THEME 2 Flashcards
CNS GLIAL CELLS
Oligodendrocytes: Form myelin around several axons
Astrocytes: Form the BBB and maintain chemical homeostasis
Ependymocytes: Line the ventricles and spinal cord and is involved in CSF production
Radial: Progenitor of neurones and assist their migration
Microglia: Phagocytes
NEURITES
Axon: Process emerging from the soma at the axon hillock and extending into an axon terminal which can form axodendritic, axosomatic, or axoaxonic connections, capable of transporting substances from the cell body to terminal (fast/slow anterograde transport via kinesin) or from the terminal to cell body (fast retrograde transport via dynein)
Dendrite: Highly branched process feeding into the soma which integrates information received from its synaptic connections
ACTION POTENTIAL PROCESS
Resting potential: Determined by ion concentration equilibrium and permeability, approx. -70mv due to efflux of K+ through leak channels
Depolarisation: Influx of Na+ through voltage gated channels which have m gates (open via + feedback) and h gates (usually open), over threshold and to overshoot
Repolarisation: Na influx is stopped by closure of h gate causing an absolute refractory period, efflux of K+ through voltage gated channels which have n gates
Hyperpolarisation: Efflux of K+ below resting potential towards K equilibrium followed by n gate closure to stop K efflux, opening of Na+ h gate causes relative refractory period
Action potentials follow the all or none law unless accommodation occurs (depolarisation to threshold is too slow to open h gates
FACTORS AFFECTING CONDUCTANCE SPEED
Axon diameter: Larger diameter allows faster conductance
Myelin: Myelinated axons have faster conductance due to saltatory conductance via nodes of Ranvier
SYNAPSES
Types: Electrical (via gap junctions) or chemical (via neurotransmitters, associated with ionotropic or metabotropic receptors)
Process: Action potential depolarises presynaptic membrane, influx of Ca2+ through voltage gated channels, fusion of vesicles to active zones by forming SNARE complexes, exocytosis of neurotransmitter, binding to postsynaptic receptors, removal from cleft and recycling via endocytosis
POST SYNAPTIC POTENTIALS
Neurotransmitters bind to post synaptic receptors causing depolarisation (EPSP, activate Na+/k+ channels) or hyperpolarisation (IPSP, activate K+ or Cl- channels)
These responses are local and decrement with distance so summate via temporal and spatial summation, combining into a composite PSP which determines if an action potential will fire
SPINAL NERVES
Posterior root: Afferent sensory fibres with a cell body in the dorsal root ganglion, which enter the dorsal horns
Anterior root: Efferent motor fibres with a cell body in the spinal cord, which enter the ventral horns
FINE TOUCH PATHWAY
DORSAL COLUMN MEDIAL LEMNISCUS PATHWAY: 1’ neurone enters dorsal horns and ascends through dorsal column cuneate/gracile nuclei in the medulla to synapse, 2’ neurone switches to contralateral side and ascends to thalamus to synapse, 3’ neurone to cortex
Face: 1’ neurone enters trigeminal ganglion and travels to pons to synapse, 2’ neurone travels to thalamus on contralateral side to synapse, 3’ neurone travels to cortex
PAIN PATHWAY
ANTEROLATERAL PATHWAY: Nociceptors detect stimuli and send 1’ neurone to superficial lamina layers of dorsal horns to synapse, 2’ neurones switch to contralateral side and ascends to thalamus via spinothalamic tract to synapse, 3’ neurone travels to cortex. Neurones then descend on the ipsilateral side though the periaqueductal gray (inhibits the pain) and medulla to the dorsal horns
Face: 1’ neurones enter trigeminal ganglion and descends to medulla to synapse, 2’ neurones switch to contralateral side and ascend to thalamus to synapse, 3’ neurones travel to cortex
GATE CONTROL THEORY
Afferent A delta (small myelinated) and C (small unmyelinated) fibres carry pain stimuli to CNS and their activation opens the ‘gate’. Afferent A fibres (large myelinated) carry non-painful stimuli to CNS and their activation closes the ‘gate’. Excess non-painful stimuli (such as rubbing an injury) over rides the painful stimuli, closing the ‘gate’ so pain is no longer detected.
ACUTE VS CHRONIC PAIN
Acute: Sudden onset lasting duration of injury, triggers fight or flight responses
Chronic: Persistent pain lasting beyond the injury. Occurs due to peripheral sensitisation (release of sensitising soup reduces pain threshold and causes 1’ hyperalgesia) and central sensitisation (reduced inhibition, increased excitation and synapses causes 2’ hyperalgesia, increased receptive field, and allodynia)
