Modulation of glutamate release from hippocampal mossy fiber nerve endings by arachidonic acid and eicosanoids.
作者： R. V. Dorman , T. F. R. Hamm , D. S. Damron , E. J. Freeman
DOI: 10.1007/978-1-4615-3426-6_11
关键词:
摘要: Arachidonic acid has been implicated in normal synaptic transmission processes, including those related to the development of hippocampal long-term potentiation. Hippocampal mossy fiber (MF) synaptosomes were used investigate role arachidonate evoked accumulation presynaptic Ca2+ and release endogenous glutamate, since these nerve terminals express potentiation selectively glutamate as excitatory transmitter. It was demonstrated that membrane depolarization Ca2+, production unesterified arachidonic acid. These events may be functionally related, exogenous phospholipase A2 activation mimicked effects on availability release, while secretion processes attenuated presence inhibitors. In addition, pretreatment with or melittin allowed for facilitated response a subsequent depolarizing stimulus. Inhibition cyclooxygenase lipoxygenase activities also potentiated responses depolarization. contrast, 12-lipoxygenase products depolarization-evoked intraterminal free release. is suggested acts positive modulator involved increased required induction potentiation, metabolites provide negative feedback signals designed limit neurotransmitter secretion.
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