physiology Flashcards
movement of signal
sensory/visceral stimuli -> afferent division -> CNS -> efferent division -> somatic NS (motor behaviour) or autonomic NS (regulate visceral structures)
what are afferent and efferent nerves part of
peripheral nervous system (PNS)
types of myelin fibres
1) alpha beta fibre: thick, myelinated
2) alpha delta fibre: thin, myelinated
3) C fibre: unmyelinated
- C slowest, alpha beta fastest
examples of afferent nerves
1) pacinian corpsucle (touch receptor, alpha beta)
2) free nerve ending pain receptor (C, alpha delta)
pacinian corpuscle
- respond to non-noxious stimulus (non-painful)
- skin receptors -> enclosed nerve ending -> myelinated axon -> cell body -> spinal cord -> break into collaterals -> axon terminal
- function of components
1) axon terminal: communicate with spinal cord
2) receptor: generate electrical signals to external stimuli
3) receptive field: area of skin wherereceptors are embedded in for stimulus to excite
free nerve ending pain receptor
- respond to noxious stimulus
- free because not covered by connective tissue
structure of neuron
soma (cell body), dendrite, axons (split into axon terminals)
synapse
- consists of presynaptic axon, synaptic cleft, postsynaptic part of neuron
- if postsynaptic connect to dendrite -> likely to be excitatory
- if postsynaptic connect to soma -> likely to be inhibitory
terminology for electrical signalling
1) action potential
- change in electrical potential
2) resting membrane potential (RMP)
- -ve value
- caused by unequal distribution of charges -> inside membrane more negatiev than outside
3) voltage gated channels
- respond to changes in membrane potential
- only opens when threshold reached
tldr process of signal generation by membrane
1) resting membrane potential
2) depolarisation
3) depolarisation until threshold (action potential)
4) recovery back to RMP
process of depolarisation (signal generation)
happen within CNS, triggered by synaptic transmission
- action potential generated by afferent (axon terminal) -> trigger opening of voltage gated Ca channel -> influx of Ca -> fusion of synaptic vesicle with membrane of axon terminal -> release neurotransmitter into synaptic cleft -> neurotransmitter diffuse and bine to receptor on postsynaptic membrane -> receptor open
- difference in effect once receptor opens
** excitatory: influx of cation -> inside more positive -> depolarisation
** inhibitory: influxof anion -> inside more negative -> hyperpolarisation (further from threshold potential)
process of depolarisation until threshold (signal generation)
1) upstroke of action potential until peak
- initial depolarisation trigger opening of voltage gated Na channel -> membrane more permeable to Na+ -> Na+ concentrate outside cell -> rapid Na+ entry through voltage gated channel -> depolarise cell
2) overshoot phase
- inside cell more positive than outside = reverse membrane potential polarity
3) downstroke of action potential
- inactivation of voltage gated Na channel
- opening of voltage gated K channel -> membrane more permeable to K+ -> K+ move out of cell -> repolarise membrane potential
recovery back to RMP (signal generation)
- voltage gated K+ closed
- membrane potential back to normal
how hypoK affect RMP
- forces acting on K+
1) concentration gradient
2) electrical gradient
- hypoK -> lower K outside -> favour movement of K from outside to inside -> hypoerpolairsation
component of CNS roles and damage consequences - cortex
1) roles
- sensation and perception (both cortices)
- voluntary control of movement
- personality trait (frontal lobe)
- learning and memory
- language
2) consequences
- damage to frontal lobe = drastic change in personality
- damage to left cortex (Brocas, Wenickes) = aphasia (affect written & spoken language)
- damage to prefrontal cortex (subgenual ACC) = affect emotions
components of CNS roles and damage consequences - limbic structures
1) hippocampus
- role: declarative memory (recall)
- damage: alzheimer
2) amygdala
- role: emotion, emotional memory important for mood change
- damage: express emotion on face but can’t recognise other people’s facial expression of emotion
principles regarding underlying sensory processing
(LAYMEN)
- each stimulus pick up specific stimulus and a specific signal produced by that stimulus is passed along a specific path that regions a specific region on brain
- n order means the number of neuron that the signal is passed to from the receptor
- more intense stimuli = more signals produced = stronger sensation
types of pain
1) spontaneous: activation of pain pathway only for that period of time
2) hyperalgesia: increased pain to given noxious stimulus (inflammation or tissue damage)
3) allodynia: pain to normally non-painful stimulus (normally sensed as touch), reduced threshold to invoke pain
identifying type of pain on pain sensation x stimulation graph
1) normal curve
- pain threshold basically the amt of stimulation where pain sensation starts to increase
2) allodynia curve
- any point on non normal curve before normal threshold is reached
3) hyperalgesia pain
- any amt of pain sensation more than normal
normal pain pathophysiology
1) touch receptors: movement of alpha beta neurons
- spinothalamic-tract pathway
** nociceptive signals synapse with second order neurons in dorsal horn of spinal cord -> relay pain signals to higher brain centre -> perception of pain - dorsal column pathway
** nociceptive signals move up dorsal column -> synapse with inhibitory neuron -> modulate/suppress transmission of pain signals -> don’t perceive pain when we sense touch
2) pain receptors
- associated with C first order neuron
- spinothalamic tract pathway ^
allodynia pathophysiology
- stimulus evoke more AP than normal = hyperexcite more and more stuff along the pathway until it overcomes the inhibitory portion
- possible effects of tissue damage
1) loss of inhibitory neuron in spinal cord -> side branch of alpha beta excite pain pathway
2) sensitisation/hyperexcitability of excitatory relay form C fibre to spinothalamic tract neuron
** how hyperexcitation/sensitisation work: increase number of receptors, decrease threshold to excite, release chemicals at damage site -> hyperexcite nociceptors -> generate more AP -> hyperexcite second order neuron
pain modulation
- regulate signal along pain pathway
- PAG
- process
1) stuff that excite PAG
2) neuron in PAG excite neuron in medulla -> excite inhibitory neuron in spinal cord -> inhibit transfer of signal from 1st order C fibre to 2nd order spinothalamic neuron
- segmental modulation (gate theory)
** stimualte larger afferent for touch -> excite inhibitory neuron -> decrease transmission of pain
types of motor behaviour generated
1) reflex: involuntary
2) rhythmic motor pattern: require voluntary initiation and termination
3) voluntary: goal directed
hierarchial features of motor control
1) Cortex
- voluntary
2) brain stem
- postural reflex, rhythmic motor pattern
3) spinal cord (efferent)
- site of motor neuron
- control of muscle activity
4) brainstem pathway
- long descending axon pathyway from brain stem to ventral horn
role of cerebellum in motor function
- bring about coordinated movement
- adjust output of efferent via cortex and brainstem
- if damaged: can’t do coordinated movement like walking in a straight line or touching nose quickly
role of basal ganglia in motor function
- initiation of movement
- selection of motor program
- if damaged: disorder of movement (even at rest) or disorder of posture (rigidity)
