Synpases and neuromuscular control Flashcards

(49 cards)

1
Q

What are the two types of synapses?

A

Electrical and Chemical

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2
Q

How do electrical synapses transmit signals?

A

Via electric current that passes directly through gap junctions between pre- and postsynaptic cells

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3
Q

How do chemical synapses transmit signals?

A

Electrical signals are converted into chemical signals via neurotransmitters

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4
Q

What forms gap junctions in synpases?

A

Docking of two hemichannels made of connexin or innexin proteins

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5
Q

What are the three main categories of neurotransmitters?

A

Classical
Peptides
Unconventional

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6
Q

Name examples of classical neurotransmitters

A

Acetylcholine
Biogenic amines (norepinphrine, dopamine, serotonin, histamine)
Amino acids (glutamate, GABA, glycine)

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7
Q

Name examples of peptide neurotransmitters

A

Substance P
Endorphins
Enkephalins

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8
Q

Name examples of unconventional neurtransmitters

A

Nitric oxide
ATP
Cannabinoids

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9
Q

What is an excitatory postsynaptic potential

A

Adepolarising response that may lead to an action potential

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10
Q

What is an inhibitory postsynaptic potential?

A

A hyperpolarising response that makes action potentials less likely

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11
Q

What triggers neurotransmitter release at the synpase?

A

Action potential opens volagte-gates Ca2+ channels, allowing Ca2+ entry, which triggers exocytosis

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12
Q

What happens after neurotransmitter release?

A

It diffuses across the synpatic cleft and binds to postsynaptic receptors, initiating a response

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13
Q

What are the precursors of ACh?

A

Choline and acetyl-CoA

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14
Q

What enzyme synthesise ACh?

A

Choline acetyltransferase

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15
Q

What enzyme degrades ACh?

A

Acetylcholinesterase, breaking it into acetic acid and choline

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16
Q

What are ionotropic receptors?

A

Chemicalls-gated ion channels that open directly

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17
Q

What are metabotropic receptors?

A

G-protein coupled recepotrs that trigger second messengers

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18
Q

What type of receptor is nAChR?

A

Ionotropic; allows Na+, K+, and Ca+ in when activated

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19
Q

What type of receptor is mAChR?

A

Metabotropic, uses G-proteins to affect second messenger system

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20
Q

What do M1, M3, N5 mAChRs do?

A

Activate phospholipase C –> DAG + IP3 –> increase Ca2+, kinase activation

21
Q

What do M2, M4 mAChRs do?

A

Inhibit adenylate cyclase –> decrease cAMP; affect K+, Ca2+ channels

22
Q

What is an agonist?

A

A molecule that binds to and activates a receptor

22
Q

What is an antagonist?

A

A molecule that blocks or interferes with receptor activation

23
Q

What does a1 receptor activation do?

A

Activates phospholipase C –> IP3 and DAG

24
What does a2 receptor do?
Inhibits adenylate cyclase --> decrease cAMP
25
What do B1-B3 receptros do?
Activate adenylate cyclase --> increase cAMP
26
How are neuotrasnmitters inactivated?
Reuptake Enzymatic breakdown Glial uptake
27
Is there reuptake for ACh?
No, but choline is recycled
28
What does the somatic motor pathway control?
Skeletal muscle via single, exciatory neurons from the CNS
29
What is a motor unit?
One motor neuron and all the muscle fibres it innervates
30
What neurtransmitter is used at the NMJ?
Acetylcholine
31
What receptor is at the NMJ?
Nicotinic ACh receptor (nAChR)
32
What triggers ACh release?
Ca2+ influx due to an action potential
33
What happens after ACh binds nAChRs?
Na+ influx --> depolarisation of muscle fibre
34
What diseases are linked to impaired neurotransmission?
Alzheimer's Parkinson's Depression Anxiety Schizophrenia Epilepsy
35
How do drugs affect neurotransmission?
Alter enzyme activiy, reuptake, or receptor interactions
36
What are the general symptoms of Myasthenic Disorders?
Muscle weakness Fatigability
37
What is Myasthenia Gravis?
Postsynaptic defect; antibodies attack nAChRs
38
How is MG treated?
What acetylcholinesterase inhibitors
39
What is Lambert-Eaton Myasthenic Syndrome
Presynaptic defect; antibodies attack Ca2+ channels --> decrease ACh release
40
WHat causes ACh receptor deficiency?
Mutation in nAChR genes --> fewer/altered receptors (postsynaptic)
41
What cause Congenital Myasthenic Syndromes? (CMSEA)
Mutation in choline acetyltransferase (presynaptic)
42
What causes AChE deficiency?
Mutation in AChE gene --> overstimulation of muscle (synaptic defect)
43
What is endogenous depression?
No clear cause, possibly genetic
44
What is exogenous depression?
Triggered by life events (PTSD)
45
What neurotransmitter imbalance is seen in depression?
Decrease in noradrenaline, serotonin, dopamine Increase in cholinergic activity
46
How do tricyclin antidepressant work?
Block reuptake of noradrenaline
47
How do SSRIs work?
Blcok reuptake of serotonin
48
How do MAO inhibitors work?
Prevent breakdown of monoamines