Abstract
In the past 2 years powerful evidence has emerged to suggest that nitric oxide functions as a neurotransmitter in both the central and peripheral nervous systems. Recent evidence suggests that it may play a role in mediating forms of synaptic plasticity such as long-term potentiation in the CA1 region of the hippocampus, and long-term depression in the cerebellum. Abnormal secretion of nitric oxide may be responsible for the neurotoxicity mediated by NMDA receptors that results in the pathophysiology of strokes and neurodegenerative diseases.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 323-327 |
| Number of pages | 5 |
| Journal | Current Opinion in Neurobiology |
| Volume | 2 |
| Issue number | 3 |
| DOIs | |
| State | Published - 1992 |
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ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Nitric oxide and neurons. / Snyder, Solomon H.
In: Current Opinion in Neurobiology, Vol. 2, No. 3, 1992, p. 323-327.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Nitric oxide and neurons
AU - Snyder, Solomon H
PY - 1992
Y1 - 1992
N2 - In the past 2 years powerful evidence has emerged to suggest that nitric oxide functions as a neurotransmitter in both the central and peripheral nervous systems. Recent evidence suggests that it may play a role in mediating forms of synaptic plasticity such as long-term potentiation in the CA1 region of the hippocampus, and long-term depression in the cerebellum. Abnormal secretion of nitric oxide may be responsible for the neurotoxicity mediated by NMDA receptors that results in the pathophysiology of strokes and neurodegenerative diseases.
AB - In the past 2 years powerful evidence has emerged to suggest that nitric oxide functions as a neurotransmitter in both the central and peripheral nervous systems. Recent evidence suggests that it may play a role in mediating forms of synaptic plasticity such as long-term potentiation in the CA1 region of the hippocampus, and long-term depression in the cerebellum. Abnormal secretion of nitric oxide may be responsible for the neurotoxicity mediated by NMDA receptors that results in the pathophysiology of strokes and neurodegenerative diseases.
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UR - http://www.scopus.com/inward/citedby.url?scp=0026874469&partnerID=8YFLogxK
U2 - 10.1016/0959-4388(92)90123-3
DO - 10.1016/0959-4388(92)90123-3
M3 - Article
C2 - 1353698
AN - SCOPUS:0026874469
VL - 2
SP - 323
EP - 327
JO - Current Opinion in Neurobiology
JF - Current Opinion in Neurobiology
SN - 0959-4388
IS - 3
ER -