Role of the Cerebellar Fastigial Nucleus in the Physiological Regulation of Cerebral Blood Flow

Takahashi, Shinichi; Crane, Alison M.; Jehle, Jane; Cook, Michelle; Kennedy, Charles; Sokoloff, Louis

doi:10.1038/jcbfm.1995.15

Cited by 8 publications

(3 citation statements)

References 52 publications

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“…In relation to potential neural control of autoregulation, a few studies have examined whether specific regions within the brain may influence autoregulation of CBF globally. For example, electrolytic lesions of the fastigial nucleus in the cerebellum had little or no effect on resting CBF or autoregulation of CBF during reductions in arterial BP (produced by hemorrhagic hypotension) in conscious rats (551). In contrast, electrolytic lesions of the nucleus tractus solitarii (NTS) in the medulla impaired autoregulation in multiple brain regions during phenylephrine-induced increases in arterial BP in anesthetized rats (276).…”

Section: Where In the Vascular Bed Does Autoregulation Take Place?mentioning

confidence: 99%

Regulation of cerebral blood flow in humans: physiology and clinical implications of autoregulation

Claassen

Thijssen

Panerai

et al. 2021

Physiological Reviews

482

418

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Brain function critically depends on a close matching between metabolic demands, appropriate delivery of oxygen and nutrients, and removal of cellular waste. This matching requires continuous regulation of cerebral blood flow (CBF), which can be categorized into four broad topics: 1) autoregulation, which describes the response of the cerebrovasculature to changes in perfusion pressure, 2) vascular reactivity to vasoactive stimuli [including carbon dioxide (CO2)], 3) neurovascular coupling (NVC), i.e., the CBF response to local changes in neural activity (often standardized cognitive stimuli in humans), and 4) endothelium-dependent responses. This review focuses primarily on autoregulation and its clinical implications. To place autoregulation in a more precise context, and to better understand integrated approaches in the cerebral circulation, we also briefly address reactivity to CO2 and NVC. In addition to our focus on effects of perfusion pressure (or blood pressure), we describe the impact of select stimuli on regulation of CBF (i.e., arterial blood gases, cerebral metabolism, neural mechanisms, and specific vascular cells), the inter-relationships between these stimuli, and implications for regulation of CBF at the level of large arteries and the microcirculation. We review clinical implications of autoregulation in aging, hypertension, stroke, mild cognitive impairment, anesthesia, and dementias. Finally, we discuss autoregulation in the context of common daily physiological challenges, including changes in posture (e.g., orthostatic hypotension, syncope) and physical activity.

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Section: Where In the Vascular Bed Does Autoregulation Take Place?mentioning

confidence: 99%

Regulation of cerebral blood flow in humans: physiology and clinical implications of autoregulation

Claassen

Thijssen

Panerai

et al. 2021

Physiological Reviews

482

418

View full text Add to dashboard Cite

show abstract

“…The area of the F N eliciting neuroprotection, the rostral ventromedial quadrant, is the region of the nucleus from which electrical stimulation potently elevates AP (Miura and Reis, 1970;Takahashi et al, 1995), elevates rCBF globally without modifying rCGU (Nakai et al, 1983), and releases catecholamines from adrenal medulla (Del Bo et al, 1983a), arginine vasopressin from pituitary (Del Bo et al, 1983b), and renin from the kidney (Manning et al, 1985), a response called the fastigial pressor response (FPR) (Miura and Reis, 1970. In unanesthetized animals, such stimulation also elicits a range of consummatory behaviors (Reis et al, 1973).…”

Section: Cerebellar Substrate For Neuroprotectionmentioning

confidence: 99%

Intrinsic Neurons of Fastigial Nucleus Mediate Neurogenic Neuroprotection against Excitotoxic and Ischemic Neuronal Injury in Rat

