THE CENTRAL NERVOUS SYSTEM
NO
has an important role in the central nervous system as a neurotransmitter .
Unlike classic transmitters such as glutamate or dopamine, which are stored in
synaptic vesicles and released in the synaptic cleft upon vesicle fusion, NO is
not stored, but rather is synthesized on demand and immediately diffuses to
neighboring cells. NO synthesis is induced at postsynaptic sites in neurons,
most commonly upon activation of the NMDA subtype of glutamate receptor, which
results in calcium influx and activation of nNOS. In several neuronal subtypes,
eNOS is also present and activated by neu-rotransmitter pathways that lead to
calcium influx. NO synthe-sized postsynaptically may function as a retrograde
messenger and diffuse to the presynaptic terminal to enhance the efficiency of
neurotransmitter release, thereby regulating synaptic plastic-ity, the process
of synapse strengthening that underlies learning and memory. Because aberrant
NMDA receptor activation and excessive NO synthesis is linked to excitotoxic
neuronal death in several neurologic diseases, including stroke, amyotrophic
lateralsclerosis, and Parkinson’s disease, therapy with NOS inhibitors may
reduce neuronal damage in these conditions. However, clinical trials have not
clearly supported the benefit of NOS inhibition, which may reflect
nonselectivity of the inhibitors, resulting in inhibition of the beneficial
effects of eNOS.
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