Central antinociceptive action of histamine: behavioural and electrophysiological studies

The effects of intracerebroventricular (i.c.v.) injection of histamine (HA), an H1-agonist (2-pyridylethylamine, 2PEA) and an H1-antagonist (pyrilamine, PYR) on hot-plate latency in rats were examined. HA (40 or 80 μg/rat) significantly enhanced the pain threshold whereas 2PEA (80 or 160 μg/rat) and PYR (20 μg/rat) had no effect. Moreover, PYR did not modify HA antinociception. These results indicate that HA-H1 receptors are not involved in the inhibition by HA of the hot-plate response. To characterize the neural pathways involved in the antinociceptive action of HA, the effect of HA (40 μg/rat, i.c.v.) on the firing of thalamic neurons in arthritic rats evoked by peripheral noxious stimuli was recorded by electrophysiological techniques. HA markedly depressed the neuronal firing evoked by ankle mobilization, suggesting that the thalamus is one important area involved in modulation of pain by HA.