Rat climbing behavior elicited by stimulation of cerebral dopamine receptors

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Abstract
The experimental conditions allowing to elicit by administration of dopamine agonists a climbing behavior in rats, apparently analogous to the stereotyped cage climbing behavior previously described in mice (Protais et al. 1976), have been established. Among the various strains of rats studied i.e. Sprague-Dawley, Long Evans and Wistar, the latters were selected as the most responsive to the dopamine agonist apomorphine. However, even in the Wistar strain, only about 60% of animals responded to a test-dose of 0.4 mg/kg apomorphine by adopting in a sustained manner the typical upright position against the walls of a suitable experimental cage. Hence responsive rats were preselected 4 days before the experimental sessions and finally rated during a 60-min observation period. Increasing the test-dose of apomorphine led to a biphasic effect, the spontaneous climbing behavior being decreased at low dosage and, then, both the percentage of climbing animals and the duration of the behavior were progressively increased at higher dosages. A scoring system based on an all-or-none evaluation of the frequency of stereotyped climbing episods over the 1 h observation period was finally adopted allowing to establish dose response curves to apomorphine and its more potent derivative N-propylnorapomorphine. Dexamphetamine (associated to L-Dopa) also produced the stereotyped climbing behavior. The latter was completely abolished in animals treated with the “atypical” antipsychotic sulpiride. The effects of lesioning various cerebral dopaminergic areas on the apomorphine-induced behavior were investigated. The response was not significantly altered following bilateral thermocoagulations of the striatum (restricted lesions), globus pallidus, nucleus interstitialis of the striae terminalis, amygdala, nucleus lateralis septi or nucleus accumbens. Intrastriatal injections of 6-hydroxydopamine were without significant effect while large striatal thermocoagulations abolished the stereotyped behavior but were accompanied by a profound motor deficiency. Bilateral lesioning of the substantia nigra by either thermocoagulation or 6-hydroxydopamine, the latter leading to a 60% decrease in 3H-dopamine uptake in striatum without significant modification in nucleus accumbens, resulted in a hypersensitive response to apomorphine. Hence, these experiments do not allow to identify a single brain area where dopamine receptors mediating the climbing behavior are located although they suggest that the receptors involved receive a dopaminergic input originating from the substantia nigra.