scholarly journals Direct stimulation of the autonomic nervous system modulates activity of the brain at rest and when engaged in a cognitive task

2012 ◽  
Vol 34 (7) ◽  
pp. 1605-1614 ◽  
Author(s):  
Barbara Basile ◽  
Andrea Bassi ◽  
Giovanni Calcagnini ◽  
Stefano Strano ◽  
Carlo Caltagirone ◽  
...  
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Cognitive Task ◽  
Direct Stimulation ◽  
Autonomic Nervous ◽  
The Brain ◽  
Stimulation Of

Vital staining of cells of the brain vegetative centers

1926 ◽  
Vol 22 (5-6) ◽  
pp. 730-731
Author(s):  
G. P.
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Vital Staining ◽  
Frozen Sections ◽  
Autonomic Nervous ◽  
The Brain ◽  
Dark Blue

V. Rakhmanov (Zhurn. Neurop. And Psych., 1925, No. 3-4) proposes to inject them with 1% Trypanblau solution in the amount of 1 cubic meter to study the vegetative centers in mice. with. weekly for 6-8 weeks. The brain is fixed in 10% formalin, frozen sections are stained with alum carmine or cochineal. In this case, dark blue dust-like grains appear in the plasma and nuclei of cells - selectively for the cells of the autonomic nervous system.

Control of noradrenergic differentiation and Phox2a expression by MASH1 in the central and peripheral nervous system

Development ◽  
1998 ◽  
Vol 125 (4) ◽  
pp. 599-608 ◽  
Author(s):  
M.R. Hirsch ◽  
M.C. Tiveron ◽  
F. Guillemot ◽  
J.F. Brunet ◽  
C. Goridis
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Peripheral Nervous System ◽  
Genetic Circuits ◽  
Autonomic Nervous ◽  
Peripheral Neurons ◽  
Dopamine Beta Hydroxylase ◽  
Targeted Mutation ◽  
The Brain ◽  
Noradrenergic Differentiation

Mash1, a mammalian homologue of the Drosophila proneural genes of the achaete-scute complex, is transiently expressed throughout the developing peripheral autonomic nervous system and in subsets of cells in the neural tube. In the mouse, targeted mutation of Mash1 has revealed a role in the development of parts of the autonomic nervous system and of olfactory neurons, but no discernible phenotype in the brain has been reported. Here, we show that the adrenergic and noradrenergic centres of the brain are missing in Mash1 mutant embryos, whereas most other brainstem nuclei are preserved. Indeed, the present data together with the previous results show that, except in cranial sensory ganglia, Mash1 function is essential for the development of all central and peripheral neurons that express noradrenergic traits transiently or permanently. In particular, we show that, in the absence of MASH1, these neurons fail to initiate expression of the noradrenaline biosynthetic enzyme dopamine beta-hydroxylase. We had previously shown that all these neurons normally express the homeodomain transcription factor Phox2a, a positive regulator of the dopamine beta-hydroxylase gene and that a subset of them depend on it for their survival. We now report that expression of Phox2a is abolished or massively altered in the Mash1−/− mutants, both in the noradrenergic centres of the brain and in peripheral autonomic ganglia. These results suggest that MASH1 controls noradrenergic differentiation at least in part by controlling expression of Phox2a and point to fundamental homologies in the genetic circuits that determine the noradrenergic phenotype in the central and peripheral nervous system.

scholarly journals The autonomic nervous system regulates pancreatic β-cell proliferation in adult male rats

2019 ◽  
Vol 317 (2) ◽  
pp. E234-E243
Author(s):  
Valentine S. Moullé ◽  
Caroline Tremblay ◽  
Anne-Laure Castell ◽  
Kevin Vivot ◽  
Mélanie Ethier ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Adrenergic Receptors ◽  
Male Rats ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Nonesterified Fatty Acids ◽  
Autonomic Nervous ◽  
The Brain

The pancreatic β-cell responds to changes in the nutrient environment to maintain glucose homeostasis by adapting its function and mass. Nutrients can act directly on the β-cell and also indirectly through the brain via autonomic nerves innervating islets. Despite the importance of the brain-islet axis in insulin secretion, relatively little is known regarding its involvement in β-cell proliferation. We previously demonstrated that prolonged infusions of nutrients in rats provoke a dramatic increase in β-cell proliferation in part because of the direct action of nutrients. Here, we addressed the contribution of the autonomic nervous system. In isolated islets, muscarinic stimulation increased, whereas adrenergic stimulation decreased, glucose-induced β-cell proliferation. Blocking α-adrenergic receptors reversed the effect of epinephrine on glucose + nonesterified fatty acids (NEFA)-induced β-cell proliferation, whereas activation of β-adrenergic receptors was without effect. Infusion of glucose + NEFA toward the brain stimulated β-cell proliferation, and this effect was abrogated following celiac vagotomy. The increase in β-cell proliferation following peripheral infusions of glucose + NEFA was not inhibited by vagotomy or atropine treatment but was blocked by coinfusion of epinephrine. We conclude that β-cell proliferation is stimulated by parasympathetic and inhibited by sympathetic signals. Whereas glucose + NEFA in the brain stimulates β-cell proliferation through the vagus nerve, β-cell proliferation in response to systemic nutrient excess does not involve parasympathetic signals but may be associated with decreased sympathetic tone.

scholarly journals Autonomic Regulation of Splanchnic Circulation

1991 ◽  
Vol 5 (4) ◽  
pp. 147-153 ◽  
Author(s):  
Kathleen A Fraser ◽  
Samuel S Lee
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Adrenergic Receptors ◽  
Splanchnic Circulation ◽  
Autonomic Nervous ◽  
Vascular Reserve ◽  
Afferent Nerves ◽  
Primary Afferent Nerves ◽  
Stimulation Of

The role of the autonomic nervous system in circulatory regulation of the splanchnic organs (stomach, small intestine, colon, liver, pancreas and spleen) is reviewed. In general, the sympathetic nervous system is primarily involved in vasoconstriction, while the parasympathetic contributes to vasodilation. Vasoconstriction in the splanchnic circulation appears to be mediated by alpha-2 receptors and vasodilation by activation of primary afferent nerves with subsequent release of vasodilatory peptides, or by stimulation of beta-adrenergic receptors. As well, an important function of the autonomic nervous system is to provide a mechanism by which splanchnic vascular reserve can be mobilized during stress to maintain overall cardiovascular homeostasis.

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