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Movement and control > Neuroscience: excitotoxicity and neurotoxicity > Flashcards

Neuroscience: excitotoxicity and neurotoxicity Flashcards

1
Q

What is excitatory transmission?

A

increase electrical excitability on post-synaptic membrane - glutamate, ACh

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2
Q

What is inhibitory transmission?

A

decrease electrical excitability on post-synaptic membrane to prevent propagation of AP - glutamate

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3
Q

What is an inotropic receptor?

A

Membrane bound protein that responds to ligand binding by opening ion channel and allowing flow into a cell

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4
Q

Process of neurotransmission

A

neurotransmitter packaged into vesicles → presynaptic membrane depolarises due to AP → depolarisation causs Ca2+ channels an Ca2+ to flow into terminal → increase of intracellular Ca2+ triggers fusion of vesicles with presynaptic membrane → transmitter is released into extracellular space and diffuses across the cleft → some transmitters bind to postsynaptic membrane → receptors open

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5
Q

How are mitochondria damaged

A

Metabolic distress causes failure of ion homeostasis
This leads to increased intracellular Ca2+ and stimulates glutamate release
This activates post-synaptic receptors
CA2+ influx to cytoplasm and mitochondria
Apoptosis and cell death

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6
Q

Inhibitory neurotransmitter

A

GABA

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7
Q

Excitatory neurotransmitter

A

Glutamate

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8
Q

Is D1 inhibitory or excitatory?

A

Excitatory

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9
Q

Is D2 excitatory or inhibitory?

A

Inhibitory

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10
Q

Metabotropic receptor

A

indirectly linked with ion channels through signal transduction mechanisms e.g. G proteins - binds to receptor which releases a messenger and this is what causes ion influx

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11
Q

Differences between neuropeptides and neurotransmitters

A

Neurotransmitters are bigger, released slowly, last longer and can’t be re-uptaken

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12
Q

Examples of neuropeptides

A

ADH, cholecystokinin, endorphins, somatostatin, ACTH

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13
Q

Slow acting molecules

A

Dopamine, noradrenaline

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14
Q

Neurotransmitter in myasthenia graves and sx

A

ACh and droopy eyelids, tiredness, ptosis

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15
Q

What are neurotoxins?

A
  • Destructive to nerve tissue
  • Endogenous or exogenous
  • E.g. heavy metals, botox, venoms, poisonous animals, ethanol
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16
Q

How is calcium removed from a cell when we are healthy?

A
  • Glutamate binds to receptors
  • Ca2+ enters from ER
  • Na+ enters cell, allowing more Ca2+ to enter via exchangers
  • Depolarisation - inhibits glutamate resorption
  • Ca2+ stored in ER ad mitochondria and then actively pumped out of cell
17
Q

How does excitotoxicity occur?

A
  • Excessive glutamate binding
  • Excessive calcium influx
  • Cell can’t get rid of it quickly enough
  • Ca2+ builds up in mitochondria
18
Q

Consequences of excitotoxicity

A

High Ca2+ = glutamate release
Proteases and lipase activated by calcium
NO synthesised
Increased arachidonic release = more free radicals

19
Q

Glial cells and excitotoxicity

A

Normally absorb glutamate
Failure = too much excitation
Glial cell destruction = Parkinson’s and Alzheimer’s

20
Q

What is ischaemic brain injury?

A

no o2 means mitochondria dysfunction = Ca2+ build up

21
Q

Organophosphate poisoning neurotransmitter and sx

A

ACh and bradycardia, SLUDGE

Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis

22
Q

Neurotransmitter for Parkinson’s and sx

A

Dopamine - bradykinesia, Parkinson’s gait, resting tremor, rigidity

23
Q

Neurotransmitter in benzodiazepine overdose and sx

A

GABA and drowsiness, blurred vision, unresponsive

24
Q

Neurotransmitter in opioid overdose and sx

A

Opiates, bradypnoea, pinpoint pupils

25
Q

Neurotransmitter in depression and sx

A

Serotonin and low mood and insomnia

26
Q

Neurotransmitter in PKU and sx

A

Phenylalanine (precursor for dopamine etc), musty breath, seizures, fair skin and blue eyes

27
Q

Examples of benzodiazepines

A

Diazepam, lorazepam

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