synapse Flashcards
action potential
rapid, large depolarisation from threshold mem potential
threshold potential more +ve > basal (RMP)
when does AP occur?
1) when external stimulus applied
2) info is transferred to neuron
steps to Action potential depolarisation
1) rest mem potential of -80/60mV (based on K, Na, Cl distribution)
2) AP begins: excitatory neurotransmitter, open ligand -gated channels (NMJ, synapse of CNS)
depolarising potential reach trigger zone, depolarise mem
3) voltage gated Na channels activated, mem more permeable to Na (EXTRACELL –> INTRA)
4) Na entry, depolarise cell
5) inside more +ve > outside, reverse mem potential polarity
6) voltage gated Na+ channels inactivated. VG K+ channels open, mem potential more permeable to K+
K+ move out, mem potential repolarises
7) VG K+ channels close. mem potential returns to normal (Na-K pump: 2 Na+ out and 3K+ in)
electrochemical gradient
ionic distribution across mem at rest (resting mem potential)
K+ (intracell > extracell)
Ca2+ (intracell < extracell)
Na+ (intracell < extracell) ** ASM
Cl- (intracell < extracell)
electrochemical gradient determines equilibrium potential
resting mem potential is usually +/-ve ??
more neg than threshold mem potential
mem must be depolarised –> threshold mem for AP signal to be evoked
forces acting on K that affects its movement
1) conc gradient favour EFFLUX of K (intracell –> extracell)
2) electrical gradient PULLS +ve K+ (extracell –> intracell)
2 gradients oppose each other
equilibrium potential
equilibrium potential (where OUT = INWARD gradients, no net movement of ion across mem
balanced at eg: -97mV, no net movement of K+
eqm potential eqn
E = 58 log (conc of ION outside/ conc of ION inside)
specific for each ion: K, Na. Given ion will either move IN/OUT cell to push mem potential towards E value
different from mem potential
mem potential
reflects conc and permeability of K, Na, other ions that are distributed across the mem
at rest, normal state movement
K move outward (push mem potential towards -97mV)
Na move inward (push mem potential towards +75mV)
mem potential maintained at -80/60mV (more neg reflects greater permeability for K+ = leak K channels)
alter K conc outside (incr extracell conc)
E value = 58 log (50/ 140) = -25mV vs -97mV
favour K outflow but now less steep than before
less K move out since E is more +ve now
greater accumulation of +ve charges inside mem.
Resting mem potential becomes less negative, closer to threshold
Depolarisation easier as less stimulus needed to initiate action potential
hypernatremia
still favour inflow of Na+ intracellularly
more positive rest mem potential
reach threshold easier, depolarisation easier as less stimulus needed to initiate AP
hypokalemia
low extracell K
more -ve E value. still favour K outflow, more steep now, more K move out
less accumulation of +ve charges inside mem.
Resting mem potential becomes MORE negative, further from threshold
Depolarisation harder as more stimulus needed to initiate action potential (less excitable)
synaptic transmission
communication b. cells (b. neurons, nerves, muscles)
3 components:
1) presynaptic terminal
2) postsynaptic cell
3) synaptic cleft
2 types synaptic transmission
electrical – current generated in presynaptic neuron FLOWS DIRECTLY into postsynaptic cell through gap-junction channels
chemical – has synaptic cleft, neurotransmitters released, receptors on postsynaptic cleft
chemical synapse
has synaptic cleft 20-40nm
1) action potential in presynaptic cell release chemical transmitters in cleft
2) transmitter diffuse across cleft, interact with specific receptors
3) depolarise/ hyperpolarise postsynaptic cell
4) depo: reach threshold mem, leads to generation of action potential in postsynaptic cell
neuromuscular junction definition
NMJ synapse/ junction of axon terminal of motoneuron with motor end plate (motor neuron excites skeletal muscle fiber)
highly excitable region of muscle fiber
plasma mem: initiates AP across muscle surface = contract muscle
CHEMICAL SYNAPSE
how depolarisation occurs at neuromuscular junction
1) transmitting (AP presynaptic)
2) receptive (Ach)
1) synaptic transmission involve release of acetylcholine from presynaptic axon terminal (open VG Ca2+ channel)
2) Ach binds to nicotinic receptor (postsynaptic mem/ muscle mem – ligand gated)
3) initiate depol of postsynap mem (influx of Na+) result in muscle contraction (motor end plate)
release of Ca2+ in presynaptic axon
presence of Ca2+ in axon terminal cause synaptic vesicles to fuse with mem
Ca2+ act on Ca2+ sensitive vesicle mem poteins (VAMPs) –> vesicle docking to presynapse –> fuse with presynaptic mem –> exocytosis
transmitters for diff synapse and their effects
Ach – excitatory at NMJ
glutamate – excitatory in CNS
GABA – inhibitory in CNS & NMJ
facilitate depolarisation at threshold mem potential
block efflux of intracell K+
incr influx of extrcell Na+
decr influx of extracell Cl-
release Ach at NMJ
incr nicotinic receptor agonist at NMJ
type of channels at membrane
ligand-gated channels (AP begins, NMJ to motor end plate)
voltage-gated channels (depol, repol)
sensation
conscious awareness of external stimuli (touch, pressure)
signal generated: external stimulus reach sensory cortex (along label line)
sensory receptor embedded in skin
specialised sensory nerve ending/ specialised epithelial cells – recognise stimulus
initiate sensory transduction by action potential in same cell/ adjacent one
sensory receptor send info –> CNS via afferent nerve fibers (1* afferents)
