Nervous Co-ordination BWO

• Structure of a myelinated moteor neurone

  A) Dendrite

  B) Cell Body

  C) Axon

  D) Axon terminal

  E) Myelin sheath

  F) Node of Ranvier

  
• Describe resting potential

  Inside of axon has a negative charge relative to outside (as more positive ions OUTSIDE compared to inside)
• Explain how a resting potential is established across the axon membrane in a neurone

  Na+/K+ pump actively transports 3 Na+ out of axon and 2 K+ into axon

  Creating an electrochemical gradient (higher K+ conc inside and higher Na+ conc outside

  Differential membrane permeability -

  More permeable to K+ - move out by facilitated diffusion

  Less permeable to Na+ (closed channels)
• 5 Stages in depolarisation and gen of action potential

  Stimulus - Depolarisation - Repolarisation - Hyperpolarisation - Resting potential
• Changes in membrane permeability lead to depolarisation and the generation of an action potential

  1. Stimulus: Na+ channels open, membrane permeability to Na+ increases

  2. Na+ diffuse into axon down electrochemical gradient

  3. Depolarisation: if threshold potential reached, action potential generated

  4. As more voltage-gated Na+ channels open (positive feedback), more Na+ diffuse in rapidly

  5. Repolarisation: voltage-gated Na+ channels close, voltage gates K+ channels open, K+ diffuse out of axon

  6. Hyperpolarisation: K+ channels slow to close so there's a slight overshoot - too many K+ diffuse out

  7. Resting potential: restored by Na+/K+ pump
• Label a graph showing an action potential

  A) Stimulus

  B) open

  C) Depolarisation

  D) Ka+ close, Na+ open

  E) Repolarisation

  F) Hyperpolarisation

  G) K+ channels close

  H) Resting potential

  I) Threshold

  
• Describe the All-or-Nothing principle

  For an AP to be produced, depolarisation must exceed threshold potential

  APs produces are always same size at same potential (bigger stimuli instead increase frequency of action potentials)
• Explain how the passage of an AP along a NON-MYELINATED axon results in nerve impulses

  Action potential passes as a wave of depolarisation

  Influx of Na+ in one region increases permeability of adjoining region to Na+ by causing voltage-gated Na+ channels to open so adjoining region depolarises
• Explain how the passage of an AP along a myelinated axon results in nerve impulses

  Myelinated provides electrical insulation

  Depolarisation of axon at nodes of Ranvier only

  Resulting in saltatory conduction (local currents circuits)

  So there is no need for depolarisation along whole length of axon
• How can damage to myelin sheath lead to slow response

  Less/no saltatory conduction; depolarisation occurs along whole length of axon - so nerve impulses take longer to reach neuromuscular junctions; delay in muscle contraction

  Ions / depolarisation may pass/leak to other neurones - casuing wrong muscle fibres to contract
• Describe the nature of the refractory period

  Time taken to restore axon to resting potential when no further action potential can be generated

  As Na+ channels are closed/inactive
• Explain the importance of the refractory period

  Ensures discrete impulses are produced (APs dont overlap)

  Limits frequence of impulse transmission at certain intensity (prevents over-reaction to stimulus)

  Higher intensity stimulus causes higher frequence of APs - but only upto certain intensity

  Ensures APs only travel in one direction - cant be propogated in a refractory region
• In the second half of the refractory period an action potential can be produced but requires greater stimulation to reach threshold
• How does myelination affect speed of conductance

  Depolarisation at nodes of ranvier only due to saltatory conduction

  Impulse doesn't have to travel/depolarise whole length of axon
• How does axon diameter affect speed of conductance

  Bigger diameter means less resistance to flow of ions in cytoplasm
• How does temperature affect speed of conductance

  Increases rate of diffusion of Na+ and K+ due to more kinetic energy

  But proteins/enzymes could denature at a certain temperature
• Describe the structure of a synapse

  A) Axon

  B) Axon terminal

  C) Synaptic Cleft

  D) Vesicle with NTMs

  E) Voltage-gated calcium ion channel

  F) Receptor

  G) Sodium ion channel

  
• What is a cholinergic synapse

  Synapses that use the neurotransmitter acetylcholine
• Describe transmission across a cholinergic synapse

  At presynaptic neurone -

  Depolarisation of pre-synaptic membrane causes opening of voltage-gated Ca2+ channels - Ca2+ diffuse into pre-synaptic knob.

  Causing vesicles containing ACh to move and fuse with pre-synaptic membrane - Releasing ACh into the synaptic cleft by exocytosis

  At post-synaptic neurone -

  ACh diffuses across synaptic cleft to bind to specific receptors on post-synaptic membrane.

  Causing Na+ channels to open - influx of Na+ diffusing into psn causing depolarisation, if threshold met = AP
• What happens to acetylcholine after synaptic transmission

  It is hydrolysed by acetylcholinesterase

  Products are reabsorbed by the pre-synaptic neurone

  To stop overstimulation (if not removed it would keep binding to receptors, causing depolarisation)
• Explain how synapses result in unidirectional nerve impulses


  Neurotransmitters only made in / released from presynaptic neurone

  Complimentary receptors only on post-synaptic membrane
• Explain summation by synapses

  Addition of a number of impulses converging on a single post-synaptic neurone

  Causing rapid buildup of neurotransmitter

  So threshold more likely to be reached to generate an action potential
• Low frequency action potentials release insufficient neurotransmitter to exceed threshold
• Describe spatial summation

  Many pre-synaptic neurones share one post-synaptic neurone

  Collectively release sufficient NT to reach threshold to trigger an action potential
• Describe temporal summation

  One pre-synaptic neurone releases NT many times over a short time

  Sufficient NT to reach threshold to trigger an action potential
• Describe inhibition by inhibitory synapses

  Inhibitory neurotransmitters hyperpolarise postsynaptic membrane as:

  Cl- channels open -> Cl- diffuse in

  K+ channels open -> K+ diffuse out

  More Na+ required for depolarisation

  Reduces likelihood of threshold being met/action potential formation at post-synaptic membranes
• Both excitatory and inhibitory neurones forming synapses with the same post-synaptic membrane gives control of whether it 'fires' an action potential
• Describe the structure of a neuromuscular junction

  Receptors are on a muscle fibre instead of post-synaptic membrane and there are more

  Muscle fibres form clefts to store enzyme e.g. acetylcholinesterase to break down NT
• Compare transmission across cholinergic synapses and neuromuscular junctions

  Cholinergic:

  Neurone to neurone

  Neurotransmitters can be excitatory or inhibitory

  Action potential may be initiated in post-synaptic neurone

  Neuromuscular junction:

  Neurone to muscle

  Always excitatory

  Action potential propagates along sarcolemma down T tubules
• Use examples to explain the effect of drugs on a synapse

  Some stimulate the nervous system leading to more action potentials e.g. :

  Similar shape to NT/ stimulate release of more NT/ inhibit enzyme that breaks down NT -> Na+ continues to enter

  Some drugs inhibit the nervous system leading to fewer action potentials e.g.:

  Inhibit release of NT e.g. prevent opening of calcium ion channels/block receptors by mimicking shape of NT