Chapter 15 - Nervous Control

• Describe the structure of a myelinated motor neurone.

  
• Describe resting potential.

  Inside of axon has a negative charge to outside

  More positive ions outside compared to inside.
• Explain how a resting potential is established across an axon membrane in a. neurone.

  Na+/K+ pump actively transports

  3Na+ out and 2K+ into axon.

  Creating an electrochemical gradient

  Higher conc. K+ inside and higher conc. of Na+ outside

  Differential membrane permeability

  More permeable to K+ - move out of FD

  Less permeable to Na+
• Explain how changes in membrane permeability lead to depolarisation and generation of an action potential.

  Na+ channels open increasing membrane permeability to Na+

  Na+ diffuse into axon down electrochemical gradient

  If threshold reached an action potential is generated

  More voltage gated Na+ channels opne

  More Na+ diffuse in rapidly
• Explain how repolarisation and hyper polarisation are caused.

  Voltage gated Na+ channels close

  Voltage gated K+ channels opne

  K+ diffuse out of the axon

  K+ channels slow too close so there is a slight overshoot of K+ diffusing out.
• Describe the graph to show an action potential.

  
• Describe the all or none principle.

  For an action potential to be produced depolarisation must exceed threshold potential.

  Action potentials produced are always same magnitude or size

  Bigger stimuli will only increase frequency of action potentials.
• Explain he passage of an action potential down a non - myelinated axon.

  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.
• Explain he passage of an action potential down a myelinated axon.

  Myelination provides electrical insulation

  Depolarisation of axon at nodes of Ranvier only

  results in saltatory conduction

  No need for depolarisation along whole length of axon.
• Suggest how damage to the myelin heath can lead to slow responses or jerky movements.

  Less/ no saltatory conduction

  Depolarisation occurs along the whole length of the axon

  Nerve impulses take longer to reach the neuromuscular junction

  Delaying muscular contraction

  Ions/depolarisation may pass to other neurones causing the wrong muscle fibres to contract.
• Describe the nature of the refectory period.

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

  Na+ channels are closed / inactive
• Explain the importance of the refectory period.

  Discrete impulses produced - action potentials don't overlap

  Limits frequency of impulse transmission at a certain intensity.

  - High intensity causes higher frequency of action potentials

  - Only unto a certain intensity

  Unidirectional travel of action potentials - cant be propagated in refectory region.
• State the three factors that affect speed of conductance.

  Myelination

  Axon Diameter

  Temperature
• Describe how myelination impacts speed of conductance.

  Depolarisation at nodes of Ranvier only - saltatory conduction

  Impulse doesn't depolarise whole length of axon
• Describe how axon diameter impacts speed of conductance.

  Bigger diameter means less resistance to flow of ions in cytoplasm.
• Describe how temperature impacts speed of conductance.

  Increased rate of diffusion of Na+ and K+ as more kinetic energy.

  Proteins and enzymes may denature at a certain temperature.
• Describe the structure of a synapse.

  
• What are cholinergic synapses?

  Synapses that use acetylcholine as their neurotransmitter
• Describe transmission across a cholinergic synapse.

  1. Depolarisation of pre - synaptic membrane causes opening of voltage gated Ca2+ ion channels

  2. Ca2+ diffuse into pre synaptic neurone

  3. casting vesicles containing ACh to move and fuse with the pre - synaptic membrane.

  4. Releasing ACh into the synaptic cleft

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

  6. Causing Na+ channels to opne

  7. Na+ diffuse into post synaptic neurone causing depolarisation.

  8. If threshold met action potential initiated.
• Explain what happens to acetylcholine after synaptic transmission.

  Hydrolysed by acetycholinesterase

  Products reabsorbed by presynaptic neurone

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

  Neurotransmitter only made in pre synaptic neurone

  Receptors only on post synaptic neurone.
• Explain summation by synapses.

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

  Causing rapid buildup of neurotransmitter (NT)

  So threshold more likely to be reached to generate an action potential
• What is the importance of summation?

  Low frequency action potentials release insufficient neurotransmitter to exceed threshold.
• Describe spatial summation.


  Many pre-synaptic neurones share one synaptic cleft /

  post-synaptic neurone

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


  One pre-synaptic neurone releases neurotransmitter many

  times over a short time

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

  Inhibitory synapses hyperpolarise post synaptic membrane

  Cl- channels open - Cl- diffuse in

  K+ channels open - K+ diffuse in

  More Na+ required for depolarisation

  Reducing likelihood of threshold being met / formation of action potential at post synaptic membranes.
• What is the importance of inhibitory synapses?

  Both excitatory and inhibitory neurones forming synapses with same post synaptic membrane give control of generation of an action potential.
• Describe the structure of neuromuscular junction.

  Receptors are on the muscle fibre instead of post synaptic membrane and are more

  Muscle fibres form clefts to store enzyme e.g acetycholinesterase.
• Compare transmission across a cholinergic receptor and a neuromuscular junction.

  Both undiriectional

  Cholinergic -

  Neurone - Neurone

  Neurones can be excitatory or inhibitory

  Action potential may be initiated in postsynaptic neurone

  
  

  Neuromuscular junction -

  Neurone - Muscle

  Always excitatory

  Action potential propagate along sarcolemma down T tubules.
• How do some drugs stimulate the nervous system?

  Similar shape to neurotransmitter

  Stimulate more release of neurotransmitter

  Inhibit enzyme to brea down neurotransmitter - Na+ continues to enter
• How do some drugs inhibit the nervous system?

  Inhibit release of neurotransmitter egg prevent calcium ion channels opening

  Block receptors by mimicking shape of neurotransmitter.
• Describe how muscles work.

  In antagonistic pairs - pull in opposite directions

  One contracts the other relaxes

  Skeleton is incompressible so muscle transmits force
• Describe the gross structure of a skeletal muscle.

  Made of many bundles of muscle fibres

  Attached to bones by tendons
• Describe the microscopic structure of a skeletal muscle.

  Sarcolemma

  Sarcoplasm

  Multiple nuclei

  Many myofibrils

  Sarcoplasm reticulum

  Many mitochondria
• Describe the ultrastructure of a myofibril.

  Made of two types of protein filament

  Actin - thin filamnet

  Myosin - thick filament

  Arranged in functional units called sarcomeres

  End - z line

  Middle - M line

  H zone - Contains only myosin
• What are I bands ?

  Light bands containing only thin actin filaments
• What are A bands?

  Dark bands containing both actin and myosin filaments
• What are H zones?

  Contain only myosin filaments.
• Explain the movement of myofibril bands during muscular contraction.

  Myosin head slide along chin filament causing contraction of sarcomere

  Simultaneous contraction of many sarcomere

  H zones get shorter

  I band gets longer

  A band stays same

  Z lines get closer
• Describe how a myofibril contracts.

  1. Depolarisation spreads down sarcolemma via T tubules causing Ca2+ release from sarcoplasmic reticulum, which diffuse to myofibrils

  2. Calcium ions bind to tropomyosin, causing it to move → exposing binding sites on actin

  3. Allowing myosin head, with ADP attached, to bind to binding sites on actin → forming an actinomyosin crossbridge

  4. Myosin heads change angle, pulling actin along myosin, (ADP released), using energy from ATP hydrolysis

  5. New ATP binds to myosin head causing it to detach from binding site

  6. Hydrolysis of ATP by ATP(hydrol)ase (activated by Ca2+) releases energy for myosin heads to return to original position

  7. Myosin reattaches to a different binding site further along actin Process is repeated as long as calcium ion conc. is high