Week 7 - Pharmacology Of The Synapse Flashcards

1
Q

How do NT move from axon to synapse?

A
  1. synthesis and storage (synethesised by golgi apparatus, synaptic vesicles to presynapse)
    2.receive AP (synaptic vesicles float)
  2. depolarisation (Ca2+ open, flood into presynapse)
  3. release of NT into cleft (exocytosis)
  4. attachment and activation (complementary receptors)
  5. deactivation (reuptake, enzymatic breakdown)
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2
Q

What does depolarisation post-synapse lead to?

A

excitatory postsynaptic potential (EPSP)

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3
Q

What does hyperpolarisation post-synapse lead to?

A

inhibitory postsynaptic potential (IPSP)

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4
Q

How do glutamatergic synapses work?

A

Excitatory
Depolarisation - EPSP - Lower threshold - More firing

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5
Q

How do GABAergic synapses

A

Inhibitory
Hyperpolarisation - IPSP - Increase threshold - Less firing

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6
Q

Examples of catecholamines

A

Dopamine
Adrenaline
Noradrenaline

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7
Q

Stages of catecholamine synthesis

A

Tyrosine
L-Dopa
Dopamine
Noradrenaline
Adrenaline

(PRE CURSORS : ONE CANNOT EXIST WITHOUT OTHER)

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8
Q

What is the purpose of the Nigrostriatal System?

A

Sensory, movement

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9
Q

What is the purpose of the Mesolimbic System?

A

Reinforcement
Reward and Emotions

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10
Q

What is the purpose of the Mesocortical System?

A

Cognition
Memory ST
Planning
Strategy

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11
Q

Are most serotenergic synapses IPSP or EPSP?

A

IPSP

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12
Q

Which enzyme allows the breakdown of monoamines?

A

Monoamine Oxidase: convert into inactive substances
Monoamine oxidase inhibitors prevent MAO action

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13
Q

Features of acetylcholine?

A

2 types of receptors - slower vs fast acting
Broken down by AchE (abundant in synaptic cleft)
Cholinergic synapses (excitatory)

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14
Q

Define Agonists

A

Speed up action of NT
eg. L-Dopa and Nicotine

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15
Q

Define Antagonists

A

Slow action of NT
(eg. Botox, Reserpine)

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