Abstract

Intracerebroventricular administration of prostaglandins E 1 or E 2 was shown to block, while PGF 2α increased the incidence of tonic convulsion due to electroshock in mice. The Prostaglandins were administered intracerebroventricularly (i.c.v.) to conscious mice by a modification of Haley and McCormick's method (1) prior to a transcorneal maximal electroshock (MES) or a transcorneal supra-maximal electroshock (SMES). PGE 1 and PGE 2 i.c.v. blocked the tonic hindlimb extension (THE) and protected the animals from death induced by MES with ED 50's for PGE 1 and PGE 2 for inhibition of the THE of 6.6 (4.3–12.0) μg/mouse i.c.v. and 13.3 (8.9–22.4) μg/mouse i.c.v. respectively. When PGE 2 was administered intraperitoneally (i.p.) in doses as high as 4.0 mg/kg it did not block the THE. However, the duration of the THE as well as the mortality were reduced by doses of 0.5–4.0 mg/kg PGE 2 i.p.. Both PGE 1 and PGE 2 were shown to cause a dose related significant (p<.001) decrease in the duration of the THE with SMES in doses of 1–10 μg/mouse i.c.v. for PGE 1 and 2–40 μg/mouse i.c.v. for PGE 2. PGF 2α, administered i.c.v. prior to a transcorneal electroshock equivalent to a current at the ED 1 level, increased the incidence of the THE as well as the mortality in doses of 20–50 μg/mouse.

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