Effects of histamine and some biogenic amines on the hippocampal after-discharge in rats.

Abstract

The stereotaxic implantation of chronic electrodes for EEG recording was done into the frontal cortex, septal region and amygdala, and simultaneous insertion of a cannula into the lateral ventricle was conducted. Indifferent electrode was placed in the occipital part of the cranium, and bipolar electrode for electrical stimulation was also implanted into the hippocampus. At least 10 days were elapsed before the initiation of experiment. The animals were placed in a plastic observation chamber, and EEG was recorded with monopolar electrodes. The after-discharge (AD) was provoked by electrical stimulation (3 msec duration, 60 Hz) to the hippocampus for 2 sec. Intraventricular application of 100 μg histamine (Hi) decreased the AD duration determined at 5 and 30 min later, significantly. However, at a dose of 500 μg, Hi caused significant increase of the AD duration even after 60 and 120 min. 2-MethylHi (100 μg) depressed AD; however, 4-MethylHi (200 μg) extended the AD duration. Diphenhydramine (1 mg/kg, i.v.) and pyrilamine (5 mg/kg, i.v.) prevented Hi-induced suppression of AD, but Cimetidine (2 mg/kg, i.v.) and ranitidine (2 mg/kg, i.v.) did not affect the AD. Although noradrenaline (200 μg), serotonin (100 μg) and dopamine (100 μg) did not affect the AD duration, acetylcholine (100 μg) induced significant prolongation. GABA (200 μg), glycine (200 μg) and taurine (200 μg) did not affect hippocampal AD. From these results, it has been assumed that the suppression of AD induced by Hi can not be attributed to the effect mediated by these amines and amino acids; and suppressive effect of Hi on AD can be associated with H1 receptor, while prolongation of AD by Hi may be related with H2 receptor.