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Physiology > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

What are the 4 criteria which need to be satisfied for a substance to be a neurotransmitter?

A
  1. Synthesis
    • The neurotransmitter must be made in the presynaptic neuron.
  2. Storage
    • The neurotransmitter must be stored presynaptically
    • (The exception is NO in vesicles)
  3. Release
    • The neurotransmitter must be released on demand.
  4. Inactivation
    • The neurotransmitter must be inactivated.
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2
Q

What are the stages in the ‘life cycle’ of a neurotransmitter?

A
  1. Uptake of precursors.
  2. Synthesis of neurotransmitter (NT).
  3. Uptake/transport of NT into vesicles.
  4. Degradation of excess NT.
  5. Depolarisation by AP.
  6. Influx of calcium caused by AP.
  7. Release of NT by exocytosis.
  8. Diffusion of postsynaptic membrane.
  9. Interaction with postsynaptic receptors.
  10. Inactivation of NT.
  11. Reuptake of NT or degraded products by nerve terminal.
  12. Reuptake and release of NT by non-neuronal cells.
  13. Interaction with presynaptic receptors.
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3
Q

What is the action of mono-oxidase?

What is it used for?

A

Mono-oxidase can prevent degradation of what is already a limited or depleated neurotransmitter.

It is used as a class of anti-depressants.

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4
Q

What are the main neurotransmitters classified by amino acid structure?

A
  • Glutamate
  • GABA
  • Glycine
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5
Q

What are the main neurotransmitters classified by biogenic amine structure?

A
  • Catecholamines
    • Noradrenaline
    • Adrenaline
    • Dopamine
  • Indolamines
    • Seratonin
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6
Q

What are the main neurotransmitters classified by peptide structure?

A
  • Encephalin
  • Endorphin
  • Dynorphin
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7
Q

What are the properties of glutamate?

A
  • Primary excitatory NT in the CNS.
  • Involved in memory, learning and cell death.
  • Action postsynaptically is mostly via ionotropic receptors.
    • NMDA receptors
      • Calcium ions
    • Kainate receptors
      • Sodium and potassium ions
    • AMPA receptors
      • Permeable to cations (eg. calcium, sodium, potassium)
  • Inactivation by reuptake and recycling to either glutamate or GABA.
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8
Q

What are the properties of gamma-aminobutyric acid (GABA)?

A
  • Principal inhibitory NT in the CNS.
  • Found predominantly in the interneurons of the CNS.
  • Also found in striatum and globus pallidus.
    • Modulates descending motor information.
  • Acts on ligand-gated chloride chanels.
  • Acts on ionotropic receptors.
  • Inactivated by presynaptic reuptake.
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9
Q

What are the properties of glycine?

A
  • Second most common inhibitory NT in the CNS.
  • BUT, it is the primary inhibitory NT in the spinal cord and brainstem.
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10
Q

Describe the distribution of glutamate within the CNS.

A
  • Widespread.
    • Neurons spanning hemispheres (intra- and inter-hemispheric connections).
    • Neurons descending to the brainstem (corticobulbar tracts) or spinal cord (corticospinal tracts).
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11
Q

Describe synaptic plasticity of glutamate.

A
  • Process by which synapses are strengthened or weakened by feedback mechanisms.
  • Is the basic process for storing long and short term memories.
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12
Q

Describe excitotoxicity of glutamate.

A
  • Excessive stimulation of NMDA receptors causes a large influx of calcium ions.
  • Through a variety of processes, can result in cell death.
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13
Q

Describe the relationship between migraine and dysfunction of glutamate.

A
  • Dysfunction of glutamate is associated with visual anomalies secondary to migraine. This is excessive production of glutamate causing depression of CNS activity.
  • Karl Lashley’s visual aura
  • Glutamate is implicated in cortical spreading depression.
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14
Q

Describe the relationship between epilepsy and dysfunction of glutamate.

A
  • Excess excitation causes a feedback loop.
  • Uncontrolled excitation over expanding areas in the brain.
  • Can begin as partial seizures.
  • If this becomes more uncontrolled, can become Grand Mal seizures.
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15
Q

How are epileptic seizures treated?

A
  • Phenytoin
    • ​Increases the refractory peroid between firings in voltage-gated sodium channels.
  • Benzodiazepines
    • ​Increase the action of GABA (because it is an inhibitory NT.
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16
Q

Describe the action of benzodiazepines.

A
  • Benzodiazepines act on a separate receptor binding site on the GABA(subA) receptor subtype than GABA.
  • This site controls the ability of GABA to open the channel.
    • When benzodiazepines are bound, GABA can open the channel more often.
  • Benzodiazepines therefore only enhance the action of existing GABA molecules.
17
Q

Describe the interaction between alcoholism and GABA.

