C-J DS Flashcards
Action potential propagation?
2 processes
Active and Passive
Passive current- triggers active AP propagation, spread of local currents to adjacent areas of the membrane, which depolarize to threshold and generate action potential, only one direction
Determines Conductions Velocity?
speed at which passive induces active
length constant?
measure of how far current spreads passively
3 resistances?
external, internal, membrane
Oligodendrocytes?
work in CNS to create myelin
Schwann cells?
work in the PNS to create myelin
what does a large space constant mean?
faster conduction velocity
Cause an increase in space constant?
increase radius
decrease internal resistance
increase membrane resistance
What does an increase in fiber size do?
increase the diameter of a nerve fiber results in decreased internal resistance, conduction velocity is therefore faster
Type of conduction on a myelinated fiber?
saltatory conduction, can only be conducted at the node of ranvier, appears that the AP is jumping
Botulinus toxin?
blocks release of ACh from presynaptic terminals, stops vesicle binding to terminal membrane
Neostigmine?
inhibits acetylcholinesterase
prolongs and enchances action of ACh at muscle end plate
Myasthenia gravis?
caused by presences of antibodies to the ACh receptor (nicotinic at NM junction)
characterized by skeletal muscle weakness and fatigability resulting from a reduced number of ACh receptors on the muscle end plate
Effect of reduced ACh receptors on the muscle end plate? (Myasthenia gravis)
size of EPP is reduced, more difficult to depolarize the muscle membrane to threshold and to produced action potentials
EPP?
an end plate potential, is not an action potential, but simply a depolarization of the specialized muscle end plate
it is formed by several positive end plate potentials, a summation
Treat myasthenia gravis?
AChE inhibitors like neostigmine
prevent degredation of ACh and prolong the action of ACh at the muscle end plate, partially compensating for the reduced number of receptors
Characteristic myasthenia gravis?
Muscles are ok at first, progressively weaker over time
autoimmune disease aganist ACh receptors
Tetanus toxin?
Tetanspasmin, enters into the body via puncture wound most commonly
makes its way to presynaptic cleft of interneurons in the spinal cord (responsible for inhibition)
there it cleaves Synaptobrevin II and prevents the release of GABA and glycine from vesicles, allowing for continued signal, continue release of Ca from SR and a continued muscle contraction
Tetanus presents?
constant muscle contraction, “Lock jaw”
Lamber- Eaton syndrome?
antibodies targeting voltage gated Ca channels, interfere with normal calcium flux needed for acetylcholine release
signs of Lambert eaton syndrome?
proximal limb weakness without signs of wasting
temporay isometric exercise can show improvement of muscle weakness
Multiple sclerosis?
in the CNS, cause demyleination
pins/needles is a common complaints
sensory loss in limbs, visual loss, many symptoms affects
Guillain-Barre syndrome?
targets schwann cells (autoantibodies) in the PNS
pins and needles also common
begins in legs generally
