Excitotoxicity begins with:

A. Excessive production of lactic acid.
B. Destruction of cellular proteins.
C. Cellular edema.
D. Persistent binding of glutamate to N-methyl-D-aspartate (NMDA)–type receptors in the postsynaptic cell membrane.
E. Interference of mitochondria functions.


ANS: D
Rationale: First, glutamate binds persistently to the NMDA-type glutamate receptor in the cell membrane. Stimulation of this receptor results in an influx of calcium ions (Ca+2) into the cell, and indirectly facilitates the release of internal Ca+2 stores. An influx of sodium ions (Na+) into the cell results in further stimulation of NMDA receptors and an additional influx of Ca+2 into the cell. Channels that are permeable to Ca+2 open because of the injury. With the increase in Ca+2 inside the cell, more potassium ions (K+) diffuse out of the cell, requiring increased glycolysis that provides energy for the Na+/K+ pump to actively transport K+ into the cell. Together, the increased glycolysis and the increased Ca+2 lead to several destructive consequences for neurons.

Health & Biomechanics

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