scholarly journals MORPHOLOGY AND FUNCTION OF THE AUTONOMOUS NERVOUS SYSTEM

Author(s):  
A.P. Stepanchuk

The autonomic nervous system consists of the sympathetic and parasympathetic divisions. The central part is represented by supra-segmental and segmental centres. Parasympathetic segmental centres in the brain are accessory nucleus of the oculomotor nerves, superior salivary nucleus of the facial nerve, inferior salivary nucleus of the glossopharyngeal nerve and dorsal nucleus of the vagus nerve. In the spinal cord, these are the intermediate lateral nuclei. Sympathetic segmental centres in the brain are absent, and in the spinal cord, intermediate-lateral nuclei are located in the lateral horns in the eighth cervical, all thoracic and 1-2 lumbar spinal segments. The peripheral part of the autonomic nervous system is represented by pre-nodal and post-nodal branches, paravertebral, prevertebral and terminal nodes and plexuses. The intramural part of the autonomic nervous system lies in the larger part of a wide and narrow-loop net and represented with a large number of nerve cells different by their shapes and sizes and clustered as intramural nodes, or individual nerve cells included along the net loops. The autonomic plexuses of the abdominal cavity are topographically divided into celiac, superior and inferior mesenteric, abdominal aortic, mesenteric, superior and inferior hypogastric region.

2021 ◽  
pp. 614-662
Author(s):  
Alastair Compston

Chapter 16: ‘Neurologie: the doctrine of the nerves: the brain and nervous stock’ summarizes Willis’s treatises in Cerebri anatome, Nervorumque descriptio et usus (1664), De motu musculari (1670) and De anima brutorum (1672). Willis’s coinage of the term ‘neurologie’, intending this as the doctrine of the nerves based on the anatomy of the cranial nerves rather than the study of diseases affecting the brain and nervous stock, is described. The chapter explains why these treatises are additionally important for assigning function to the cerebrum and cerebellum rather than the ventricles; the concept of cerebral localization; the distinction between voluntary and involuntary, or reflex, movement; Willis’s account of the autonomic nervous system; and his ideas on muscular movement. Apart from these innovative contributions, Willis’s description of the arrangement of blood vessels supplying the brain and spinal cord, for which the book is celebrated, is described. The fifteen engraved plates are included. {148 words}


1926 ◽  
Vol 22 (5-6) ◽  
pp. 730-731
Author(s):  
G. P.

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.


Development ◽  
1998 ◽  
Vol 125 (4) ◽  
pp. 599-608 ◽  
Author(s):  
M.R. Hirsch ◽  
M.C. Tiveron ◽  
F. Guillemot ◽  
J.F. Brunet ◽  
C. Goridis

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.


2015 ◽  
Vol 3 (3) ◽  
pp. 197-205 ◽  
Author(s):  
Jill M. Wecht ◽  
Michael F. La Fountaine ◽  
John P. Handrakis ◽  
Christopher R. West ◽  
Aaron Phillips ◽  
...  

2019 ◽  
Vol 317 (2) ◽  
pp. E234-E243
Author(s):  
Valentine S. Moullé ◽  
Caroline Tremblay ◽  
Anne-Laure Castell ◽  
Kevin Vivot ◽  
Mélanie Ethier ◽  
...  

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.


1978 ◽  
Vol 48 (6) ◽  
pp. 895-902 ◽  
Author(s):  
John Yen ◽  
Frederick L. Reiss ◽  
Harold K. Kimelberg ◽  
Robert S. Bourke

✓ The kinetics of distribution of 3H methotrexate (3HMTX) in the central nervous system, plasma, and urine after intraventricular, lumbar percutaneous puncture, and spinal catheter injections were compared. Levels of 3HMTX in whole brain after lumbar percutaneous injection were 40 times less than after intraventricular injection. Injection of 3HMTX via a spinal catheter increased the level of 3HMTX in whole brain but this was still tenfold less than after direct intraventricular instillation. Also, it was found that a disproportionately high amount of 3HMTX was in the brain-stem-cerebellum region which would further reduce the concentration of methotrexate in the cerebral hemispheres. Both intraventricular and lumbar spinal catheter administration of 3HMTX produced 3HMTX levels greater than 10−6M (moles/kg wet weight) in spinal cord tissue as measured by 3H specific activity between 2 to 8 hours after injection. Administration by lumbar percutaneous puncture, however, rarely resulted in this suggested therapeutic level of 10−6M. Initial 3HMTX levels in plasma after lumbar percutaneous instillation was 24 times greater than after intraventricular or lumbar spinal catheter injections. This indicated significant and unavoidable extradural leakage after lumbar percutaneous puncture, which may account for the substantially lower levels of 3HMTX in the brain and spinal cord tissue. It is concluded that intraventricular instillation of methotrexate is the best route of administering the drug to achieve therapeutic levels of methotrexate in both whole brain and throughout the spinal cord.


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