RESUMEN
OBJECTIVES: To better understand the sleep-wake cycle characteristics in the female Neotropical rodent Proechimys guyannensis related to comparative neurobiology. METHODS: Surface neocortical and hippocampal electrodes were chronically implanted in the brains of female Wistar and Proechimys animals. In addition, electrodes for the study of muscle activity were implanted into the neck muscle of both species. After surgical recovery and a period of adaptation, animals were continuously registered for periods as long as 48 h. RESULTS: In both the light and dark phases of the cycle, significant differences in some electrographic patterns were observed between the Proechimys and Wistar animals. Although Proechimys has nocturnal activities and a pattern of polyphasic sleep similar to Wistar rats, the analysis of its sleep-wakefulness cycle indicates that the Neotropical rodent sleeps less with consequent longer periods of wakefulness when compared to Wistar rats. CONCLUSIONS: Together with previous findings of different neuroanatomical, neurophysiologic and behavioral characteristics, this study allow us to better understand adaptive differences of the Neotropical rodent Proechimys.
RESUMEN
Acute electrolytic lesions of the commissural nucleus of the solitary tract (commNTS) reduce blood pressure (BP) in SHR but not in normotensive Wistar-Kyoto and Wistar rats and abolish the pressor response to intravenous injection of potassium cyanide. We investigated the chronic effect of commNTS lesions on mean arterial pressure (MAP), and on baroreceptor and chemoreceptor reflex responses in SHR. The contribution of the sympathetic nervous system and the hormones vasopressin and angiotensin II to maintenance of BP in lesioned SHR was also investigated. MAP fell to normotensive levels the day after lesioning the commNTS but returned to the hypertensive level 9 days later. The reflex tachycardia evoked by sodium nitroprusside remained attenuated for 10 days after commNTS lesions but became enhanced 30 days after commNTS lesions. The pressor component of the chemoreflex elicited by potassium cyanide remained blocked for 30 days after lesions. Vasopressin antagonist or ACE blocker did not change MAP in sham or commNTS-lesioned SHR. Ganglionic blockade with hexamethonium elicited similar reductions in MAP in sham and commNTS-lesioned SHR. Results demonstrated that commNTS lesions in SHR produce a transient fall in BP and a long-lasting inhibition of the pressor response of the chemoreflex. Therefore, the blockade of the pressor response to peripheral chemoreflex activation is not sufficient to chronically reduce MAP in SHR. In the chronic absence of the commNTS, other subnuclei of the NTS or other brain stem nuclei may reorganize to replace the function of commNTS neurons, restoring sympathetic activity and high BP in SHR.