Involvement of opioid and non-opioid mechanisms in footshock-induced enhancement of brain histamine turnover in mice.

Naloxone (1-10 mg/kg, i.p.) dose-dependently inhibited the footshock-induced elevation in levels of tele-methylhistamine (t-MH), a predominant metabolite of brain histamine (HA), although this compound had no effect on the HA dynamics in the non-shocked control mice. Footshock significantly enhanced the HA depletion induced by alpha-fluoromethylhistidine, a specific inhibitor of histidine decarboxylase. However, in mice treated with naloxone (5 mg/kg, i.p.) footshock did not significantly facilitate the alpha-fluoromethylhistidine-induced HA depletion. In mice which had been rendered morphine-tolerant following an s.c. implantation of a pellet containing 50 mg of morphine base 3 days before, footshock produced no significant elevation of the t-MH level. The treatment with alpha-methyl-p-tyrosine, p-chlorophenylalanine or atropine had no significant influence on the footshock-induced t-MH elevation. The t-MH elevation was the most marked in the midbrain. In the hypothalamus and pons-medulla oblongata, no significant change in the t-MH level was produced by footshock. These results suggest that footshock increases the HAergic activity in the mouse brain partly through activation of opioid-related mechanisms and that alterations in HA dynamics differ with region of the brain.