Abstract
Bilateral injections of kainic acid (KA) in doses of 100 ng (but not of 20 ng) into the rat striatum caused behavioral disturbances, which were manifested as an increase in the latency of the movement initiation, a decrease in the indices of the locomotor activity in an “open field” test, an increase in muscle tone, and ptosis appearance. Intrastriatal bilateral administration of galanin (10 or 50 ng) decreased the number of crossing movements and rearings in the open field, without affecting the latency of the first crossing movement and the level of muscle tone, and with no ptosis. Combined administration of galanin (10, 20 or 50 ng) and KA (20 ng) into the striatum led to the dose-dependent emergence of behavioral disturbances, which resembled those caused by injections of 100 ng of KA into the caudate nuclei. Behavioral disturbances associated with intrastriatal injection of KA, galanin, and their combination were partially antagonized by naloxon, ketamine, and atropine. It is concluded that galanin potentiates specific behavioral effects of injected KA by modulation of receptors for endogenous opioids, excitatory amino acids, and acetylcholine.
Published Version
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