nerves and muscles Flashcards
describe the sliding filament model
- Ap spreads down T tubules and Calcium released from sarcoplasmic reticulum and travels down sarcoplasm to myofibrils
- calcium ions binds to tropomyosin and changes shape and exposes myosin binding site on actin
- Myosin heads (ADP attached) bind to binding sites which requires ATP
- power stroke- myosin head ‘cocks’ sliding actin along myosin (ADP released)
- ATP causes myosin to detach from actin binding site which breaks cross bridge
- Hydrolysis of ATP provides energy for myosin to return to its original position (recovery stroke)
- Myosin head attaches to different binding site further along actin filament
how does myelination affect speed of conduction
depolarisation at nodes of ranvier only (saltatory conductance)
AP doesn’t travel down whole axon so there’s no need to depolarise whole axon unlike unmyelinated neurone
how does axon diameter effect speed of diameter
bigger diameter= less leakage of ions
how does temperature affect speed of conductance
more kinetic energy= increased movement of sodium and potassium ions
which increases rate of respiration which increases ATP therefore AT faster
what is the refractory period
time taken to restore axon to resting potential
what is the importance of the refractory period
- discrete and discontinuous impulses (action potentials don’t over lap)
- limits frequency of impulse transmission at a certain intensity
- unidirectional action potential
what is summation
addition of number of impulses covering a post synaptic neurone
what is temporal summation
one pre synaptic neurone produces many impulses over short period
what is spatial summation
many pre synaptic neurone share same post synaptic neurone
describe a myelinated neurone
depolarisation on nodes of ranvier only, saltatory conduction, whole axon doesn’t need to be depolarised
describe a non myelinated neurone
AP passes as a wave of depolarisation and there is influx of sodium ions in 1 region which increases permeability to sodium ions in adjoining region therefore influx of sodium ions and therefore adjoining region depolarised
how is a resting potential established
- sodium/ potassium ion pump
- 3 NA+ out of axon
-2K+ in axon - creates electrochemical gradient
- more sodium ions out of axon and more potassium ions inside axon - membrane more permeable to potassium ions therefore K+ channels open
- therefore K+ leaves axon
- inside axon relatively negative to outside therefore polarised= resting potential
transmission across cholinergic synapse
- AP arrives causing Ca2+ channels to open
- influx of Ca2+ causes vesicles to move and fuse with presynaptic membrane
- neurotransmitter released into synaptic cleft and diffuse across synaptic cleft
- NT bind to specific receptors on post synaptic membrane
- causes Na+ channels to open
- influx of Na+ into post synaptic knob causes depolarisation and induces action potential
- neurotransmitter removed from synaptic cleft
all or nothing principle
- stimulus- membrane more permeable to sodium ions so sodium channels open and sodium diffuses into neurone
- depolarisation -pd reaches threshold and action potential generated because more sodium channels open and sodium ions diffuse more rapidly
- repolarisation- Na+ channels close and K+ channels open so K+ diffuse out of neurone
- hyperpolarisation- K+ channels slow to close and slight overshoot
- resting potential restored through sodium potassium pump
role of phosphocreatine
Per stored in cells
rapidly produces ATP by phosphorylating ADP