Brain stem regions mediating the cardiovascular responses elicited from the posterior cerebellar cortex in the rabbit.

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Abstract
1. In this study we have examined the roles of the lateral parabrachial nucleus (lateral PBN) and nucleus tractus solitarius (NTS) as sites mediating the circulatory responses evoked from lobule IXb of the posterior cerebellar vermis in the decerebrate and anaesthetized decerebrate rabbit. Microinjection of either kainic acid or bicuculline into the lateral PBN and NTS was undertaken to assess the importances of neurones and GABAergic mechanisms, respectively, in expressing the cardiovascular responses evoked from lobule IXb. 2. In both the decerebrate and anaesthetized decerebrate rabbit activation of neurones within the lateral PBN with a microinjection of glutamate elicited tachycardia and a pressor response together with an increase in renal sympathetic nerve discharge and vasoconstriction in the hindimb. A microinjection of GABA into the lateral PBN evoked and opposite pattern of response. Chemical lesioning of neurones within the rostal region of the lateral PBN or pharmacological blockade of GABAA receptor, abolished or significantly attenuated the cardiovascular response (bradycardia/depressor effect) evoked from lobule IXb in the anaesthetized decerebrate rabbit. 3. In the decerebrate animal the tachycardia/pressor response elicited from lobule IXb was suppressed when either kainic acid or bicuculine was microinjected into the caudal division of the lateral PBN. 4. A bradycardia, depressor response, an abolition of on-going renal nerve activity and vasodilatation in the femoral bed were evoked by activating neurones within a restricted region of the NTS with glutamate in the decerebrate and anaesthetized decerebrate rabbit. A microinjection of GABA into the NTS produced a qualitatively opposite pattern of response. The bradycardia/depressor response evoked from lobule IXb in the anaesthetized decerebrate rabbit was not altered significantly following a microinjection of either kainic acid or bicuculline into the ipsilateral NTS. However, in the decerebrate preparation folloenin a microinjection of bicuculline into the ipsilateral NTS the tachycardia/pressor resoinse evoked from IXb was either abolished or in many cases reversed to the pattern of response seen in the anaesthetized decerebrate rabbit. 5. The present experiments provide evidence for two functionally distinct pathways from the cardiovascular region of lobule IXb to the lateral PBN. One projection relays via the rostal lateral PBN and mediates the cardiovascular changes evoked from IXb in the anaesthetized decerebrate rabbit whereas a second pathway impinges upon the caudal aspect of the lateral PBN and plays a major role in expressing the tachycardia/pressor response associated with the decerebrate preparation. 6. These pathways have been shown to act through bicuculline-sensitive mechanisms. Furthermore, in the decerebrate animal the integrity of GABAA receptors within the NTS was also shown to be essential for the tachycardia/pressor response evoked from IXb. 7. The nature of the input from lobule IXb on physiologically identified neurones within the NTS is investigated in the following paper but as yet the influence of cerebellar inputs on neurons in the lateral PBN remains to be elucidated.