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MD2001 > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

What 4 criteria does a neurotransmitter need to satisfy?

A
  1. Synthesis: the NT must be made in the pre-synaptic neuron
  2. Storage: the NT must be stored pre-synaptically in vesicles (exception is NO)
  3. Release: NT must be released on demand
  4. Inactivation: NT must be inactivated
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2
Q

What can happen to the NT after it binds and activates post-synaptic receptors?

A

+ Enzyme activation
+ Diffusion
+ Re-uptake

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3
Q

What is a receptor?

A

A protein that is either in the plasma or inserted in the outer membrane of a cell

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4
Q

What is the relationship between the receptor and a NT?

A

+ The receptor binds to and is activated by a NT

+ Lock and key hypothesis

+ Most receptors types are activated by only one NT but there are families of receptors sensitive to a single NT. exceptions include co-agonists, constitutively active receptors

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5
Q

What are the neurotransmitter classifications by structure?

A

+ Amino acids (simple compound with carboxyl group and amino group)

+ Biogenic amines:

  • catecholamines
  • indolamines

+ Peptides

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6
Q

What are the different amino acid neurotransmitters?

A

+ Glutamate

  • primary excitatory NT of CNS
  • acts through calcium ions

+ GABA

  • inhibitory
  • aminobutyric acid

+ Glycine
- inhibitory

(Other AAs: Aspartate, proline, taurine, beta-alanine)

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7
Q

What are the different biogenic amine neurotransmitters (catecholamines)?

A

+ Norepinephrine
+ Epinephrine
+ Dopamine

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8
Q

What are the different biogenic amine neurotransmitters (indolamines)?

A

+ Serotonin

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9
Q

What are the different peptide neurotransmitters?

A

+ Encephalin
+ Endorphin
+ Dynorphin

(Others include: Substance P, neuropeptide Y, neurotensin, cholecystokinin)

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10
Q

Where are the amino acid neurotransmitters produced?

A

In the bouton

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11
Q

What are functions of NT glutamate?

A

+ Action at post synapse predominantly by opening cation (e.g Na+) channels

+ Inactivation is by re-uptake and is recycled to either glutamate or GABA

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12
Q

What is the term for neurons within or spanning hemispheres?

A

Intra and inter-hemispheric connections

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13
Q

What are the terms for neurons descending to the braintstem or spinal cord?

A

+ Corticobulbar tracts

+ Corticospinal tracts

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14
Q

What other receptors are also permeable to calcium ions?

A

+ AMPA
+ Kainate
+ NMDA

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15
Q

What type of transmission are kainate glutamate receptors involved in?

A

Fast synaptic transmission and synaptic plasticity

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16
Q

What type of transmission are NMDA receptors involved in?

A

Slow synaptic transmission

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17
Q

Which neurotransmitter is involved in memory, learning and cell death?

A

Glutamate

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18
Q

What is synaptic plasticity?

A

+ The process by which synapses are strengthened or weakened by feedback mechanisms

+ Basic process for storing long and short term memories

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19
Q

What is the result of excessive glutamatergic stimulation of NMDA receptors?

A

A large influx of calcium ions; through a variety of processes this can result in cell death known as EXCITOXICITY

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20
Q

Which neurotransmitters is involved in migraines?

A

Glutamate

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21
Q

What can happen in regards to excess excitation?

A

It can feedback on itself to cause uncontrolled waves of excitation over expanding areas in the brain

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22
Q

What do the results of excess excitation manifest as at first?

A

+ Begin as PARTIAL COMPLEX seizures (partial - not the whole brain, complex - due to an alteration of consciousness)

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23
Q

What can the partial complex seizures progress to, and what causes the progression?

A

Grand Mal seizures (involve the whole brain):

- if the waves of depolarisation become more uncontrolled

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24
Q

How are seizures treated, and what do the treatments do?

A

With BENZODIAZEPINES:

  • increase the action of GABA and drugs like PHENYTOIN which increase inactivation (refractory) period between firings in voltage activated Na+ channels
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25
Q

Why do benzodiazepines increase the action of GABA?

A

+ They act on a separate receptor binding site on the GABAa receptor, compared to GABA

+ This binding site controls the ability of GABA to open the channel; more benzodiazepines bound => GABA can open the channel more often

+ Benzodiazepines therefore only enhance the action of existing GABA molecules

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26
Q

What are some features of GABA?

