C-J DS

Question 1

Action potential propagation?

Answer 1

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

Question 2

Determines Conductions Velocity?

Answer 2

speed at which passive induces active

Question 3

length constant?

Answer 3

measure of how far current spreads passively

Question 4

3 resistances?

Answer 4

external, internal, membrane

Question 5

Oligodendrocytes?

Answer 5

work in CNS to create myelin

Question 6

Schwann cells?

Answer 6

work in the PNS to create myelin

Question 7

what does a large space constant mean?

Answer 7

faster conduction velocity

Question 8

Cause an increase in space constant?

Answer 8

increase radius
decrease internal resistance
increase membrane resistance

Question 9

What does an increase in fiber size do?

Answer 9

increase the diameter of a nerve fiber results in decreased internal resistance, conduction velocity is therefore faster

Question 10

Type of conduction on a myelinated fiber?

Answer 10

saltatory conduction, can only be conducted at the node of ranvier, appears that the AP is jumping

Question 11

Botulinus toxin?

Answer 11

blocks release of ACh from presynaptic terminals, stops vesicle binding to terminal membrane

Question 12

Neostigmine?

Answer 12

inhibits acetylcholinesterase

prolongs and enchances action of ACh at muscle end plate

Question 13

Myasthenia gravis?

Answer 13

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

Question 14

Effect of reduced ACh receptors on the muscle end plate? (Myasthenia gravis)

Answer 14

size of EPP is reduced, more difficult to depolarize the muscle membrane to threshold and to produced action potentials

Question 15

EPP?

Answer 15

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

Question 16

Treat myasthenia gravis?

Answer 16

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

Question 17

Characteristic myasthenia gravis?

Answer 17

Muscles are ok at first, progressively weaker over time

autoimmune disease aganist ACh receptors

Question 18

Tetanus toxin?

Answer 18

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

Question 19

Tetanus presents?

Answer 19

constant muscle contraction, “Lock jaw”

Question 20

Lamber- Eaton syndrome?

Answer 20

antibodies targeting voltage gated Ca channels, interfere with normal calcium flux needed for acetylcholine release

Question 21

signs of Lambert eaton syndrome?

Answer 21

proximal limb weakness without signs of wasting

temporay isometric exercise can show improvement of muscle weakness

Question 22

Multiple sclerosis?

Answer 22

in the CNS, cause demyleination
pins/needles is a common complaints
sensory loss in limbs, visual loss, many symptoms affects

Question 23

Guillain-Barre syndrome?

Answer 23

targets schwann cells (autoantibodies) in the PNS
pins and needles also common
begins in legs generally