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Effects of low ammonia levels on NAD(P)H levels and glutamate secretion during calcium‐dependent depolarization of CNS slices
Author(s) -
Cummins J. T.,
Hamberger A.,
NystróOum B.
Publication year - 1981
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490060208
Subject(s) - nad+ kinase , depolarization , glutamate receptor , stimulation , biophysics , endogeny , ammonium , chemistry , calcium , biochemistry , biology , endocrinology , enzyme , receptor , organic chemistry
Simultaneously with an evoked release of endogenous glutamate, redox changes in NAD(P)H levels occur as a response to electrical or chemical stimulation of the isolated CNS tissue. While electrical‐field stimulation induces a transient increase in tissue NAD(P)H, KCl stimulation produces a decrease in NAD(P)H. One possible interpretation for this difference is that elevated KCl induces glutamate release from larger cell populations, including glia, while electrical stimulation might have a more neuro‐specific action. In the present report, it is shown that the electrically or biochemically evoked release of endogenous glutamate is strongly inhibited by ammonium ions at 3–5 mM in the hippocampus and frontal cortex. At the same time, ammonium ions inverted the NAD(P)H response of the tissue during electrical stimulation, making both electrical and KCl depolarization induce a decrease in NAD(P)H. There was no effect of ammonium ions per se on the NAD(P)H levels, and to obtain the effects on both NAD(P)H and glutamate release, the tissue had to be exposed for 40–60 minutes to ammonium ions. The results are interpreted to indicate that ammonium ions influence regulatory control mechanisms in cell populations in the tissue slice that secretes glutamate in response to depolarization.