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Phay0003 > Nerves And Neurotransmission > Flashcards

Nerves And Neurotransmission Flashcards

1
Q

Nerves

A

Bundle of fibres that transmit impulses between areas of the body and within the brain

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2
Q

Peripheral nervous system

A

Afferent (sensory)
Efferent (motor)

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3
Q

Efferent (motor) has what two systems

A

Somatic - voluntary
Autonomic - involuntary and reflex

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4
Q

The autonomic system can be subdivided into what

A

Sympathetic
Parasympathetic

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5
Q

What is nervous system made up of

A

Glial cells (structure and support)
Schwann cells
Neurons ( generate and send impulses)

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6
Q

Structure of neuron

A

Cell body / soma
Axon
Axon hillock is that connects cellbody to axon
Dendrites

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7
Q

Neurons generate impulses called what

A

Action potentials

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8
Q

Action potential impulses transmission

A

Presynaptic neurone:
Generated in axon hillock
Travel down axon to axon terminals
Axon terminals forms a junction with another cell = synapse
Release of chemicals= neurotransmitters

Post synaptic neurone:
Neurotransmitter diffuses across synapse to target cell
Binds to receptors
Drug receptor complex
Generation of signals in receiving cell

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9
Q

Sodium Ion concentration outside the cell compared to inside

A

Outside= high conc of sodium ions
Intercellular= relatively low conc of sodium ions

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10
Q

Potassium ion conc inside and outside of the cell

A

Intercellular= high potassium conc
Outside the cell= low potassium con

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11
Q

How is the ion concentrations maintained

A

Various ion channels and ion pumps

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12
Q

Sodium potassium ATPase

A

Transports Na+ from inside cell to outside and K+ from outside to inside
Resting conformation has 3 binding sites for sodium ions
Pump can also bind to atp
When atp becomes dephosphorylated, the pump becomes phosphorylated
Conformation of the pump changes so is now exposed to extra cellular side and sodium ions is released into extra cellular fluid
Binding sites for potassium open
Pump becomes dephosphorylysed and phosphorus is released
Potassium ions released back into cell
Repeat

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13
Q

Equilibrium potential of an ion equation

(Not needed)

A

RT/ZF ln [ion out/ ion in]

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14
Q

Equilibrium potential of potassium

A

-90mV
No movement of potassium ions

Typical membrane potential of cell is -70

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15
Q

Voltage gated ion channel states

A

Change in voltage across cell membrane
Voltage gated ion channels are activated
Voltage channel open state
Ions cross channel
Time dependent
Ion channel conformation changes
Ball and chain closes the end part of the ion channel (inactive state)
Membrane potential changes to near rest, ion channel returns to closed state

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16
Q

Types of receptors in dendrites

A

Glutamate, acetylcholine = neurotransmitters in brain
NMDA receptors= Sodium and calcium, more positive ions goes into the cell, excitatory post synaptic potential (EPSP)
Ampa receptor = sodium ions causes an excitatory response

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17
Q

Inhibitory post synaptic potential

A

Inhibitory ensures neurones don’t become overactive
Hyper polarisation

18
Q

Action potentials initiated at axon initial segment

A

High conc of sodium channels/ potassium
Epsp reach soma/ cell body
Membrane potential becomes more positive (depolarisation)
Reaches threshold potential
Sodium channels open up, fast depolarisation
Membrane potential decreases= repolarisation
Potential becomes less than resting potential (hyperpolaristaion)/ refractory state
Reaches resting potential

19
Q

Resting membrane of cell

A

-70mV
‘Leak’ K+ channels

20
Q

Depolarisation

A

Na+ channels begin to open
Membrane depolarised
Regenerative

21
Q

Peak of action potentials

A

Na+ channels begin to inactivate
Prevents their activation a second time
Blocks initiation of another action potentials within a short period of time= Absolute refractory period
Voltage gated K+ channels open more slowly than Na+

