2. Physio Flashcards
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
2 forces acting on K+
- concentration gradient - more K+ inside cell (favours movement of K+ out of cell)
- electrical gradient - cell inside more negative (favours entering of K+)
how does hypokalemia affects RMP
- in hypokalemia (less K+ outside cell) → more K+ will move out of cell → neuron cell hyperpolarise (more negative inside)
- moves RMP away from threshold (cell become less excitable) → cause muscle paralysis
how does hyper-excitable neurons cause altered RMP
- normally, inhibition of neurons by GABA cause hyperpolarisation
- Decrease in GABA cause uncontrolled excitation → seizures/ epilepsy
describe the generation of AP when touch is applied
- through pharmacological receptors (eg TRPV1/nociceptor open when exposed to heat) - receptors transduce external stimuli to an electrical charge
- mechanical pressure opens the channel → allows influx of cations → depolarisation
what type of activities does the cortex control?
needed for all activities that need consciousness (aware and responsive to surrounding)
what type of activities does the frontal lobe control?
personality trait
what type of activities does the Broca’s area (in left hemisphere) control?
expressing language
what type of activities does the Wernicke’s area (in left hemisphere) control?
comprehending language
what type of activities does the Subgenual Anterior Cingulate Cortex (Subgenual ACC) control?
emotions
- hyperactivity of subgenual ACC leads to depression (sadness and lost of interest)
what does the medial temporal lobe contain?
hippocampus and amygdala
what type of activities does the Cortical and sub-cortical regions control?
cognition (learning and memory), emotions and mood
what type of activities does the hippocampus control?
involved in declarative memory that involves recall (eg memory of events, names, numbers)
- lesion of hippocampus/ medial temporal → loss of memory (eg Alzheimer)
what type of activities does the amygdala control?
for emotion and emotional memory
eg of excitatory and inhibitory NT
excitatory: glutamate, epinephrine and norepinephrine
inhibitory: GABA
