Flipped lecture Synapses + NT

Question 1

What is ChAT?

Answer 1

Choline acetyltransferase

Question 2

What is the role of Choline acetyltransferase (CHaT)?

Answer 2

ChAT catalyzes the transfer of an acetyl group from acetyl-CoA to choline, producing acetylcholine

Essentially synthesises ACh

Question 3

Where is Acetyl Coa produced?

Answer 3

Produced by cellular respiration in mitochondria

Question 4

What are nicotinic acetylcholine receptors (nAChRs)?

Answer 4

nAChRs are a type of cholinergic receptors, meaning they respond to ACh

Question 5

How is ACh recycled after being released into the synaptic cleft?

Answer 5

AChe breaks down Ach into Choline and Acetic acid which the choline is then reuptaked by choline transporter

Question 6

How many types of Muscarinic receptors?

Answer 6

5

M1,M2,M3,M4,M5

Question 7

Where are Musarinic (mAChRs) found?

Answer 7

CNS and autonomic nervous system

Question 8

Which muscarinic receptors are excitatory and inhibitory?

Answer 8

M1, 3, 5: excitatory via Gq
M2, 4: inhibitory via GI

Question 9

Are there more mAChRs (muscarinic) or nAChRs (nicotinic) in the brain?

Answer 9

Brain has 10-100x more mAChRs than nAChRs

Question 10

What is the neurotransmitter at the NMJ?

Neuromuscular junction

Answer 10

Acetylcholine

Question 11

What blocks the release of acetylcholine?

Answer 11

• Botulinum toxin - destroys SNARE’s protein
• Black widow spider venom - Causes large Ca2+ influx but then completely stops it

Question 12

What blocks the AChE?

Answer 12

• Nerve gas
• Organophosphate pesticides
• Alzheimer’s treatments

Buildup of Ach resulting in excessive stimulation of ACh receptors

Question 13

What activates ACh receptors?

Answer 13

• Nicotine, muscarine (agonists)
• Neonicotinioid pesticides

Question 14

What blocks the ACh receptors?

Answer 14

• Nicotinic: curare, a-bungarotoxin
• Muscarinic: atropine

Atropine can be an antidote for nerve gas

Question 15

What 4 ways could interfere with Acetylcholine’s role?

Answer 15

1) Block release
2) Block AChE
3) Activate ACh receptors
4) Block Ach receptors

Question 16

Why is atropine used to treat nerve gas poisoning?

Answer 16

• Nerve gases are potent inhibitors of AChE (breaks down ACh) - causes a buildup of ACh
• Atropine is a muscarinic acetylcholine receptor antagonist - means it blocks ACh from binding to muscarinic receptors

Atropine acts as a competitive inhibitor, preventing the excess ACh from overstimulating the muscarinic receptors

Question 17

What is VMAT?

Answer 17

Vesicular monoamine transporters

Question 18

What gets packed into vesicles by VMAT?

Answer 18

Monoamines

Question 19

What is MAO?

Answer 19

Monoamine oxidase

Question 20

What can destroy monoamines?

Answer 20

Monoamina oxidase (MAO) and catechol-O-methyltransferase

Question 21

What are monoamine receptors mostly like?

Answer 21

Monoamine receptors are mostly GPCRs

Question 22

What are the receptors for epinephrine/ norepinephrine?

Answer 22

Adrenergic receptors: alpha and beta types

Question 23

What are the receptors for Serotonin?

Answer 23

7 receptors - one is a ligand-gated Na+/K+ channel

Question 24

Where is dopamine produced?

Answer 24

Produced in the substantia nigra

Question 25

Where are dopaminergic neurons in the substantia nigra projected to?

Answer 25

They are projected to the striatum ## Footnote Dopaminergic neurons go from the substantia nigra to the striatum

Question 26

What is the pathway responsible for motor movement called?

Answer 26

The nigrostriatal pathway

Question 27

What happens if dopamingeric neurons are damaged?

Answer 27

Damage to the dopamine-producing neurons in the substantia nigra leads to a decrease in dopamine in the striatum, which is the primary cause of Parkinson's disease

Question 28

What is TH?

Answer 28

Tyrosine hydroxylase

Question 29

Does dopamine cross the blood-brain barrier ?

Answer 29

No it does not cross

Question 30

Why can Parkinson's be treated by increasing dopamine?

Answer 30

Parkinson's disease is primarily caused by the loss of dopamine-producing neurons in the substantia nigra, leading to a dopamine deficiency in the striatum. This deficiency disrupts the delicate balance of neurotransmitters in the brain, resulting in the characteristic motor symptoms of Parkinson's, such as tremors, rigidity, and slowness of movement.   Therefore, a major focus of Parkinson's treatment is to increase dopamine levels in the brain to compensate for this loss

Question 31

What is VTA?

Answer 31

Ventral tegmental area

Question 32

Where does the ventral tegmental area project to?

Answer 32

The VTA projects to the cortex and limbic system

Question 33

What does the mesolimbic pathway mediate?

Answer 33

Reward/motivation

Question 34

Where do noradrenergic neurons live?

Answer 34

They live in the locus coeruleus

Question 35

How much noradrenergic neurons are there in the brain?

Answer 35

12,000 per hemisphere

Question 36

What is the role of noradrenergic neurons in the brain?

Answer 36

Noradrenergic neurons, particularly those in the locus coeruleus, are vital in regulating wakefulness and vigilance. They increase alertness and responsiveness to stimuli. ## Footnote Also regulate sleep/wake, attention, arousal, mood, memory, anxiety, pain etc

Question 37

Where do serotonergic neurons live?

Answer 37

They live in the Raphe nuclei

Question 38

What is the role of serotonergic neurons?

Answer 38

Serotonin is heavily involved in regulating mood, feelings of well-being, and happiness. Imbalances in serotonin levels are often linked to mood disorders like depression and anxiety

Question 39

What do cocaine and amphetamines do?

Answer 39

Block reuptake of dopamine and norepinephrine

Question 40

What do antipsychotics do?

Answer 40

They block dopamine receptors (possible side effect: Parkinson's-like symptoms)

Question 41

Give me exampls of antidepressants

Answer 41

- Tricyclics: block reuptake of NE, serotonin - Selective serotonin reuptake inhibitors (SSRIs), e.g. fluoxetine (Prozac) - MAO-A inhibitors