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Involvement of nitric oxide in low glucose‐mediated inhibition of hippocampal long‐term potentiation
Author(s) -
Izumi Yukitoshi,
Zorumski Charles F.
Publication year - 1997
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(199703)25:3<258::aid-syn4>3.0.co;2-a
Subject(s) - long term potentiation , nmda receptor , tetanic stimulation , chemistry , nitric oxide , glutamate receptor , synaptic plasticity , stimulation , hippocampal formation , nitric oxide synthase , endocrinology , medicine , neuroscience , pharmacology , receptor , biochemistry , biology
Hypoglycemia is associated with deficits in learning and memory, yet there is little information about how changes in extracellular glucose alter processes involved in memory. To address these issues, we examined the effects of low glucose on long‐term potentiation (LTP) in the CA1 region of rat hippocampal slices. When slices were exposed to 2–3.3 mM glucose for 5–30 min before tetanic stimulation, baseline synaptic responses were unaltered, but LTP could not be induced. However, exposure to 2 mM glucose immediately following a tetanus failed to inhibit LTP. An inhibitor of N‐methyl‐D‐aspartate (NMDA) receptors prevented the inhibition of LTP by 3.3 mM glucose, but was ineffective against 2 mM glucose. Similarly, nitric oxide synthase (NOS) inhibitors prevented LTP inhibition by 3.3 mM but not by 2 mM glucose. These results suggest that untimely activation of NMDA receptors and release of NO contributes to low glucose‐mediated LTP inhibition, but that different mechanisms may be responsible for LTP inhibition depending on the severity of hypoglycemia. Synapse 25:258–262, 1997. © 1997 Wiley‐Liss, Inc.