A

+ Principle inhibitory NT of the CNS

+ Made from glutamate

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27
Q

Where is GABA found?

A

+ Predominantly in the interneurons of the CNS

+ Neurons of the striatum and globus pallidus, where it modulates descending motor information

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28
Q

GABA acts at ligand gated chloride channels (not K+ channels). What is it inactivated by?

A

Pre-synaptic reuptake

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29
Q

Name disease resulting from GABAergic dysfunction

A

Huntington’s

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30
Q

What is the role of GABA in Huntington’s, and what is the treatment?

A

+ GABAergic neurons degenerate, which can lead to uncontrolled movement

+ Treatment: GABA mimetic

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31
Q

What are the effects of alcoholism on GABA, and what are the treatments?

A

+ Causes a change in GABA transmission such that withdrawal results in convulsive movements and seizures

+ Treatment: Benzodiazepines (Diazepam, temazepam) and phenytoin

32
Q

For what are GABA agonies sometimes used?

A

+ Treatment of anxiety
+ Treatment of sleeplessness
+ Treatment of epilepsy
+ Anaesthetics (e.g propofol)

33
Q

What are some features of glycine?

A

+ Second most common inhibitory NT of the CNS

+ Synthesised from serine

+ Predominant inhibitory NT in the interneurons of the spinal cord and brain stem but also present in the brain

34
Q

What is glycinergic dysfunction thought to be the cause of?

A

Inherited mammalian myoclonus

  • most are benign
  • others are late symptoms of more serious diseases
35
Q

What causes tetanus, and how does it do so?

A

+ Caused by a toxin from the bacteria clostridium tetani

+ It inhibits the release of glycine resulting in a shift of the excitation-inhibition balance

36
Q

What are the mild and serious effects of tetanus/shifts in excitation-inhibition balance?

A

Mild effects:
- restricted to muscles in Webster by cranial nerves

Serious effects:
- loss of inhibition in the cerebra => epiform fits

37
Q

What is the treatment for tetanus/shifts in the excitation-inhibition balance?

A

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

38
Q

What are some features/functions of norepinephrine?

A

+ Aka noradrenaline

+ Sympathetic NT: inhibition

+ Used in treatment for:

  • Parkinson’s
  • ADHD

+ Agonsists:

  • cocaine
  • tricyclic antidepressants

+ Projects major centres of the brain

39
Q

What are some features/functions of epinephrine?

A

+ Aka adrenaline
+ Peripheral hormone from adrenal medulla
+ Pharmacological target for cardiac and circulatory problems

40
Q

What are some features/functions of dopamine?

A

+ NT and neuromodulator
+ Involved in pleasure, addiction and movement
+ Dopaminergic axons project to the majority of the CNS (excluding cerebellum)
+ Act at G-protein linked metabotropic receptors

41
Q

Where are catecholamine NTs synthesised?

A

+ In the bouton

+ Inactivated principally by re-uptake

42
Q

What are adrenoceptors?

A

G-protein linked metabotropic receptors

43
Q

What NTs are involved in the fight or flight response (gut, heart, respiration etc)?

A

Epinephrine and norepinephrine

44
Q

What does the brainstem in the CNS use norepinephrine to influence?

A 
\+ Sleep
\+ Wakefulness
\+ Attention (via reticulum)
\+ Feeding behaviour (via hypothalamus)
\+ Involved in bi-polar disorder
45
Q

What is the Locus Coeruleus?

A

The part of the brainstorm whose neurons project norepinephrinergic axons

46
Q

How many different central systems is dopamine found in and what is it involved in?

A

+ 3 different central systems

  1. The control of movement
  2. Certain symptoms of psychiatric disease
  3. Regulation of the release of certain hormones
47
Q

Control of hormone release is exerted by dopamine. Where does this occur, and what is the role of dopamine?

A

+ Anterior pituitary

+ Dopamine released into portal vessels by hypothalamic neurons

48
Q

What is the role of dopamine in Parkinson’s?

A

Parkinson’s sufferers who experience tremors, muscle rigidity and bradykinesia or akinesia have DEPLETED dopamine in the MOTOR CO-ORDINATION CIRCUITS

49
Q

What is the role of dopamine in schizophrenia?

A

+ Can be caused by an OVER PRODUCTION of dopamine in the Mesolithic system

+ Treatment with antipsychotics

50
Q

How is dopamine related to addiction of drugs of abuse, decide, and certain behaviours such as sexual activity?

