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2.1 T1: Fundamental Neuroscience and the Brain > T1 L4: Chemicals in the brain > Flashcards

T1 L4: Chemicals in the brain Flashcards

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1
Q

How do neuropeptides act as neurotransmitters and how are they released?

A

They are synthesised in the cell soma and transported to the terminal and then stored in secretory granules. They are much larger than normal neurotransmitters. They’re released in response to global increase in Ca2+

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2
Q

Are amino acids as neurotransmitter fact or slow?

A

Fast

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3
Q

Are neuropeptides as neurotransmitters fact or slow?

A

Slow

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4
Q

What is the main excitatory neurotransmitter?

A

Glutamate (Glu)

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5
Q

How does Glutamate excite neurones?

A

It slightly depolarises the postsynaptic cell’s membrane

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6
Q

What are the 2 main inhibitory neurotransmitter?

A

GABA (gamma-aminobutyric acid) and Glycine (Gly)

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7
Q

How do GABA and Glycine excite neurones?

A

They slightly hyperpolarise the postsynaptic cell’s membrane

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8
Q

Where is GABA used within the body?

A

In the brain

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9
Q

Where is Glutamate used within the body?

A

In the CNS

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10
Q

Where is Glycine used within the body?

A

In the spinal cord and the brain stem

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11
Q

What functions does the Serotonergic system have?

A

Mood, sleep, pain, emotion, and appetite

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12
Q

Where is Glutamate produced?

A

It’s synthesised in the presynaptic terminal

  • from glucose via the krebs cycle
  • from glutamine converted by glutaminase into glutamate
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13
Q

What do vesicular glutamate transporters (VGLUT’s) do?

A

They load and store glutamate in vesicles

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14
Q

Which cells convert Glu into glutamate?

A

Glial cells

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15
Q

Which transporters reuptake glutamate (Glu) and where are they?

A

Excitatory amino acid transporters (EAAT’s) found in the plasma membrane of presynaptic cell and surrounding glia

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16
Q

What is GABA synthesised from?

A

Glutamate (Glu)

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17
Q

What catalyses the synthesis of GABA?

A

Glutamic acid dehydrogenase (GAD)

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18
Q

Which transporter loads and stores GABA?

A

Vesicular GABA transporter (GAT). Gly uses this transporter too

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19
Q

How is GABA cleared from a synapse?

A

Reuptake by transporters on glia and neurones

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20
Q

How much of GABA is recycled?

A

Not a lot. Most of it is made de novo to refill vesicles

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21
Q

What are the effects of too much Glu/ too little GABA?

A

Hyper-excitability (epilepsy) and excitotoxicity

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22
Q

What are the effects of too much GABA?

A

Sedation/ coma

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23
Q

What is cerebral ischaemia and what are the consequences?

A

It’s the metabolic events that retain the electrochemical gradient are abolished leading to reversal of the Na+/K+ gradient. It causes transporters to release glutamate by reverse operation causing excitotoxic cell death (too much Ca2+ release activates digestive enzymes that break down the cell)

24
Q

What is GHB (gamma-hydroxybutyrate) and how does it work?

A

It the date rape drug. It’s a metabolite that can be converted back into GABA to increase the levels of GABA which will lead to unconsciousness and coma

25
Q

Give some examples of Cetecholamines

A

Dopamine, Adrenaline, and Noradrenaline

26
Q

Give examples of Indolamines

A

Serotonin

27
Q

Describe the steps to synthesising dopamine

A

Tyrosine - dopa - dopamine

28
Q

Does dopamine cross the blood-brain barrier?

A

No

29
Q

What is the drug Levodopa used for?

A

Treating Parkinson’s disease

30
Q

Describe the steps of synthesising adrenaline

A

Dopamine - Noradrenaline - Adrenaline

31
Q

Which is the only neurotransmitter synthesised within vesicles?

A

Noadrenaline

32
Q

What is Levodope (L-dopa) and how is it used?

