Further studies concerning the role of nitric oxide in LTP induction and maintenance
| Autor: | Michel Baudry, Wael Musleh, Kavian Shahi |
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| Rok vydání: | 1993 |
| Předmět: |
Male
N-Methylaspartate Potassium Channels Stimulation In Vitro Techniques Pharmacology Hippocampal formation Arginine Nitric Oxide Hippocampus Nitroarginine Nitric oxide Rats Sprague-Dawley Hemoglobins Cellular and Molecular Neuroscience chemistry.chemical_compound Postsynaptic potential LTP induction Animals Evoked Potentials Neuronal Plasticity biology musculoskeletal neural and ocular physiology Long-term potentiation Free Radical Scavengers Tetraethylammonium Compounds Electric Stimulation Rats Nitric oxide synthase 2-Amino-5-phosphonovalerate nervous system chemistry Synapses biology.protein Amino Acid Oxidoreductases Nitric Oxide Synthase Neuroscience |
| Zdroj: | Synapse. 13:370-375 |
| ISSN: | 1098-2396 0887-4476 |
| DOI: | 10.1002/syn.890130409 |
| Popis: | Nitric oxide (NO) has recently been proposed to act as a retrograde messenger to produce long-term potentiation (LTP) in hippocampal area CA1. This notion is based largely on the absence of LTP when hippocampal slices are incubated in the presence of inhibitors of NO synthase (NOS) or of NO scavengers. In the present study, we tested the effects of such compounds on both the induction and maintenance of LTP in field CA1 of hippocampal slices. Incubation of slices in the presence of N-methyl-L-arginine (MLA) or L-nitro-arginine (LNA), two inhibitors of NOS, or in the presence of hemoglobin (Hb), a NO scavenger, produced a large reduction in the magnitude of LTP induced by a theta burst stimulation (TBS) paradigm. These compounds had no effect on the degree of paired-pulse facilitation but produced a significant reduction of the facilitation of postsynaptic responses occurring during TBS. On the other hand, MLA did not prevent the potentiation induced by application of tetraethylammonium (TEA). These results suggest that the inhibition of LTP produced by these agents could be due to an effect on a physiological mechanism that triggers LTP and not necessarily on an event that follows the triggering step. |
| Databáze: | OpenAIRE |
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