effects of lidocaine reversible inactivation of the dorsal raphe nucleus on passive avoidance learning in rats

Introduction: The role of serotonergic fibers in avoidance learning is controversial. Involvement of the dorsal raphe nucleus [DRN], the main source of hippocampal projecting serotonergic fibers in acquisition, consolidation and retrieval of passive avoidance [PA] learning, was investigated by functional suppression of this area. Materials and Methods: DRN functional inactivation was done by lidocaine [0.5µl, 2%] injection into the DRN, 5 min before training [n=10]; and 5 [n=9], 90 [n=10] and 360 min [n=9] after acquisition trial. In the last experiment, lidocaine was injected into the DRN 5 min before the retrieval test, which was 48 h after the training [n=10]. Results: Our results showed that PA learning was not impaired by DRN inactivation 5 min before training nor 5 and 360 min after training. Lidocaine injected 90 min after the acquisition trial significantly reduced avoidance of the dark compartment [P<0.001]. Intra-DRN injection of lidocaine before retrieval significantly increased PA retention [P<0.001]. Therefore, it seems that DRN has opposite effects on consolidation and retrieval of passive avoidance learning, but it has no effect on PA acquisition. Discussion: It is suggested that functional ablation of DRN may disrupt integrity of subcortical circuits participating in PA consolidation, but DRN inactivation by increasing brain awareness may affect PA retrieval in rats

effect of nucleus tractus solitarius nitric oxidergic neurons on blood pressure in diabetic rats

It has been shown that nitric oxide is synthesized in the central nervous system as well as in vascular endothelial cells. Recently, it was reported that nitric oxide was involved in central cardiovascular regulation, baroreflex modulation, and involved in a reciprocal release with excitatory amino acids in the nucleus tractus solitarii of rats. The purpose of the present study was to investigate the possible interaction of nitric oxide and glucose in the nucleus tractus solitarii on blood pressure regulation. Male Wistar stereptozotocin induced diabetic rats were anesthetized with urethane. A cannula was inserted above the nucleus tractus solitarii and blood pressure was monitored intra-arterially. Unilateral microinjection of L-glutamate [2.3 nmol/60 nL] into the nucleus produced a decrease in blood pressure in diabetic rats. Microinjection of lidocaine [0.5 Mul%2] increased blood pressure. Unilateral microinjection of sodium nitroprusside [100 mmoV6O nL] into the nucleus increased blood pressure in diabetic rats. After microinjection of sodium nitroprusside, the depressive responses to glutamate were significantly attenuated. These results demonstrated the probable role of glucose on blood pressure regulation in diabetic animals affecting on nitric oxidergic neurons and so it implicates an interaction between nitric oxide and glucose in central cardiovascular regulation

[ effect of hyperglycmia on nitric oxidergic neurons in nucleus tractus solitarius and blood pressure regulation in rats with induced diabetes]

The role of nucleus tractus solitarius in cardiovascular system regulation is controversial. On the other hand, study on the problem of hypertension in diabetic animals is the subject of many research programs. The aim of the present study was to determine wheather inactivation of nucleus can affect blood pressure in diabetic rats. To this end, stereptosotocin-induced diabetic rats were anesthetized with Urethane and a cannula was inserted above nucleus. Blood pressure and heart rate were monitored using an intraarterial cannula. The cannulas were filled with L-glutamate [78 pmol/60 nL, to functionally identify the NTS; see below], L-NAME[1nmol, to inhibit the nitric oxidergic neurons] and sodium nitroprusside [100mmol,as a NO-donor]. The results indicated that inactivation of nucleus in diabetic rats, had no effect on systolic and mean arterial pressure but enhanced diastolic blood pressure [P<0.05]. There was no significant difference in heart rate between control and test groups. Glucose affect on increasing blood pressure in rats with induced diabetes, in part, is caused by nitric oxidergic neurons resided in neucleus tractus solitarius