A

It a precursor of dopamine and is used to treat Parkinsons disease. Dopa decarboxylase converts it into dopamine

33
Q

How are catecholamines released?

A

By Ca2+ dependent exocytosis

34
Q

How is the catecholamine signal terminated?

A

They are taken up into the axon terminal by transporters powered by electrochemical gradient (Dopamine transporters (DAT’s), and Norepinephrine transporters (NET’s))

35
Q

Which enzymes degrade Catecholamines?

A

Monoamine oxidases (MOA’s)

36
Q

Which molecules deactivate Catecholamines?

A

Catechol-O-methyl-transferases (COMT)

37
Q

What effect does the drug Amphetamine have on Catecholamines?

A

It increases the release and decreases the reuptake of catecholamines like Dopamine and Norepinephrine

38
Q

What effect does the drug Cocaine have on Catecholamines?

A

It increases the release of norepinephrine and of dopamine and inhibits their neuronal reuptake. This leaves more of them in the synaptic cleft and which extends their action on the postsynaptic neuron

39
Q

What effect does the drug Methylphenidate (Ritalin) have on Catecholamines?

A

Methylphenidate preferentially increases catecholamine neurotransmission within the prefrontal cortex at low doses that enhance cognitive function

40
Q

What effect does the drug Selegiline have on Catecholamines?

A

It’s an MOA inhibitor found in dopaminergic nerve terminals which prevents the breakdown of dopamine

It’s used as treatment for depression and dementia

41
Q

What effect does the drug Entacapone have on Catecholamines?

A

It’s a COMT inhibitor that increases the amount of neurotransmitter

42
Q

Describe the process of serotonin synthesis

A

Tryptophan - 5-HTP - 5-HT (serotonin)

43
Q

Which precursor of serotonin is found in chocolate?

A

Tryptophan

44
Q

How is the signal for serotonin terminated?

A

By reuptake by serotonin transports (SERT’s) on the presynaptic membrane or it’s destroyed by MAO’s in the cytoplasm

45
Q

What effect does the drug Fluoxetine (Prozac) have on serotonin?

A

It’s an SSRI that blocks the reuptake of serotonin. It’s used as treatment for for depression and OCD

46
Q

What effect does the drug Fenfluramine have of serotonin?

A

It stimulates the release of serotonin and inhibits it’s reuptake. It has also been used to supress appetite in obesity

47
Q

What effect does MNDA (methylenedioxymethamphetamine) (ecstasy) have on serotonin?

A

It causes norepinephrine and serotonin transporters to run backwards so that they release neurotransmitter into the synapse. It has been assessed for therapeutic potential in PTSD

48
Q

What does Choline acetyltransferase do?

A

It converts choline and acetyl CoA into acetylcholine

49
Q

Which transporters package acetylcholine into vesicles?

A

Vesicular acetylcholine transporters (VAChT)

50
Q

Which molecule rapidly degrades acetylcholine in the synapse?

A

Acetylcholinesterase (AChE). The choline is transported back into the presynaptic terminal and converted to acetylcholine again

51
Q

What is the drug Neostigmine used to treat?

A

Myasthenia gravis. It’s a type of acetylcholinesterase inhibitor

52
Q

What is Myasthenia gravis?

A

A rare long-term condition that causes muscle weakness. It most commonly affects the muscles that control the eyes and eyelids, facial expressions, chewing, swallowing and speaking

53
Q

What triggers the degradation of neuropeptides?

A

Ca2+

54
Q

How long do neuropeptides last?

A

The signal can be maintained for longer but they are released slowly

55
Q

What role does nitric oxide have in the guanylyl cyclase pathway?

A

NO activates guanylyl cyclase which makes the second messenger cGMP

56
Q

What do endocannabinoids do?

A

They are small lipids which mostly cause reduced GABA release at certain inhibitory terminals. They are believed to be related to addiction

57
Q

What is the active component of cannabis?

A

A cannabinoid

2.1 T1: Fundamental Neuroscience and the Brain (24 decks)

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