2. Physio Flashcards
(38 cards)
Resting membrane potential is determined by
distribution of K+, Na+, Cl-
where is AP generated
AP will only be generated if depolarisation reach threshold membrane potential at trigger point/ axon hillock
Describe rising phase in AP cycle
As neuron depolarises, voltage gated Na+ channels are opened.
Rapid entry of Na+ into the cell through voltage-gated Na channels depolarises the cell
Describe overshoot phase of AP cycle
- at one point, the inside of the cell become more positive than outside → reverse membrane potential polarity → drop in voltage
- at peak: no influx of Na+ and efflux of K+ through voltage gated channels
Describe falling phase of AP cycle
- Inactivated voltage-gated Na channels
- Open voltage-gated K channels (K more concentrated inside cell)
- K+ moves out of cell → membrane rapidly repolarises
2 events that occur at Neuromuscular Junction
Receptive step and Translating/transmitting step
Receptive step
- arrival of AP at presynaptic cell/ axon terminal → depolarisation of presynaptic neuron → opening of voltage-gated Ca channels → influx of Ca →
- fusion of synaptic vesicle with presynaptic membrane → release of NT into synaptic cleft
Translating/transmitting step
binding of NT (eg acetylcholine) to postsynaptic ligand gated receptor (eg nicotinic receptor) → influx of Na into postsynaptic membrane
how does hypokalemia affect signalling
causes hyperpolarisation → impairs ability to generate AP at NMJ → skeletal muscle membrane becomes less excitable → muscle cannot contract → weakness and paralysis of skeletal muscles
how does hyperkalemia affect signalling
reduce efflux of K+ from inside to outside of the cell
sensory transduction
Transformation of an external stimulus to AP
describe the sensory transduction pathway
- Depolarisation of sensory receptor
- Generation of action potential
- depolarisation at trigger point generate AP
- Depolarisation from the receptor travels to the axon hillock/ tigger zone → generates AP
- Propagation to CNS
- Synaptic transmission
- Excitation of neuron in spinal cord/ CNS
types of sensory receptors and their stimuli
- mechanoreceptor - mechanical energy (non-noxious)
- nociceptor/free nerve ending - noxious stimuli
- chemoreceptor - chemicals
- photoreceptor - light
- thermoreceptor - heat
- proprioceptor - position of body in space
Afferent (nerve fiber)
carry signals from periphery to CNS
receptive field
area on skin where stimulus will excite a receptor
afferent eg 1
- Pacinian corpuscle (touch): a type of afferent nerve fiber embedded in the skin
- receptor in the receptive field will convey physical energy to signal → travels to CNS via Aß myelinated axon fiber
afferent eg 2
- Nociceptors/ free nerve endings (pain): pain receptors that respond to tissue damaging stimuli
- Eg of nociceptor is TRPV1: opens when there is a painful stimuli → cations enter
- signal travels via unmyelinated C axon fiber or thinly myelinated Aδ axon fiber to CNS
type of fibers and their stimuli
- Aß thickly myelinated axon fiber (largest diameter): for touch, non noxious stimuli
- Aδ thinly myelinated axon fiber (bigger diameter than C): for pain
- C unmyelinated axon fiber (smallest diameter): for pain
how does myelination and size affects speed of conduction of signal
Aß (fastest) > Aδ > C (slowest)
Significance of different fibers (eg loss/damage)
- loss of Aß fibers: cannot feel touch/vibration but can still feel pain
- absence of Aδ & C fibers (eg CIPA): cannot feel pain, touch sensation normal
Postsynaptic target for excitatory and inhibitory
- dendrite for excitatory synapse
- soma for inhibitory synapse
where is AP generated
AP generated in axon hillock/trigger zone
how is NT released into synaptic cleft
- AP trigger opening of voltage-gated Ca2+ channels
- Influx of Ca2+ cause fusion of synaptic vesicles to membrane of axon terminal.
- NT released into synaptic cleft
- NT diffuse across synaptic cleft and bind to receptor on postsynaptic dendrite/soma membrane
what happen when NT bind to receptor on postsynaptic neuron
- on dendrite (excitatory): ligand-gated Na+ opens → Na+ enters → depolarisation
- on soma (inhibitory): ligand gated K+ opens, ligand gated Cl- opens → K+ leaves, Cl- enters → hyperpolarisation