Arachidonic acid inhibits sodium currents and synaptic transmission in cultured striatal neurons

Content Provider	Semantic Scholar
Author	Fraser, Douglas D. Hoehn, Katja Weiss, Samuel Bruce Vicar, Brian A. Mac
Copyright Year	1993
Abstract	In the striatum, dopamine generates arachidonic acid (AA) and induces synaptic depression. Here, we report that Na+ channels are a target for AA in both cultured and acutely isolated striatal neurons. AA depressed veratrine-induced Na+ influx and neurotransmitter release. Whole-cell voltage clamp revealed that peak Na+ currents are depressed, and steady-state inactivation shifts -15 mV in the presence of AA. Furthermore, inactivation was accelerated, and recovery from inactivation was delayed. These actions of AA were not produced by AA metabolites or protein kinase C activation. In addition, AA reduced both the amplitude and frequency of action potentials and depressed spontaneous inhibitory postsynaptic currents without affecting miniature inhibitory postsynaptic currents. These data suggest that AA modulates presynaptic, Na(+)-dependent action potentials, thereby contributing to striatal synaptic depression.
Starting Page	633
Ending Page	644
Page Count	12
File Format	PDF HTM / HTML
DOI	10.1016/0896-6273(93)90075-3
PubMed reference number	8398152
Journal	Medline
Volume Number	11
Alternate Webpage(s)	https://api.elsevier.com/content/article/pii/0896627393900753
Alternate Webpage(s)	https://www.sciencedirect.com/science/article/pii/0896627393900753?dgcid=api_sd_search-api-endpoint
Alternate Webpage(s)	https://doi.org/10.1016/0896-6273%2893%2990075-3
Journal	Neuron
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article