Gamma radiation (10 Gy at 10 Gy/min from a60 Co source) induces a decrease in the release of norepinephrine in the hippocampus 48 h after exposure. The purpose of this study was to determine the effect of Bay K 8644 [methyl-1, 4-dihydro-2, 6-dimethyl-3-nitro-4-2(trifluoromethylphenyl)pyridine-5-carboxylate], an agonist for L- and N-type calcium channel subtypes; calcimycin {6S-[6α(2S*, 3S*), 8β(R*), 9β,11α]-5(methylamino)-2-[[3,9,11-trimethyl-8-[1-methyl-2-oxo-2(1H-pyrrol-2-yl)ethyl]1,7-dioxaspiro[5,5]undec-2-yl]methyl]-4-benzoxazolecarboxylicacid}, a calcium ionophore which increases intracellular Ca2+; and phorbol 12-O-tetradecanoate 13-acetate (TPA), which stimulates protein kinase C (PKC) alone or in combination with decreases in the release of norepinephrine in the hippocampus 48 h after irradiation. Neither Bay K 8644 (1-100 nM), calcimycin nor TPA prevented the radiation-induced decreases in the release of norepinephrine in the hippocampus. However, 10 nM of Bay K 8644 or calcimycin in combination with 1-100 nM of TPA or 10 nM of TPA in combination with 1-100 nM of Bay K 8644 or calcimycin did prevent the radiation-induced decreases in the release of norepinephrine. These results suggest that stimulation of PKC by TPA and mobilization of calcium by Bay K 8644 or calcimycin are necessary to prevent the radiation-induced decreases in the release of norepinephrine in the hippocampus.

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