22
Q

Repolarisation

A

Voltage gated K+ channels are open

23
Q

Hyperpolarisation/ relative refractory period

A

More k+ channels are open than at rest
Membrane potential approaches Ek
Allows Na+ channels to recover from inactivation

24
Q

Resting potential

A

Voltage gated K+ channels close
Membrane returns to rest
Ready for another action potentials

25
Q

Action potential travel

A

Axon is unmyelinated
Sodium ion channels open
Generates action potential, passive spread of electric current

Slow, action potentials tend to fail or stop because of leakage

26
Q

Effect of myelin sheath on axon

A

Insulates axon
Action potentials travel faster

Peripheral= Schwann, glial
Central= oligodendrocyte, glial

27
Q

Node of ranvier with myelinated

A

High concentration of sodium channels/ potassium
Action potential is generated
Saltatory conduction= impulses travel very quickly from axon to axon terminals by jumping
Less chance of failing

28
Q

Why is saltatory conduction important

A

The myelin sheath provide the neurones to reach from the spinal chord to the leg quickly
Communication of impulses from brain to body

29
Q

Drugs affecting action potential generation

A

Local anaesthetic are weak bases (lidocaine)
Unionised form travels through cell membrane
Turns to ionised form
Binds to sodium ions channel on the intracellular
Stops sodium ions from being activated
Stops action potential

30
Q

Neuromuscular junction

A

Sodium moves into terminal= more positive
Calcium going into terminal
Acetylcholine released into synaptic choline

31
Q

Acetylcholine synthesis

A

Ach made from choline and acetyl coA
In the synaptic cleft, ach rapidly broken down by the enzyme acetylcholineesterase
Choline transported back into the axon terminals and used to make more ach
Acetate washed away , choline is reused

32
Q

How does calcium cause synaptic release

A

Vesicles are transported and anchored to presynaptic terminal - docking
Dependent at ATP- primed
Ready to release
Only release when ca2+ conc increases
Binds to a protein in SNARE COMPLEX
initiates fusion with membrane to release into synaptic cleft

33
Q

What happens to motor end plate when acetylcholine binds to receptors

A

Ion channels open up
Permeable to sodium and potassium
Electrochemical gradient is smaller for potassium
Sodium moves into motor end plate, end plate potential produced
Large end plate potential= action potential

34
Q

Excitation contraction coupling

A

Nicotine ach receptors causes depolarisation
Depolarisation travels to T tubule
Sodium channels open and sodium moves into the cell
Attaches to receptors linked to the calcium stores in sarcoplasmic reticulum
When receptors are activated, calcium is released
Initiates contraction

35
Q

Muscle contraction

A

Calcium released from sarcoplasmic reticulum and binds to troponin C
Unravels trypomosin
Exposes binding sites on the actin
Myosin head can bind to actin
ATP is hydrolysed so myosin binds to actin (cross bridge)
Phosphate released
Myosin head pivots, power stroke
Sliding actin filament
ADP released (low energy configuration)
New atp attaches, cross bridge detaches

36
Q

Why are neuromuscular junction blockers used

A

To cause skeletal muscle paralysis for surgeries

37
Q

Two groups of neuromuscular junction blockers

A

Depolarising
Non depolarising

38
Q

How do depolarising neuromuscular blockers work

A

Nicotinic receptor agonist
Bind to nicotinic receptor and opening
Sodium influx into muscle cell
Remain bound to receptor for long time
Ion channel remains continuously open
No more sodium going into cell= equilibrium
No further depolarisation
No muscle contraction

39
Q

How do non depolarising neuromuscular blocker work

A

Competitive reversible antagonist at nicotinic receptor
Bind to same binding site as acetylcholine
Nicotinic receptor not activated
Channel stays closed

40
Q

Acetylcholinesterase inhibitors

A

Blocks the enzyme which breaks down acetylcholine
Increase in acetylcholine in the synaptic cleft

Phay0003 (11 decks)

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