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Neuro > Axonal and Synaptic Neural Transmission > Flashcards

Axonal and Synaptic Neural Transmission Flashcards

1
Q

Ions involved

A

Anions (negative protein), Na+, K+, Cl-

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2
Q

Final resting potential

A

-70 mV

Na+ high conc. outside but with both forces pushing in.
Membrane and pump resists Na+ inward movement.
K+ and Cl- move both ways across membrane so reach steady state determine by diffusion and electrostatic pressure.

Some Na+ leaks back in but is expelled by pump.

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3
Q

Sodium-potassium pump

A

Keeps resting potential by pumping 3 Na+ ions out and 2 K+ in.
Active and requires ATP

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4
Q

What do neurotransmitters do?

A

Activate receptors on dendrites . soma

Ion channels open

Ions cross
Membrane potential changed
Potential changes spread through cell

If large enough, action potential triggered

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5
Q

What does a positive voltage mean

A

Depolarised

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6
Q

What would hyperpolarisation do to voltage

A

More negative

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7
Q

Excitatory neurotransmitters

A

Depolarises cell membrane (more positive)

Increases probability of action potential (more likely to cross threshold of -60mV)

Cause an Excitatory Post Synaptic Potential (EPSP)

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8
Q

Inhibitory neurotransmitters

A

Hyperpolarises cell membrane

Decreases probability of action potential (less likely to cross threshold of -60mV)

Causes Inhibitory Post Synaptic Potential (IPSP)

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9
Q

Spatial summation

A
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10
Q

Temporal summation

A
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11
Q

Passive conduction

A

Voltage changes spread away (decrementally) from point of origin

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12
Q

What part determines whether an action potential is generated?

A

Axon hillock

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13
Q

What happens after action potential generated?

A

When -60mV reached, voltage gated Na+ channels open and influx of Na+ into neuron.

Polarity becomes +30 mV in neuron.

Membrane potential reverses with neuron becoming positive.

Voltage gated Na+ channels close. K+ channels open and K+ rushes out of neuron.

This makes resting membrane potential more negative again to restore it to the resting membrane potential.

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14
Q

Myelination

A

Speeds up axonal conduction.

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15
Q

Where does myelin come from?

A

Oligodendrocytes in CNS and Schwann cells in PNS

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16
Q

Chemical Synapse

A

Action potential reaches terminal buttons on pre-synaptic side.

Voltage gated Ca2+ channels activated.

Ca2+ ions flood in.

Causes exocytosis, neurotransmitter molecules cross synaptic cleft.

Attach to receptors on post-synaptic membrane

17
Q

What happens to the neurotransmitter on post-synaptic side?

A

Acetylcholinesterase breaks down acetylcholine.

Other enzymes break down other neurotransmitters.

Reuptake.

18
Q

Blockers

A

eg Novichok

Blocks enzyme to breakdown the neurotransmitter so it stays in synapse continuing to have effect

(could cause excessive activation of muscles leading to convulsions –> paralysis, failure of heart muscle, respiration, eye, muscles, GI tract)

19
Q

Parts of Synaptic Transmission that can be blocked (targets of drugs)

A

Manufacture (intracellular biochemical processes)

Storage (vesicles)

Release (action potential)

Post-synaptic receptors

Inactivation (break down or reuptake)

20
Q

Common Fast neurotransmitters (short lasting effects)

A

Acetylcholine
Glutamate
Gamma-aminobutyric acid (GABA)

21
Q

Common Slower acting neurotransmitters

A

Dopamine (DA)
Noradrenalin (NA)
Serotonin (5HT)

22
Q

How do local anaesthetics work?

A

Na+ channels blockers

Blocks progress of action potential

23
Q

Substances affecting ACh

A

Nictotine, curare, black widow spider toxins, nerve gas)

24
Q

Substances affecting NA (noradrenaline)

A

Antidepressant drugs (imipramine blocks re-uptake, MAO inhibitors block break-down)
Stimulants (amphetamine - increases release and blocks re-uptake)

25
Q

Substances affecting Dopamine

A

Antipsychotic drugs, stimulants, anti-Parkinson drugs

26
Q

Substances affecting Serotonin

A

Anti-depressant drugs, Hallucinogens (eg mushrooms, LSD, ketamine), ecstasy

27
Q

Substances affecting GABA

A

Anti-anxiety drug,
Anticonvulsant drugs,
Anaesthetics

Neuro (27 decks)

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