Stimulation of the nucleus basalis of Meynert increases cerebral cortical blood flow in rats

Biesold, D; Inanami, Osamu; Sato, Akio; Sato, Yuko

doi:10.1016/0304-3940(89)90370-4

Cited by 199 publications

(112 citation statements)

References 7 publications

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“…ZI-SVA projects further to the BF (Ricardo, 1981;Jones 1995) and makes it a good candidate to mediate cerebrovasodilator effects of SVA excitation. Electrical or chemical stimulation of the BF produces global and independent of metabolism increase in rCBF (Biesold et al, 1989;Lacombe et al, 1989;Kimura et al, 1990;Sato and Sato, 1992). However, failure of electrolytic lesion of BF to reverse the vasodilator effect of SVA stimulation refuted a possible relay role of the BF.…”

Section: Discussionmentioning

confidence: 99%

“…Pathways ascending from the parvicellular reticular formation innervate the SVA and project further to the BF (Jones, 1995), chemical or electrical stimulation of which increases rCBF ipsilaterally to stimulation (Biesold et al, 1989;Lacombe et al, 1989;Vaucher et al, 1995). The rCBF increase evoked from BF is independent of metabolism (Kimura et al, 1990) and mediated by cholinergic mechanisms (Dauphin et al, 1991;Scremin et al, 1991;Sato and Sato, 1992;Zhang et al, 1995).…”

Section: Effects Of Electrolytic Lesion Of Basal Forebrain On Svaevokmentioning

confidence: 99%

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Neurons of a Limited Subthalamic Area Mediate Elevations in Cortical Cerebral Blood Flow Evoked by Hypoxia and Excitation of Neurons of the Rostral Ventrolateral Medulla

2001

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Sympathoexcitatory reticulospinal neurons of the rostral ventrolateral medulla (RVLM) are oxygen detectors excited by hypoxia to globally elevate regional cerebral blood flow (rCBF). The projection, which accounts for Ͼ50% of hypoxic cerebral vasodilation, relays through the medullary vasodilator area (MCVA). However, there are no direct cortical projections from the RVLM/MCVA, suggesting a relay that diffusely innervates cortex and possibly originates in thalamic nuclei. Systematic mapping by electrical microstimulation of the thalamus and subthalamus revealed that elevations in rCBF were elicited only from a limited area, which encompassed medial pole of zona incerta, Forel's field, and prerubral zone. Stimulation (10 sec train) at an active site increased rCBF by 25 Ϯ 6%. Excitation of local neurons with kainic acid mimicked effects of electrical stimulation by increasing rCBF. Stimulation of the subthalamic cerebrovasodilator area (SVA) with single pulses (0.5 msec; 80 A) triggered cortical EEG burst-CBF wave complexes with latency 24 Ϯ 5 msec, which were similar in shape to complexes evoked from the MCVA. Selective bilateral lesioning of the SVA neurons (ibotenic acid, 2 g, 200 nl) blocked the vasodilation elicited from the MCVA and attenuated hypoxic cerebrovasodilation by 52 Ϯ 12% ( p Ͻ 0.05), whereas hypercarbic vasodilation remained preserved. Lesioning of the vasodilator site in the basal forebrain failed to modify SVA-evoked rCBF increase. We conclude that (1) excitation of intrinsic neurons of functionally restricted region of subthalamus elevates rCBF, (2) these neurons relay signals from the MCVA, which elevate rCBF in response to hypoxia, and (3) the SVA is a functionally important site conveying vasodilator signal from the medulla to the telencephalon.

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Section: Discussionmentioning

confidence: 99%

Section: Effects Of Electrolytic Lesion Of Basal Forebrain On Svaevokmentioning

confidence: 99%

Neurons of a Limited Subthalamic Area Mediate Elevations in Cortical Cerebral Blood Flow Evoked by Hypoxia and Excitation of Neurons of the Rostral Ventrolateral Medulla

2001

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“…For example, cortical perfusion can be directly increased by stimulating the cholinergic basal forebrain (Biesold et al, 1989), the main source of cholinergic innervation to the neocortex. On stimulation, perivascular cortical afferents release acetylcholine (ACh) onto endothelial M 5 muscarinic ACh receptors (Elhusseiny and Hamel, 2000;Yamada et al, 2001).…”

