Non-neuronal cardiac cholinergic system influences CNS via the vagus nerve to acquire a stress-refractory propensity

2016 ◽  
Vol 130 (21) ◽  
pp. 1913-1928 ◽  
Author(s):  
Shino Oikawa ◽  
Yuko Kai ◽  
Masayuki Tsuda ◽  
Hisayuki Ohata ◽  
Asuka Mano ◽  
...  

Choline acetyltransferase gene-overexpressing transgenic mice (ChAT tgm), a model of the non-neuronal cardiac cholinergic system (NNCCS), protects the heart from ischaemic insults, shows specific central phenotypes compatible with vagus nerve stimulation (VS), and consequently re-educate the central nervous system (CNS) to reset stress responses.

Neurosurgery ◽  
1996 ◽  
Vol 39 (2) ◽  
pp. 426-431 ◽  
Author(s):  
David Ko ◽  
Christi Heck ◽  
Scott Grafton ◽  
Michael L.J. Apuzzo ◽  
William T. Couldwell ◽  
...  

2001 ◽  
Vol 77 (4) ◽  
pp. 1136-1144 ◽  
Author(s):  
Nelson E. Loureiro-dos-Santos ◽  
Ricardo A. M. Reis ◽  
Regina C. C. Kubrusly ◽  
Olga M. M. S. De Almeida ◽  
Patricia F. Gardino ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Jaromir Myslivecek

Social species form organizations that support individuals because the consequent social behaviors help these organisms survive. The isolation of these individuals may be a stressor. We reviewed the potential mechanisms of the effects of social isolation on cholinergic signaling and vice versa how changes in cholinergic signaling affect changes due to social isolation.There are two important problems regarding this topic. First, isolation schemes differ in their duration (1–165 days) and initiation (immediately after birth to adulthood). Second, there is an important problem that is generally not considered when studying the role of the cholinergic system in neurobehavioral correlates: muscarinic and nicotinic receptor subtypes do not differ sufficiently in their affinity for orthosteric site agonists and antagonists. Some potential cholinesterase inhibitors also affect other targets, such as receptors or other neurotransmitter systems. Therefore, the role of the cholinergic system in social isolation should be carefully considered, and multiple receptor systems may be involved in the central nervous system response, although some subtypes are involved in specific functions. To determine the role of a specific receptor subtype, the presence of a specific subtype in the central nervous system should be determined using search in knockout studies with the careful application of specific agonists/antagonists.


Cell ◽  
1994 ◽  
Vol 76 (1) ◽  
pp. 117-129 ◽  
Author(s):  
David Westaway ◽  
Stephen J. DeArmond ◽  
Juliana Cayetano-Canlas ◽  
Darlene Groth ◽  
Dallas Foster ◽  
...  

2005 ◽  
Vol 66 (4-6) ◽  
pp. 546-549 ◽  
Author(s):  
Diego Clemente ◽  
Francisco Javier Arenzana ◽  
Rosario Sánchez-González ◽  
Ángel Porteros ◽  
José Aijón ◽  
...  

2002 ◽  
Vol 76 (23) ◽  
pp. 12223-12232 ◽  
Author(s):  
Susanna Freude ◽  
Jürgen Hausmann ◽  
Markus Hofer ◽  
Ngan Pham-Mitchell ◽  
Iain L. Campbell ◽  
...  

ABSTRACT Targeted expression of biologically active interleukin-12 (IL-12) in astrocytes of the central nervous system (CNS) results in spontaneous neuroimmunological disease of aged mice. Borna disease virus (BDV) can readily multiply in the mouse CNS but does not trigger disease in most strains. Here we show that a large percentage of IL-12 transgenic mice developed severe ataxia within 5 to 10 weeks after infection with BDV. By contrast, no disease developed in mock-infected IL-12 transgenic and wild-type mice until 4 months of age. Neurological symptoms were rare in infected wild-type animals, and if they occurred, these were milder and appeared later. Histological analyses showed that the cerebellum of infected IL-12 transgenic mice, which is the brain region with strongest transgene expression, contained large numbers of CD4+ and CD8+ T cells as well as lower numbers of B cells, whereas other parts of the CNS showed only mild infiltration by lymphocytes. The cerebellum of diseased mice further showed severe astrogliosis, calcifications and signs of neurodegeneration. BDV antigen and nucleic acids were present in lower amounts in the inflamed cerebellum of infected transgenic mice than in the noninflamed cerebellum of infected wild-type littermates, suggesting that IL-12 or IL-12-induced cytokines exhibited antiviral activity. We propose that BDV infection accelerates the frequency by which immune cells such as lymphocytes and NK cells enter the CNS and then respond to IL-12 present in the local milieu causing disease. Our results illustrate that infection of the CNS with a virus that is benign in certain hosts can be harmful in such normally disease-resistant hosts if the tissue is unfavorably preconditioned by proinflammatory cytokines.


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