2. motor unit: consist of an alpha motor neuron & the muscle
it synapses on
3. motor end plates are synaptic structures made up of
A. the ending of a motor neuron
B. a muscle fiber
4. Myasthenia Gravis: antibodies disable ACH receptors
A. this causes weakness of the skeletal muscle
B. Treatments include
a. anti-acetylcholinesterase drugs are used
as treatment
II. muscle spindles: convey information about muscle length:
1. these are found in extrafusal muscle
2. intrafusal muscle fibers are inside muscle spindles
3. these are sensory organs that are served by
A. two sensory axons
a. annulospiral (1A) fibers:
b. flower spray (II)
B. one motor axon called the gamma motor fiber
a. generally stimulation of this axon causes
the intrafusal fibers to adjust
so that sensitivity
to muscle length can be maintained (keep intrafusal
fiber from becoming
limp when we shorten extrafusal muscle)
4. musle stretch reflex (MSR)
A. an example of the MSR
a. Stimuli that cause a skeletal muscle
to stretch (e.g., the thigh muscle)
b. This initiates action potentials in
the sensory axons of the intrafusal
Fibers
which travel to he spinal cord
c. the sensory axon has 2 branches in
the cord
?one branch of the axon excites
the alpha motor neurons of thigh
?another branch inhibits alpha
motor neurons of antagonist muscles
B. PNS injury or disease can reduce or eliminate the MSR
a. damage or disease to the muscle (muscular
dystrophies)
b. nerve disease: e.g.,
?peripheral neuropathy:
?prolonged syphilis
?polio myeltis
?myasthenia gravis
III. golgi tendon organ:
1. these detect muscle tension, how hard it is pulling.
2. stimulation results in the clasp knife reflex
A. golgi tendon organ sends sensory information from a
tendon to the cord
via afferent fibers (1B)
B. affterents fiber synapse on to inhibitory interneurons.
C. These interneurons inhibit alpha motor neurons &
prevent more
contraction
Damage to the PNS
2. retrograde degeneration
A. cutting axons may also kill the neuron:
B. often axon damage does not kill the cell (common in adults)
a. within 24-48 hrs. the cell body chromatolysis
3. effects of muscle denervation
A. injury potentials: depolarization of the membrane at the
cite of the lesion
a. resulting in a visible twitch in the muscle fibers
(fasciculations)
b. terminal branches become isolated & cause
uncoordinated contractions
(fibrillations) )Kingsley
p. 226)
B. the muscle ultimately becomes electrically silent
C. the muscle then undergoes atrophy (degeneration atrophy)
D. the degenerated muscle develops many ACH receptors
4. cells also show degeneration if afferent fibers have been damaged
A. trophic chemicals
II. regeneration after damage:
1. the proximal axons can regrow in the PNS (axonal regeneration)
2. this begins with protein synthesis
A. the axon develops a bulbous ending (growth cones)
a. sprouts called neurites grow from the cone
B. Schwann tube: this is a line of Schwann cells that the neurite follows
C. the neurite is attracted to the ACH receptor
D. If the severed ends are too widely separated or if something
blocks the
appropriate growth, the fiber
may whorl (producing a neuroma)
E. regrowth occurs at about 1.5 mm/day
4. myelination begins at the lesion & moves in a proximodistal direction
5. the motor unit is larger than uninjured motor units