNS)

64
Q

where do acetylcholine neurons project to?

A

the hippocampus and cortex

65
Q

what are the hippocampus and the cortex important in?

A

the formation of new memories and learning

66
Q

which disease is associated with reduction in Acetylcholine?

A

Alzheimer’s disease

67
Q

what do anticholinesterases do?

A

prevent the breakdown of ACh (include insecticides DDT; nerve gases and alzheimer’s treatments)

68
Q

what do the drugs nicotine, muscarine, atropine, tropicamide do?

A

act on ACh receptors

69
Q

The diet of an alcoholic is often poor and can result in thiamine deficiency which causes damage to which structures?

A

the thalamus and mammillary bodies

70
Q

what are the maxillary bodies involved in?

A

memory formation

71
Q

what are some symptoms of damage to the thalamus and maxillary bodies?

A

amnesia, confabulation, lack of insight and apathy

Nervous tissue (7 decks)

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