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Theme 1 - 202 > Chemicals in the Brain > Flashcards

Chemicals in the Brain Flashcards

1
Q

In the presynaptic membrane, where are vesicles anchored and what anchors them here?

A

Vesicles are anchored to the cytoskeleton by synapsin

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2
Q

What activates synapsin?

A

The influx of Ca2+ activates calcium calmodulin kinase II (CaMKII), which then activates synapsin (by phosphorylating it).

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3
Q

What does the activation of synapsin lead to?

A

Prevents it from being able to to bind to the cytoskeleton so vesicles dock towards the active zone.

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4
Q

What effect do botox and tetanus have on neurotransmitters?

A

They prevent the release of neurotransmitter

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5
Q

What does botox do on the neuromuscular junction, and what can it be used to treat?

A

Blocks the release of ACH at the NMJ, so muscles lose their input and become permanently relaxed.

Can be used to treat muscle spasms

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6
Q

How does the tetanus toxin work?

A

Inhibits the release of GABA and glycine at inhibitory neurons, which dis-inhibits the cholinergic neurons.

This then causes permanent muscle contraction.

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7
Q

What are the different categories of neurotransmitters?

A
  • Amino acids (synthesised in locally in presynaptic terminal)
  • Monoamines (stored in vesicles)
  • Acetylcholine (released in response to Ca2+)
  • Neuropeptides
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8
Q

What are the two sources of glutamate?

A

1) Glucose (via Krebs cycle)

2) Glutamine (hydrolysed by glutaminase to give glutamate)

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9
Q

How is GABA synthesised?

A

From glutamate via glutamic acid decarboxylase (GAD)

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10
Q

How does glutamate get reuptaken?

A

Glial cells converts glutamate into glutamine, which then gets transported back into the nerve terminal where it gets converted back into glutamate.

This is done by excitatory amino acid transporters (EAATs)

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11
Q

What makes a neurotransmitter fast?

A

Their vesicles are located close to Ca2+ channels at the terminal

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12
Q

What can too much GABA lead to?

A

Sedation / Coma

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13
Q

What can too much glutamate or to little GABA lead to?

A

Hyper-excitability

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14
Q

What is cerebral ischaemia?

A

When the Na+/K+ gradient is reversed, due to the abolishment of the metabolic events that retain the metabolic gradient.

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15
Q

How does GHB (date rape drug) work?

A

It is a GABA metabolite that can be converted back into GABA.

This increases the GABA levels and too much of it can lead to unconsciousness/coma

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16
Q

What are the two types of monoamine neurotransmitters?

A
  • Catecholamines (e.g. dopamine, epinephrine and norepinephrine)
  • Indolamines (e.g. serotonin)
17
Q

How are catecholamines synthesised?

A

1) Tyrosine ——> L-Dopa (via tyrosine hydroxylase)
2) L-Dopa ——> Dopamine (via Dopa decarboxylase)
3) Dopamine ——> Norepinephrine (via dopamine B-hydroxylase)
4) Norepinephrine ——-> Epinephrine (via Phentolamine N-methyltransferase)

18
Q

Why is L-Dopa used to treat Parkinson’s disease (PD)?

A

It is a precursor of dopamine so dopa decarboxylase can convert it into dopamine.

This can treat PD because there are insufficient levels of dopamine in PD sufferers.

19
Q

What does SNARE stand for and what is its function?

A

Soluble NSF Attachment Protein Receptor

To dock vesicles to the plasma membrane

20
Q

How does exocytosis occur?

A

1) When the vesicle docks to the plasma membrane, SNARE complexes pull the two membranes together.
2) Ca2+ entering the cell binds to synaptotgamin on the vesicle, now allowing it to catalyse the fusion of the two membranes by binding to SNARE.
3) Neurotransmitter gets released and endocytosis then occurs to recover the vesicle to be refilled again.

21
Q

What does CaMKII stand for?

A

Calcium Calmodulin Activated Kinase II

22
Q

How do catecholamines get loaded into vesicles?

A

Via vesicular monoamine transporters (VMATs) along a proton gradient

23
Q

How does glutamate get loaded into vesicles?

A

Via vesicular glutamate transporters (VGLUTs)

24
Q

Is the supply of GABA always recycled?

A

Although it is reuptaken, a lot is also newly synthesised

25
Q

How is GABA loaded into vesicles, and what other neurotransmitter can the protein load into vesicles?

A

Via vesicular GABA transport (VAT)

Can also load glycine into vesicles

26
Q

What is the function of Monoamine Oxidases (MAOs) and Catechol-O-Methyltransferase (COMT)?

A

MAOs enzymatically degrade catecholamines

COMTs inactivate catecholamines

27
Q

What is entacapone and what can it be used to treat?

A

A COMT inhibitor and can be used to treat Parkinson’s disease

28
Q

What is selegilline and what can it be used to treat?

A

A MOA inhibitor that can be used to treat to treat depression, dementia and Parkinson’s disease.

29
Q

How does amphetamine act on the body?

A

Reverses catecholamine transporters so more gets released into synapse (DA and NA)

30
Q

How does cocaine act on the body?

A

Blocks DA reuptake transporters so they have a prolonged effect in the synapse

31
Q

How is serotonin produced?

A

1) Tryptophan —-> 5-HTP (via tryptophan hydroxylase)

2) 5-HTP —–> 5-HT (via 5-HTP decarboxylase)

32
Q

What is an example of an SSRI and what can it be used to treat?

A

Fluoxetine (Prozac)

Can be used to treat depression

33
Q

How is ACh produced?

A

The enzyme choline acetyltransferase converts choline and acetyl CoA into ACh.

34
Q

What is neostigmine and what can it be used to treat?

A

An AChE inhibitor used to treat myasthenia gravis

35
Q

What are some examples of neuropeptide neurotransmitters?

A
  • Vasopressin
  • Substance P
  • Endorphins
36
Q

What activates NO synthase, and what can this activation lead to?

A

1) Binding of Ca2+ and CaMKII activates NO synthase, which then produces NO.
2) NO then diffuses into the presynaptic cell and activates guanylyl cyclase.
3) Guanylyl cyclase then activates cGMP (2nd messenger) which can trigger a cascade to then release more neurotransmitter

Theme 1 - 202 (16 decks)

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