Abstract
Following the intracerebroventricular administration of kainic acid (KA), rats showed wet dog shakes (WDS) in a dose-dependent manner. dl-α-aminoadipic acid and l-glutamic acid diethylester blocked WDS behavior induced by 0.05 μg of KA. Noradrenaline, clonidine, yohimbine and apomorphine also significantly blocked KA-induced WDS. Phentolamine and propranolol did not affect WDS. FLA 63, 6-OHDA lesion and bilateralis electrolytic lesion to locus coeruleus markedly enhanced, but l-Dopa blocked WDS behavior. Moreover, the KA-induced shaking behavior was blocked by α-methyl-p-trosine and haloperidol. Cyproheptadine and methergoline also blocked WDS. p-Chlorophenylalanine, 5,6-DHT lesion, electrolytic lesions to dorsal and medial raphe nuclei showed no effect on WDS behavior, but l-5-hydroxytryptophan efficiently blocked it. Atropine and morphine considerably blocked KA-induced WDS behavior, but pilocarpine and nalorphine showed no effect. Bicuculline significantly enhanced, but aminooxyacetic acid blocked WDS. Intracerebroventricularly administered KA dose-dependently decreased the concentrations of noradrenaline and dopamine in the whole rat brain. The brain concentration of 5-hydroxytryptamine was unchanged. In contrast, the concentration of 5-hydroxyindoleacetic acid increased. KA was ineffective regarding the GABA concentration and GAD activity. KA dose-dependently accelerated the disappearance of brain noradrenaline and dopamine after inhibition of catecholamine synthesis. KA, following inhibition of monoamine oxidase, increased the accumulation of 5-hydroxytryptamine, but failed to change the rate of decline of 5-hydroxyindoleacetic acid. KA failed to change the disappearance of brain 5-hydroxytryptamine after inhibition of its synthesis by PCPA. It is suggested that KA-induced WDS behavior is independent from the increased activity of serotonergic neurons in the central nervous system. KA-induced WDS appears to be under the inhibitory control of noradrenergic and GABA-ergic activity. The weaker inhibitory effect upon this behavior showed also dopaminergic and serotonergic neurons. The present experiments showed the close relationship between KA-induced WDS and shaking behavior in morphine abstinence, but basic differences in WDS behavior caused by excessive stimulation of serotonergic receptors.
Published Version
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