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Medial vestibular nucleus mediates the cardiorespiratory responses to fastigial nuclear activation and hypercapnia

¹Pathophysiology Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico 87108; and ²Department of Physiology, School of Medicine, University of Kentucky, Lexington, Kentucky 40536

Submitted 5 February 2004 ; accepted in final form 14 April 2004

Electrical stimulation of the cerebellar fastigial nucleus (FN) evokes hyperventilation and hypertension responses that are similar to those induced by stimulation of the medial region of the vestibular nucleus (VN_M). Because there are mutual projections between these two nuclei morphologically, we hypothesized that the FN-mediated cardiorespiratory responses were related to the integrity of the VN_M. Experiments were conducted on 21 anesthetized, tracheotomized, and spontaneously breathing rats. Electrical stimulation (10 s) of the FN was used to evoke cardiorespiratory responses, and the same stimulus was repeated 30–45 min after bilateral lesions of the VN_M by local microinjection of ibotenic acid (100 mM, 100 nl). We found that FN stimulation-induced hyperventilation and hypertension were attenuated significantly by the lesions. The role of the VN_M in the ventilatory responses to chemical challenges was subsequently defined. The animals were exposed to hypercapnia (10% CO₂) and hypoxia (10% O₂) for 1–2 min randomly before and after VN_M lesions. The results showed that VN_M lesions significantly attenuated the cardiorespiratory responses to hypercapnia but not to hypoxia, with little effect on baseline respiratory variables. These findings suggest that the VN_M is required for full expression of the cardiorespiratory responses to electrical stimulation of the FN as well as to hypercapnia. However, neurons within the VN_M do not appear to be critical for maintaining eupneic breathing and the cardiorespiratory responses to hypoxia.

electrical stimulation; hypoxia; ibotenic acid; rats

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