nerve impulse
action potential
sodium ions and potassium ions
when nerve cell is stimulated, action potential is generated
Na+ ions channel open: positively charged Na+ ions flow into cell
K+ ion channels open in response to the depolarisation
Na+ channels close
Positively charged K+ ions flow out of the cell
K+ channels close
Na+ channels rest
return to rest
action potential moves along axon
one way travel: refractory period = time immediately following AP when new AP cannot be initiated in same area of membrane
how does an action potential start, dendrites
multiple inputs from multiple dendrites
- excitatory pre-synaptic potentials (EPSPs)
- inhibitory pre-synaptic potentials (IPSPs)
- vary in magnitude
how does an action potential start, summation
summation of changes in membrane potential.
- EPSP increases chance of AP initiation, IPSP decreases chance.
- if overall membrane potential reaches threshold voltage, Na+ channels open and AP initiated
summation
spatial summation- summation of inputs from different areas of cell eg. from different dendrites
temporal summation- input occurs multiple times from the same are/dendrite
- repeated inputs in short time period- summation
- summation -> APs generated more or less frequently
AP magnitude
signalling between nerve cells
neurotransmitter
neurotranmitter function
amino acids and derivatives
catecholamines (monoamines)
acetylcholine
-derived from choline
- neuromuscular junction
peptides
eg substance P, endorphins
GABA binding to GABA-A receptors
GABA-A receptor
-chloride ion channel
- channel opened by GABA binding, Cl- flows into cell, hyper polarisation -> harder to reach threshold voltage for AP formation in post-synaptic cell
- benzodiazepines, ethanol, some anaesthetics, potentiate GABA activation of GABA-AR, so more inhibition of APs- sedative action
what is a neuromuscular junction
NMJ = junction between motor neuron (nerve that controls muscle) and muscle cell
-similar to synapse between 2 neurons
acetylcholine “switching off’
-nAChR- sodium ion channel receptor
ACh binding allows Na+ entry
Na+ influx- depolarisation of muscle cell membrane
depolarisation initiates contraction
acetylcholinesterase I cleft removes ACh “switches off”
myasthenia gravis
muscle weakness
-autoimmune antibodies attack ACh receptors at neuromuscular junction
- treatment: AChE inhibitors used to enhance NMJ transmission
electrical signalling via gap junctions
connexion proteins form connection with channel
- ions carry charge from one cell to another (diffusion)
cardiac myocytes