A
  • Alcoholism causes a change in GABA transmission.
  • Withdrawal results in convulsive movements and seizures.
  • Can be treated with benzodiazepines and phenytoin.
  • Decrease in production of GABA so inhibitory effect is reduced.
18
Q

What are the properties of dopamine?

A
  • NT and neuromodulator.
  • Involved with pleasure, addiction and movement.
  • Synthesised in the bouton and inactivated principally by reuptake.
19
Q

What are the properties of noradrenaline?

A
  • Sympathetic NT.
  • Decrease potentialls associated with Parkinson’s disease and ADHD.
  • Synthesised in the bouton and inactivated principally by reuptake.
20
Q

What are the properties of adrenaline?

A
  • Sympathetic.
  • Peripheral hormone from adrenal medulla.
  • Synthesised in the bouton and inactivated principally by reuptake.
21
Q

Describe the pathways of noradrenaline in the brain.

A
  • Adrenoreceptors are G-protein linked metabotropic receptors.
  • Locus coeruleus
    • ​Sleep
    • Wakefulness
    • Alterness
    • Attention
  • Medulla / hypothalamus
    • ​Feeding behaviour
    • Blood pressure regulation
22
Q

Describe the pathways of dopamine in the brain.

A
  • Dopaminergic receptors are G-protein linked metabotropic receptors.
  • Nigrostriatal
    • Motor control
  • Mesolimbic and mesocortical
    • Behavioural effects
  • Tuberohypophyseal system
    • Endocrine control, via the anterior pituitary
  • Dopamine pathways don’t overlap in the same way that noradrenaline pathways do.
23
Q

Adrenoceptors are which type of receptor?

A

G-protein linked metabotropic receptors.

24
Q

Dopaminergic receptors are which type of receptors?

A

G-protein linked metabotropic receptors

25
Q

What effect does dopamine have on Parkinson’s disease?

A

Tremor, muscle rigidity and bradykinesia or akinesia due to depleted dopamine in the motor coordination circuits.

26
Q

What effect does dopamine have on Schizophrenia?

A

Over-production of dopamine in the mesolimbic system, treatment is with antipsychotics.

27
Q

Describe the interaction between dopamine and addiction.

A
  • Addiction can be to drugs of abuse, exercise and certain behaviours such as sexual activity.
  • Works through the pleasure centres ofthe CNS located in the mesolimbic dopamine system.
28
Q

Describe the effects of serotonin.

A
  • Depression and obsessive compulsive disorder
    • Associated with serotonin dysfunction (reduction)
    • Fluoxetine (‘prozac’) is a serotonin re-uptake inhibitor
  • Associated with some drugs of abuse
    • Receptor agonists include LSD, psilocybin and mescaline.
    • Major effect of MDMA (‘Ecstasy’) is by causing the release and preventing subsequent re-uptake of serotonin.
29
Q

Describe the pathways of serotonin in the brain?

A
  • Serotonin is a large family of both excitatory and inhibitory receptors in the CNS and PNS.
  • Modulates a range of NTs such as glutamate, GABA and dopamine.
  • Locus coeruleus - sensory signals
  • Raphe nuclei - sleep, wakefullness and mood
30
Q

What are the neurotransmitters / neuromodulators classified by the peptide structure?

A
  • Dynorphin
  • Encephalin
  • Substance P
  • Neuropeptide Y
  • Neurotensin
  • Cholecystokinin
31
Q

What is the main action of substance P?

A

Pain transmission

32
Q

Which peptides are implicated in schizophrenia?

A
  • Neuropeptide Y
  • Neurotensin
  • Cholecystokinin
33
Q

What are the effects of endorphins and encephalins on pain?

A
  • Act on opioid receptors as endogenous ligands.
  • Opioids (morphine, codeine, pethidine, methadone and diamorphine) cause downregulation of opioid receptors in the CNS.
    • Leads to opioid tolerance and increased intake.
34
Q

What are the effects of endorphins and encephalins on emotional perception?

A
  • Opioid receptors also present in the limbic system and periaqueductal grey.
  • Emotional element to withdrawl avoidance.
  • Naloxone (opioid receptors antagonist) can reduce symptoms.
35
Q

Where is Acetylcholine found?

A
  • Found in both the PNS and CNS.
  • Also the NT at the NMJ.
  • In the CNS, neurons project to the hippocampus and cortex.
    • ​Regions essential for formation of new memories and learning.
36
Q

How is ACh implicated in Alzheimer’s disease?

A

Alzheimer’s disease associated with dysfunction (reduction) of ACh in the CNS.

37
Q

How do nicotine and ACh interact?

A

Acts on nicotinic acetylcholine receptors found in the CNS and PNS.

38
Q

What is the action of acetylcholinesterase inhibitors?

A
  • Prevent breakdown of ACh, therefore prolonging its activity.
  • Can be theraputic (donepezil in Alzheimer’s), but also toxic (insecticides, nerve gases).

Physiology (10 decks)

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