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This study was undertaken to dynamically examine the effects of ethanol on the striatal dopaminergic transmission, in terms of N-methyl-D-aspartate (NMDA)-evoked dopamine release and dopamine uptake. In the striatum of urethane-anesthetized Sprague-Dawley rats, extracellular dopamine was measured using in vivo electrochemical detection coupled with a nafion-coated carbon fiber working electrode. Micro-ejection of NMDA evoked a transient dopamine release from the dopamine-containing nerve terminals in striatum. Local application of ethanol by pressure ejection did not elicit significant changes in spontaneous dopamine release. However, with ethanol pretreatment, the time course of NMDA-induced dopamine release was markedly prolonged while the magnitude and the rate of clearance were significantly reduced. These effects were compared to those of nomifensine, a dopamine uptake blocker. Nominfensine pretreatment was found to augment the time course of NMDA-evoked dopamine release analogous to those by ethanol pretreatment. Furthermore, pretreatment with ethanol did not increase the time course parameters of dopamine signals if dopamine releases were induced by co-application of NMDA and nominfensine. These data suggest that in addition to the attenuation of NMDA-evoked dopamine release, ethanol inhibits dopamine uptake in a similar fashion to that observed with nomifensine in situ in the striatum. Indeed, ethanol altered the uptake of exogenous dopamine from the extracellular space of striatal cortex. The time course of dopamine signals was prolonged and the rate of clearance was reduced after ethanol treatment. Taken together, our data demonstrate that ethanol simultaneously inhibits NMDA-evoked dopamine release and dopamine uptake in the striatum, suggesting the importance of the interplay between release and uptake in ethanol effects on striatal dopaminergic transmission.

In chloralose-urethane-anesthetized cats, electrical stimulation and glutamate injection on a small reticular area just dorsal to the facial nucleus (DFA) elicited an ipsilateral reduction in the common carotid resistance (CCR-reduction) with no or minimal change in other cardiovascular parameters. CCR-reduction was mediated via facial and glossopharyngeal nerves, involving partially muscarinic and partially non-muscarinic mechanisms.

Bradycardia was produced by electrical stimulation and injection of glutamate (200 nl, 1 M) to the regions in and around the extremely caudal parts of the inferior olivary nucleus (ION) in chloralose-urethane anesthetized cats. Either medullary transection at 4 mm rostral to the obex, spinal transection at C2–3 or both transections together did not abolish the ION-induced bradycardia. Bradycardia induced by stimulating one ION was slightly reduced and completely abolished by unilateral and bilateral vagotomies, respectively. The ION-evoked bradycardia was also slightly reduced by a raphe lesion. This lesion together with unilateral vagotomy abolisted only the bradycardia induced from the ION on the vagotomized side. In 28 left vagotomized cats, the left ION-induced bradycardia was subjected to the effects of destroying the right ION, dorsal motor/solitary nucleus (DM/SN) and ambiguus nucleus (AN). The bradycardia was completely abolished by ION lesion (7/7), greatly reduced (7/13) or completely abolished (6/13) by DM/SN lesion, and slightly increased (5/8) or decreased (3/8) by AN lesion. We concluded that cells and/or fibers in and around the ION may project fibers to the ipsilateral DM/SN and through the raphe nucleus to the contralateral ION which may send fibers to the other DM/SN.

In chloralose-urethane anesthetized cats, bilateral destruction of the caudal part of the inferior olivary nucleus (ION) produced neither apparent alteration of the basal arterial blood pressure and heart rate, nor discernible influence on the degree of the induced reflex bradycardia by phenylephrine and reflex tachycardia by nitroglycerin. Apart from directly producing cardioinhibition, stimulation of the ION was capable of interacting synergistically with the reflex bradycardia and antagonistically with the reflex tachycardia. Stimulation of the ION was also capable of potentiating the bradycardias induced from stimulating other cardioinhibitory areas, including the ION of the other side and the gigantocellular reticular nuclei of both sides of the medulla. These interactions were still feasible when one vagus nerve remained intact, but not after both nerves were cut. The results suggest that the ION may not be a primary component of the neural loops subserving the baroreceptor reflex arch, but instead, assumes modulatory actions to this reflex mechanism via both vagus nerves.