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
Action potential travel
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
Effect of myelin sheath on axon
Insulates axon Action potentials travel faster Peripheral= Schwann, glial Central= oligodendrocyte, glial
27
Node of ranvier with myelinated
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
Why is saltatory conduction important
The myelin sheath provide the neurones to reach from the spinal chord to the leg quickly Communication of impulses from brain to body
29
Drugs affecting action potential generation
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
Neuromuscular junction
Sodium moves into terminal= more positive Calcium going into terminal Acetylcholine released into synaptic choline
31
Acetylcholine synthesis
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
How does calcium cause synaptic release
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
What happens to motor end plate when acetylcholine binds to receptors
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
Excitation contraction coupling
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
Muscle contraction
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
Why are neuromuscular junction blockers used
To cause skeletal muscle paralysis for surgeries
37
Two groups of neuromuscular junction blockers
Depolarising Non depolarising
38
How do depolarising neuromuscular blockers work
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
How do non depolarising neuromuscular blocker work
Competitive reversible antagonist at nicotinic receptor Bind to same binding site as acetylcholine Nicotinic receptor not activated Channel stays closed
40
Acetylcholinesterase inhibitors
Blocks the enzyme which breaks down acetylcholine Increase in acetylcholine in the synaptic cleft