Anatomical basis for the fastigial pressor response

Electrical stimulation of rostromedial portion of cerebellar fastigial nucleus elicits integrated cardiovascular effects, which are neurally and humorally mediated. In this study, we sought to demonstrate the anatomical substrates of the fastigial pressor response (FPR) in the rat. The response was electrophysiologically localized in anesthetized, paralyzed-ventilated rats. Anterograde transport techniques were used to study the efferent projections of the fastigial pressor area; the distribution of efferent projection cells were then mapped by injecting retrograde tracers into anterogradely labeled sites. Electrolytic lesions were then placed bilaterally in selected brainstem areas in the attempt to block the pressor response. Sites of cerebellar stimulation and of brainstem lesions were subsequently histologically identified. The following lesions abolished the FPR: in nine animals lesions involved portions of the nucleus gigantocellularis dorsalis (NGCd), paramedian reticular formation (PMN) and the nucleus tractus solitarii (NTS) (in two animals fairly selectively the caudal NTS); in two other animals lesions destroyed the rostral ventrolateral medulla (C1 area) and in one animal the area encompassing the dorsal convexity of the superior cerebellar peduncle bordering the locus coeruleus-lateral parabrachial complex; partially effective were unilateral lesions of NGCd and NTS (three), bilateral lesions confined to NGCd and PMN (two), to vestibular complex and uncinate fasciculus (UF) (three), to UF and locus coeruleus (three) and to nucleus reticularis ventralis (two). Ineffective lesions involved A1 area, the nucleus gigantocellularis ventralis (NGCv), the spinal trigeminal nucleus and nucleus reticularis parvocellularis, the A5 area of the ventrolateral pons, the central gray and lateral mesencephalic tegmentum. It seems therefore that the pressor response elicited by stimulation of the cerebellar fastigial nucleus utilizes central specific pathways, as lesions involving other brainstem regions also known to participate in cardiovascular control do not affect the response. Furthermore, the FPR persisted after midbrain decerebration, thus demonstrating that it is organized beneath the midbrain.