Chapter 6. Nervous Tissue
The blood–brain barrier protects the brain from exposure to large toxic molecules, but presents a serious hurdle for delivering therapeutic drugs to the central nervous system. What is the cellular basis of the blood–brain barrier?
A. End feet of astrocytes covering brain capillaries
B. Fenestrations between brain capillary endothelial cells
C. Gap junctions between brain capillary endothelial cells
D. Tight (occluding) junctions between brain capillary endothelial cells
E. Tight (occluding) junctions between ependymal cells
F. Tight (occluding) junctions between microglia
The answer is D: The barrier function of the blood–brain barrier is formed by tight (occluding) junctions (zonulae occludens) between the endothelial cells that comprise the lining of brain capillaries. Adding to the impermeability are the nonfenestrated nature of the capillary endothelium and the paucity or absence of pinocytotic vesicles that represent the physiologic pores seen in other endothelia. Astrocytes form end-foot processes around the brain capillaries that induce and maintain the blood–brain barrier, but do not form the barrier itself.
A 33-year-old woman is referred to the neurology clinic because she has experienced weakness of the eye muscles for the past 2 months. Subsequently, she has experienced diplopia (double vision) and difficulty swallowing, and her speech is slurred. Physical examination shows bilateral ptosis (drooping eyelid), unstable gait, and shortness of breath. Laboratory studies show autoantibodies to the acetylcholine receptor, the receptor for the transmitter that mediates synaptic transmission between motor neurons and skeletal muscle. In which of the following structures do these antibodies bind?
A. Axon hillock of motor neurons
B. Dendrites of motor neuron
C. Presynaptic motor neuron membrane
D. Postsynaptic muscle membrane
E. Synaptic vesicles in motor neurons
The answer is D: The patient has myasthenia gravis, an autoimmune disease in which the body produces antibodies to receptors for the neurotransmitter acetylcholine (ACh), which are expressed on the postsynaptic membrane of muscles. In normal individuals, motor nerve terminals release ACh, which binds to ACh receptors on muscle cells, resulting in depolarization and muscle contraction. Because of the autoantibodies, the number of receptors is reduced in myasthenia gravis, which results in reduced synaptic transmission and consequently in reduced muscle activation.
What event results in the generation of action potentials in a typical neuron?
A. Closing of Na+ channels