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Superior vestibular neurons were penetrated with horseradish peroxidase (HRP)-loaded glass microelectrodes in anesthetized cats. Responses to electrical stimulation of the oculomotor complex and the vestibular nerves were characterized and selected neurons were injected with HRP. Neurons antidromically activated by oculomotor complex stimulation were generally monosynaptically excited by the ipsilateral vestibular nerve. Notable was the absence of strong commissural inhibition by stimulation of the contralateral vestibular nerve. Light microscopy of antidromically identified injected cells demonstrated that these cells are predominantly located at the central levels of the superior vestibular nucleus along the incoming vestibular nerve fibers but a few are found at more caudal levels. Cell bodies, elongated or pyramidal, are mainly medium-sized to large (30-50 micrometers). Dendritic trees extend in a plane at an acute to the collaterals of the vestibular nerve fibers. Dendrites remain within the nuclear territory and generally display an isodendritic branching pattern. Dendritic spines and appendages are mainly distributed on secondary and distal dendrites. A few terminal enlargements similar to growth cones are observed in these neurons. Axons of these neurons project rostrally via the medial longitudinal fasciculus, while a minor projection via the brachium conjunctivum is also found. Axon collaterals, when present, originate in the nucleus itself and in the pontine reticular formation.

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Background:The endocannabinoid system interacts extensively with other neurotransmitter systems and has been implicated in a variety of functions, including regulation of basal ganglia circuits and motor behavior. The present study examined the effects of repeated administration of the nonselective cannabinoid receptor 1 agonist WIN55,212-2 on locomotor activity and on binding and mRNA levels of dopamine receptors and transporters and GABAA receptors in mesostriatal dopaminergic regions of the rat.Methods:Rats received systemic injections of WIN55,212-2 (0, 0.1, 0.3, or 1mg/kg, intraperitoneally) for 20 consecutive days. Locomotor activity was measured on days 1, 10, and 20. Following the last measurement, rats were euthanized and prepared for in vitro binding and in situ hybridization experiments.Results:Acutely, 0.3 and 1mg/kg of WIN55,212-2 produced hypolocomotion, which was sustained for the next 2 measurements, compared to vehicle. Repeated administration of WIN55,212-2 decreased the mRNA levels of the D2 autoreceptors in substantia nigra and ventral tegmental area and increased D1 receptor mRNA and binding in nucleus accumbens. Furthermore, both dopamine receptor and transporter binding and mRNA levels were decreased in substantia nigra. Moreover, repeated administration of WIN55,212-2 decreased GABAA receptor binding levels in dorsal striatum and substantia nigra.Conclusions:Our data indicate that chronic WIN55,212-2 administration results in sustained effects on locomotor activity, similar to those observed after acute administration, and modulates the dopaminergic and GABAergic systems in a region-, dose-, and neurotransmitter-selective manner

We studied the binding parameters, the pharmacological profile and the anatomical distribution of the dopamine transporter in the mouse cerebellum by using the specific dopamine uptake antagonist [(3)H]GBR12935 and an antidopamine transporter monoclonal antibody. Competition experiments in cerebellar and striatal membrane preparations showed that [(3)H]GBR12935 binds to a specific binding site, sensitive to dopamine and low concentrations of mazindol. The affinity of dopamine for the cerebellar binding site was one order of magnitude lower than the affinity for the striatal binding site. Saturation experiments in cerebellar membrane preparations and thin frozen sections showed that the affinity of [(3)H]GBR12935 for this binding site is similar to its affinity for the striatal dopamine transporter. Saturable binding was lobule specific and in general was higher in the molecular layer compared to the granule cell layer. The immunohistochemical signal was mostly concentrated in the Purkinje cell layer and the cerebellar nuclei. The results suggest that the cerebellar dopamine transporter is similar but not identical to the striatal dopamine transporter and that it is present in the mouse cerebellum in a lobule and lamina specific pattern.

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