A

Dopamine works through the pleasure centres of the CNS located in the mesolimbic dopamine system

51
Q

What are some features/functions of serotonin?

A

+ Neorons originate principally in Raphe nuclei in the brainstem

+ Project to the majority of the brain and brainstem

+ Large family of both excitatory and inhibitory receptors, in the CNS & PNS

+ Modulates a range of NTs such as glutamate, GABA and dopamine

+ Functions associated with sleep, anxiety, depression and mood swings

52
Q

What is serotonin dysfunction (reduction) associated with, and how can it be treated?

A

+ Associated with depression and obsessive compulsive disorder (OCD)

+ Treatment: fluoxetine (Prozac a 5-HT re-uptake inhibitor)

53
Q

What are the receptor agonists involved in the serotonergic systems (often exploited by drug users) and what do they do?

A

+ LSD
+ Psilocybin
+ Mescaline

Inhibiting mono amine catabolism generally with MAOIs (monoamine oxidative inhibitors)

OR

Inhibiting serotonin re-uptake

=> increases 5-HT levels

54
Q

What are examples of psychostimulants?

A

+ Amphetamines

+ Ecstasy

55
Q

What are features of amphetamines?

A

+ Cause release of amines such as NA, 5-HT and dopamine

+ Also inhibit re-uptake of NA, 5-HT and dopamine thus causing enhanced activation of these receptors

56
Q

What are features of ecstasy?

A

+ Amphetamine analogue: methylenedioxymethamphetamine or MDMA

+ Has numerous actions but its major effect is by causing the release of and preventing re-uptake of 5-HT

57
Q

Which peptide NT is involved in Pain transmission

A

Substance P

58
Q

Which peptide NTs are all implicated in schizophrenia?

A

+ Neuropeptide Y
+ Neurotensin
+ Cholecystokinin

59
Q

Which NTs are associated with the perception of pain?

A

Endorphins and encephalins

60
Q

What are the features/functions of endorphins and encephalins?

A

+ They act as opitate receptors in the brain and spinal cord where they are the endogenous ligand

61
Q

What are some examples of opiates?

A 
\+ Morphine
\+ Codeine
\+ Pethidine
\+ Methadone
\+ Diamorphine (heroin)
62
Q

What does taking opiates lead to?

A

+ Down regulation of opiate receptors throughout the CNS

+ This causes opioid tolerance and increased intake

63
Q

What is the result of there being opioid receptors in the limbic system (and the periaqueductal grey)?

A

+ Opiates affect emotional perception as well as pain

+ Emotional element to withdrawal avoidance

64
Q

To whom is naxalone given, and what is its purpose?

A

It is given to withdrawing heroin addicts to reduce symptoms

65
Q

What is naxalone?

A

An opiate receptor agonist

66
Q

Give an example of an ester NT?

A

Acetylcholine (ACh)
+ An unusual NT but first one discovered
+ Used as a standard setter for defining NTs

67
Q

What are features/functions of the NT- acetylcholine?

A

+ Principle excitatory NT

+ Found in both CNS and PNS

68
Q

Where do the neurons of ACh project to?

A

The hippocampus & the cortex: essential for the formation of new memories and learning

69
Q

What is associated with ACh dysfunction (reduction)?

A

Alzheimer’s disease

70
Q

Which drugs act on AChs receptors?

A

+ Nicotine (drug of abuse)
+ Muscarine (agonist)
+ Atropine (antagonist)
+ Tropicamide (antagonist to dilate pupils during surgery)

71
Q

What do anticholinesterases prevent?

A

The breakdown of ACh

72
Q

What are some examples of anticholinesterases?

A

+ Insecticides (DDT)
+ Nerve gasses (Sarin)

Alzheimer’s treatments: Donepezil (aricept)

73
Q

What is Korsakoff’s psychosis?

A

The diet of an alcoholic often leads to a thiamine deficiency causing famage to the thalamus and the mammillary bodies

74
Q

What are the syptoms of Korsakoff’s psychosis?

A

+ Amnesia
+ Confabulation
+ Lack of insight
+ Apathy

75
Q

Are there treatment options for Korsakoff’s psychosis?

A

The cells involved are cholinergic and partial recovery can sometimes be achieved by using anticholinesterases

MD2001 (52 decks)

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