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form of neurotransmitter release. The neurotransmitter (from the synaptic
vesicles) crosses the synaptic cleft (between the pre- and postsynaptic
membranes) and interacts with receptors on the postsynaptic membrane
(answer b),which results in changes in the permeability of this membrane
(answer c).Numerous mitochondria and synaptic vesicles are typically found
on the presynaptic side of the synapse. The postsynaptic surface typically is
denser than the presynaptic membrane.


149.The answer is b.(Kasper, pp 2461–2463. Kumar, pp 1382–1384.
Kierszenbaum, pp 210–212. Junqueira, p 163.)The patient is suffering from
multiple sclerosis (MS), a demyelinating disease in which both CD4+and
CD8+-T cells as well as autoantibodies are targeted to oligodendrocytes. MS
is twice as prevalent in women as in men and demyelination is most com-
monly found in the anterior corpus callosum. Alterations in the CSF shows
pleocytosis (increase in the number of mononuclear cells above normal
levels), increase in protein, elevated gamma globulin (antibodies to oligo-
dendrocytes as represented by oligoclonal bands on gel electrophoresis).
Microglia (answer a)are the phagocytes of the CNS, astrocytes (answer c)
induce and maintain the blood-brain barrier and form the glial scar follow-
ing injury, and Schwann cells (answer d)are responsible for myelination in
the PNS. On autopsy, plaques are found that contain lymphocytes and
monocytes in infiltrates around small veins in what is known as perivascu-
lar cuffing. Axons (answer e)are generally preserved. The main identifying
feature on histopathological examination is the paucity of oligodendrocytes.
Astrocytic proliferation and gliosis may increase with the duration of MS.


150.The answer is e.( Junqueira, pp 154, 194. Ross and Pawlina, pp
291–292, 311–313. Kasper, pp 2518–2521. Kumar, pp 212, 1344.)The junc-
tional folds are the site of acetylcholine (ACh) receptors which are reduced
in number in myasthenia gravis. The normal neuromuscular junction
releases acetylcholine (ACh) from the motor nerve terminal in discrete
packages (quanta). The ACh quanta diffuse across the synaptic cleft and
bind to receptors on the folded muscle end-plate membrane. Stimulation
of the motor nerve releases many ACh quanta that depolarize the muscle
end-plate region and then the muscle membrane causing muscle contrac-
tion. In myasthenia gravis, the postsynaptic muscle membrane is smooth
and lacks the normal folded shape. The concentration of ACh receptors on
the muscle end-plate membrane is reduced, and antibodies are attached to


Nervous System Answers 249
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