Two neural mechanisms in rat fastigial nucleus regulating systemic and cerebral circulation

We have studied in anesthetized (alpha-chloralose) and paralyzed (d tubocurarine) rats the effects of electrical stimulation of the fastigial nucleus (FN) on local cerebral blood flow (lCBF) and its relationship to intracerebral PO2, and PCO2 and to the systemic arterial pressure (Pa). Mass spectrometry was used to measure quantitatively lCBF (repetitively) and cerebral PO2 and PCO2 (continuously). A systematic exploration of the FN for an increase in Pa and/or lCBF revealed that the most active sites for the rise in Pa were localized within the rostral FN, while those that elicited an increase in lCBF were found throughout the rostrocaudal extent of the FN. The increase in lCBF elicited from the caudal FN was not associated with changes in Pa. The increase in lCBF was concomitant with an increase in intracerebral PO2 and a slight decrease in PCO2. Although the increases in Pa and lCBF were dependent on stimulus frequency, their frequency-response curves were different. We conclude that 1) in contrast to the neurons or fibers of passage of the rostral FN, which mediate an increase in Pa, the neurons or fibers of passage that elicit changes in lCBF are localized along the rostrocaudal axis of the FN; 2) changes in the local gas partial pressures are not responsible for the vasodilation observed; and 3) the cerebral vasodilation and systemic vasoconstriction evoked by FN stimulation are probably mediated by two different neural mechanisms.