Section: The Neurogliovascular Unitmentioning

confidence: 99%

Neurovascular function in Alzheimer's disease patients and experimental models

Nicolakakis

Hamel

2011

J Cereb Blood Flow Metab

131

118

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The ability of the brain to locally augment glucose delivery and blood flow during neuronal activation, termed neurometabolic and neurovascular coupling, respectively, is compromised in Alzheimer's disease (AD). Since perfusion deficits may hasten clinical deterioration and have been correlated with negative treatment outcome, strategies to improve the cerebral circulation should form an integral element of AD therapeutic efforts. These efforts have yielded several experimental models, some of which constitute AD models proper, others which specifically recapture the AD cerebrovascular pathology, characterized by anatomical alterations in brain vessel structure, as well as molecular changes within vascular smooth muscle cells and endothelial cells forming the bloodbrain barrier. The following paper will present the elements of AD neurovascular dysfunction and review the in vitro and in vivo model systems that have served to deepen our understanding of it. It will also critically evaluate selected groups of compounds, the FDA-approved cholinesterase inhibitors and thiazolidinediones, for their ability to correct neurovascular dysfunction in AD patients and models. These and several others are emerging as compounds with pleiotropic actions that may positively impact dysfunctional cerebrovascular, glial, and neuronal networks in AD.

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“…Both electrical and chemical BF stimulations cause an ipsilateral increase in cortical blood¯ow (Biesold et al 1989;Lacombe et al 1989;Adachi et al 1990). The eects predominate on frontal and parietal cortices and are attenuated by muscarinic and nicotinic antagonists.…”

Section: Cerebral Blood¯ow As a Marker Of Neuronal Activity During Sleepmentioning

confidence: 99%

Functional neuroimaging of normal human sleep by positron emission tomography

Maquet

2000

Journal of Sleep Research

557

304

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Functional neuroimaging using positron emission tomography has recently yielded original data on the functional neuroanatomy of human sleep. This paper attempts to describe the possibilities and limitations of the technique and clarify its usefulness in sleep research. A short overview of the methods of acquisition and statistical analysis (statistical parametric mapping, SPM) is presented before the results of PET sleep studies are reviewed. The discussion attempts to integrate the functional neuroimaging data into the body of knowledge already acquired on sleep in animals and humans using various other techniques (intracellular recordings, in situ neurophysiology, lesional and pharmacological trials, scalp EEG recordings, behavioural or psychological description). The published PET data describe a very reproducible functional neuroanatomy in sleep. The core characteristics of this ‘canonical’ sleep may be summarized as follows. In slow‐wave sleep, most deactivated areas are located in the dorsal pons and mesencephalon, cerebellum, thalami, basal ganglia, basal forebrain/hypothalamus, prefrontal cortex, anterior cingulate cortex, precuneus and in the mesial aspect of the temporal lobe. During rapid‐eye movement sleep, significant activations were found in the pontine tegmentum, thalamic nuclei, limbic areas (amygdaloid complexes, hippocampal formation, anterior cingulate cortex) and in the posterior cortices (temporo‐occipital areas). In contrast, the dorso‐lateral prefrontal cortex, parietal cortex, as well as the posterior cingulate cortex and precuneus, were the least active brain regions. These preliminary studies open up a whole field in sleep research. More detailed explorations of sleep in humans are now accessible to experimental challenges using PET and other neuroimaging techniques. These new methods will contribute to a better understanding of sleep functions.

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Stimulation of the nucleus basalis of Meynert increases cerebral cortical blood flow in rats

Cited by 199 publications

References 7 publications

Neurons of a Limited Subthalamic Area Mediate Elevations in Cortical Cerebral Blood Flow Evoked by Hypoxia and Excitation of Neurons of the Rostral Ventrolateral Medulla

Neurons of a Limited Subthalamic Area Mediate Elevations in Cortical Cerebral Blood Flow Evoked by Hypoxia and Excitation of Neurons of the Rostral Ventrolateral Medulla

Neurovascular function in Alzheimer's disease patients and experimental models

Functional neuroimaging of normal human sleep by positron emission tomography

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