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pacinian corpuscle - transducer
unmyelinated sensory neurone in centre, pressure changes distort lamellae allowing na+ channel to open so ions can flood in and depolarise membrane, potential generated, impulse sent down neurone
resting potential
when neurone is doing nothing, it already has a charge (resting potential) of -65mv/ -70 mv, potential difference, this is due to na+ k+ pump where 3 na+ out and 2 k+ in, k+ diffuses out faster than na + diffuses in as more k+ gate so overall excess of positive ions outside axon leading to more pos charge outside than inside axon
depolarisation - first stage of generator potential
pressure forces na+ channels open allowing them to flood into cell down conc gradient, p.d. becomes less negative as more pos ions inside, threshold p.d. of -40mv reached, voltage gated sodium channels open so more na+ floods in until p.d. reaches +40mv (depolarisation)
repolarisation - second stage of generator potential
voltage gated na+ channels close, k+ channels open so k+ flood out lowering p.d. until cell is hyperpolarised ( lower than -65mv)
refractory period - third stage of action potential
p.d. remains below -65mv for a short time so impossible to generate action potential, then returns to -65mv because all excess stretch-mediated and voltage gated channels closed and depolaristion not likely to be enough to reach threshold as axoplasm hyperpolarised, na+ k+ pump continues and any gates open at beginning stay open
importance of refractory period
ensures action potentials are discreet and do not overlap, ensures unidirectional flow
propagation of action potential
when na+ floods in both charge and conc of na+ ions increases generating steep conc gradient allowing diffusion along inside of axon, if the na+ ions increase p.d. enough on next section of the axon, so that it reaches -40mv, this will trigger voltage-gated na+ channels to open so more na+ floods in until p.d. reaches +40mv (depolarising membrane so can be repolarised, local circuit established)
absolute refractory period
represents time when impossible to initiate another action potential
relative refractory period
could generate another action potential in this phase, but stimulus would have to have been very strong/intense
saltatory condition
action potentials jump from node to node, uninsulated nodes of ranvier are the only places along the axon where ions are exchanged across the axon membrane
non-myelinated neurones
smooth conduction of action potentials, much slower, all points on membrane can exchange ions because no myelin sheath to stop it
how does temperature affect speed of nerve conduction
increased temp increases conduction velocity because higher ke of ions for diffusion
how does width of axon affect speed of nerve conduction
increased width increases conduction velocity becuase lower sa:v ratio so less ions leaked
how does myelination affect speed of nerve conduction
increased myelination increases conduction velocity as sheath blocks ion movement
synpatic transmission
action potential depolarises axon terminal which opens voltage gated ca2+ channels, ca2+ ions enter the cell and trugger exocytosis of synaptic vesicle contents, n.transmitter diffuses across synpatic cleft and binds to receptors on post-synaptic neurone, ligand gated sodium channel open and if enough na+ ions then voltage gated na+ channels open
function of synapse
filter out low level background stimuli, ensure unidirectionality of signal transmission
spatial summation (rod cells at retina)
diff presynaptic neurones together release enough n.transmitter to exceed threshold value of post-synaptic neurone - together they trigger a new action potential
temporal summation (cone cells)
single presynatpic neurone releases n.transmitter many times over short period, if conc of n.transmitter exceeds threshold value of post-synaptic neurone, action potential is triggered
acetylcholinesterase
embedded in post synaptic neurone, breaks down acetylcholine into acetate and choline, no longer complementary to receptor so diffuse back to presynaptic membrane where endocytosed back in a vesicle
excitatory n.transmitters
open na+ channels on post-synaptic neurone
inhibitory n.transmittors
causes opening of chloride ion channels – produces an inhibitory post synaptic potential
how to synapses ensure unidirectionality
n.transmitter made only in presynaptic neurone, receptor proteins only found on post-synaptic neurone
addictive drugs
tend to inhibit the activity of GABA which increases dopamine activity, body associates dopamine with feelings of pleasure and reward, causing addictive properties