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Arachidonic acid induces a long-lasting facilitation of hippocampal synaptic transmission by modulating PKC activity and nicotinic ACh receptorsстатья
Информация о цитировании статьи получена из
Web of Science
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 11 ноября 2019 г.
- Авторы: Nishizaki T., Nomura T., Matsuoka T., Enikolopov G., Sumikawa K.
- Журнал: Molecular Cancer Research
- Том: 69
- Номер: 2
- Год издания: 1999
- Издательство: American Association for Cancer Research
- Местоположение издательства: United States
- Первая страница: 263
- Последняя страница: 272
- DOI: 10.1016/S0169-328X(99)00117-5
- Аннотация: The present study was conducted to understand the effect of arachidonic acid on nicotinic acetylcholine (ACh) receptor-mediated synaptic plasticity. Arachidonic acid persistently (≥1 h) potentiated currents through neuronal nicotinic ACh receptors (α7 and α4β2) expressed in Xenopus oocytes, and the effect was blocked by the selective protein kinase C (PKC) inhibitors, such as GF109203X, PKCI, and co-expressed active PKC inhibitor peptide. This free fatty acid markedly increased nicotine-sensitive glutamate release from hippocampal slices and enhanced the rate of nicotine-sensitive miniature excitatory postsynaptic currents without affecting the amplitude in cultured hippocampal CA1 neurons under the influence of PKC. Furthermore, arachidonic acid induced a long-lasting (≥3 h) facilitation of hippocampal CA1 synaptic transmission in slices, and the effect was blocked by nicotinic ACh receptor antagonists, α-bungarotoxin and mecamylamine. The facilitation, whereas independent of N-methyl-d-aspartate (NMDA) receptors, shares a common mechanism with long-term potentiation (LTP) induced by tetanic stimulation. The results of the present study thus suggest that arachidonic acid sustains enhanced activity of nicotinic ACh receptors by interacting with a PKC pathway, thereby increasing glutamate release from presynaptic terminals, and then leading to an ’LTP-like’ facilitation of hippocampal synaptic transmission. Copyright (C) 1999 Elsevier Science B.V.
- Добавил в систему: Ениколопов Григорий Николаевич