6B - neurons Coordination Flashcards
Resting membrane potential
Outside of membrane more positively charged than inside ( -70 mV )
- so membrane polarised - difference in charge ( potential difference/ voltage )
Resting potential maintained by sodium potassium pump and potassium channels
- Nak uses active transport to move 3 NA out and 2 K in ( produces electrochemical gradient )
- K channels ( facilitated diffusion) to move K out , down concentration gradient
Action potential
When neurons stimulated other ion channels ( sodium channel ) opens
- if stimulus big enough - will trigger rapid change in potential difference- cell membrane depolarised
Stimulus
Depolarisation
Repolarisation
Hyper polarisation
Resting potential maintained
Stimulus
It excites the neuron, causes the Na+ channels to open
- membrane becomes more permeable to sodium- diffuse down the electrochemical gradient into neuron
- makes the inside of neuron less negative
Depolarisation
When reach the threshold of -55mV, more Na+ channel open
More sodium ions diffuse
Repolarisation
Potential difference of around +30 mV Na+ channel closes, K+ channels opens
Membrane more permeable to potassium- diffuse out of the neuron down the potassium gradient
Hyperpolarisation
K+ channel slow to close, potential difference lower then -70 mV (too many K+ ion out )
Resting potential
Ion channels at rest
- sodium potassium pump returns the membrane into resting potential
- maintains resting potential until membrane’s excited by other stimulus
Action potential
When neurons stimulated - ion channels in cell membrane opens
If stimulus big enough - trigger rapid change in potential difference . This causes cell membrane to be depolarised
Have sequence of events
- stimuli
- depolarisation
- repolarisation
- hyper polarisation
- resting potential
refractory period
Ions channels recovering and can’t be opened
- acts as a time delay between one action potential to the next
- make sure action potential don’t overlap but pass along as separate impulse
Refractory period means = there is a limit to frequency at which nerve impulses can be transmitted and action potential are unidirectional
Waves of depolarisation
- some sodium ions enter the neurone sideways
- causes sodium channel in the next region of neurons to open and sodium ion diffuse into that part
- wave move away from the refractory period - these part can’t fire action potential difference lower
All or nothing principle
Only Once threshold reached = action portential will be fired
Bigger stimulus won’t cause bigger action potential but will cause them to fire more frequently
what effects speed of conduction
- myelination ( saltatory conduction )
- axon diameter
- temperature
myeloination
- nerons = have myelin sheath
- made of schwann cell, between schwann cell tiny patches of bare membrane called nodes of ranvier
- sodium ion channels concentrated at nodes of ranvier
- saltatory conduction
saltatory conduction
- myelinated neuron, depolarisation only happens in nodes of ranvier
- neurons cytoplasm conducts enough electrical charge to depolarise next node
- impluse jumps from node to node
non neylinated - impulse travels along whole length of axon membrane, so depolarisation on whole length
axon diameter
- conducted quiker with bigger diameter
- less resisstance to flow of ions
- less resistance = depolarisation reacher to other part of neuron quicker
Temperature
- speed of temp increases - ions diffuse faster
- if too high, protein becomes to denature
synaptic and neurotransmitters
- draw it ( pg : 335 )
- when Ap reach the end of neurone release NT into synaptic cleft
- receptor only on postsynaptyic membrane - inpulses are unidirectional
- neurotransmitor break down by enz ( so respond doesn’t keep on hapenning)
NT you need to know
acetycholine (ACh)
binds to cholinergoc synapes
Cholinergic Synapes - 1
- Arrival of action potential
- AP arrives at the end of synaptic knob
- action potential stimulates voltage-gated calcium ion channels open
- calcium ions (Ca2+) diffuse into synaptic knob
Cholinergic Synapes - 2
Fusion of vessicles
- influx of calcium ions into synaptic knob casues vessicle to fuse to presynaptic membrane
- vesicle release NT acetycholine (ACh) into synaptic cleft by exocytosis
Cholinergic synapes - 3
Diffusion of ACh
- ACh diffues across thhe synaptic cleft and bind to jchlorinergic receptor on postsynaptuc menbrane
- causes sodium ion channels open ( post synap memb)
- influx of Na+ ions = causes depolarisation
ACh removed from synaptic cleft - response don’t keep on happening
- broken down by an enz , acetycholinesterase (AChE) and the products are reabsorbed
Excitatory neurotransmitor
- depolarise the postsynaptic membrane making it fire and action potential if the threshold is reached
Inhibitory membrane
- hyperpolarise the postsysnaptic membrane ( make the potential difference more negative ) preventing it fires AP
Spactial summation
2 or more neurons releasing neurotransmitor
- all the NT releases = enough to meet the threshold in postsynaptic nerve and trigger AP