1999

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Electrical stimulation of the cerebellar fastigial nucleus (FN) elevates regional cerebral blood flow (rCBF) and arterial pressure (AP) and provides long-lasting protection against focal and global ischemic infarctions. We investigated which neuronal element in FN, perikarya or axons, mediates this central neurogenic neuroprotection and whether it also protects against excitotoxicity. In anesthetized rats, the FN was stimulated for 1 hr, and ibotenic acid (IBO) was microinjected unilaterally into the striatum. In unstimulated controls, the excitotoxic lesions averaged approximately 40 mm3. Stimulation of FN, but not dentate nucleus (DN), significantly reduced lesion volumes up to 80% when IBO was injected 15 min, 72 hr, or 10 d, but not 30 d, thereafter. In other rats, intrinsic neurons of FN or DN were destroyed by pretreatment with IBO. Five days later, the FN was stimulated, and 72 hr later, IBO was microinjected into the striatum. Lesions of FN, but not DN, abolished neuroprotection but not the elevations of rCBF and AP elicited from FN stimulation. Excitotoxic lesions of FN, but not DN, also abolished the 37% reduction in focal ischemic infarctions produced by middle cerebral artery occlusion. Excitation of intrinsic FN neurons provides long-lasting, substantial, and reversible protection of central neurons from excitotoxicity, as well as focal ischemia, whereas axons in the nucleus, probably collaterals of ramified brainstem neurons, mediate the elevations in rCBF, which do not contribute to neuroprotection. Long-lived protection against a range of injuries is an unrecognized function of FN neurons transmitted over pathways distinct from those regulating rCBF.

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“…It is known that the vasomotor centers and their nuclei are implicated in the regulation of CBF. Electrical stimulation of the cerebellar fastigial nucleus can lead to a significant increase in CBF (Mraovitch et al, 1986;Takahashi et al, 1995), which is mainly mediated by rostral ventrolateral nucleus in the medulla (Chida et al, 1990). Therefore, cSCSinduced cerebral vasodilation may initially activate vasomotor centers that include the cerebellar fastigial nucleus and rostral ventrolateral medulla nucleus via ascending spinocerebellar pathways (Patel et al, 2004.…”

Section: Vasomotor Mechanisms-transectionmentioning

confidence: 99%

Putative mechanisms behind effects of spinal cord stimulation on vascular diseases: A review of experimental studies

Linderoth

Foreman

2008

Autonomic Neuroscience

159

106

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Spinal cord stimulation (SCS) is a widely used clinical technique to treat ischemic pain in peripheral, cardiac and cerebral vascular diseases. The use of this treatment advanced rapidly during the late 80's and 90's, particularly in Europe. Although the clinical benefits of SCS are clear and the success rate remains high, the mechanisms are not yet completely understood. SCS at lumbar spinal segments (L2-L3) produces vasodilation in the lower limbs and feet which is mediated by antidromic activation of sensory fibers and decreased sympathetic outflow. SCS at thoracic spinal segments (T1-T2) induces several benefits including pain relief, reduction in both frequency and severity of angina attacks, and reduced short-acting nitrate intake. The benefits to the heart are not likely due to an increase, or redistribution of local blood flow, rather, they are associated with SCS-induced myocardial protection and normalization of the intrinsic cardiac nervous system. At somewhat lower cervical levels (C3-C6), SCS induces increased blood flow in the upper extremities. SCS at the upper cervical spinal segments (C1-C2) increased cerebral blood flow, which is associated with a decrease in sympathetic activity, an increase in vasomotor center activity and a release of neurohumoral factors. This review will summarize the basic science studies that have contributed to our understanding about mechanisms through which SCS produces beneficial effects when used in the treatment of vascular diseases. Furthermore, this review will particularly focus on the antidromic mechanisms of SCS-induced vasodilation in the lower limbs and feet.

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Role of the Cerebellar Fastigial Nucleus in the Physiological Regulation of Cerebral Blood Flow

Cited by 8 publications

References 52 publications

Regulation of cerebral blood flow in humans: physiology and clinical implications of autoregulation

Regulation of cerebral blood flow in humans: physiology and clinical implications of autoregulation

Intrinsic Neurons of Fastigial Nucleus Mediate Neurogenic Neuroprotection against Excitotoxic and Ischemic Neuronal Injury in Rat

Putative mechanisms behind effects of spinal cord stimulation on vascular diseases: A review of experimental studies

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