In different species, rapid eye movement sleep (REMS) is characterized by a thermoregulatory impairment. It has been postulated that this impairment depends on a general insufficiency in the hypothalamic integration of autonomic function. This study aims to test this hypothesis by assessing the hypothalamic regulation of body fluid osmolality during the different wake-sleep states in the rat. Arginine-vasopressin (AVP) plasma levels were determined following intracerebroventricular (ICV) infusions of artificial cerebrospinal fluid (aCSF), either isotonic or made hypertonic by the addition of NaCl at three different concentrations (125, 250 and 500 mM). Animals were implanted with a cannula within a lateral cerebral ventricle for ICV infusions and with electrodes for the recording of the electroencephalogram. ICV infusions were made in different animals during Wake, REMS or non-REM sleep (NREMS). The results show that ICV infusion of hypertonic aCSF during REMS induced an increase in AVP plasma levels that was not different from that observed during either Wake or NREMS. These results suggest that the thermoregulatory impairment that characterizes REMS does not depend on a general impairment in the hypothalamic control of body homeostasis.
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http://dx.doi.org/10.1111/j.1365-2869.2009.00810.x | DOI Listing |
Alzheimers Dement
December 2024
Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by synapse and memory failure, and severe cognitive impairment. Physical exercise stimulates neuroprotective pathways, has pro-cognitive actions, and has been reported to alleviate memory impairment in AD. Irisin, an exercise-induced hormone, is secreted following proteolytic cleavage of fibronectin type-III-domain-containing 5 (FNDC5).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Federal University of Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.
Background: Alzheimer's disease (AD) stands as the predominant form of dementia worldwide. The pathogenesis of AD encompasses elevated brain levels of amyloid-β oligomers (AβOs), recognized as central neurotoxins linked to AD. The accumulation of AβOs is neurotoxic, resulting in detrimental effects such as synapse loss, mitochondrial dysfunction, and impairment of proteostasis mechanisms.
View Article and Find Full Text PDFNature
November 2024
Division of Pediatric Hematology/Oncology/Stem Cell Transplant and Regenerative Medicine, Department of Pediatrics, Stanford University, Stanford, CA, USA.
H3K27M-mutant diffuse midline gliomas (DMGs) express high levels of the disialoganglioside GD2 (ref. ). Chimeric antigen receptor-modified T cells targeting GD2 (GD2-CART) eradicated DMGs in preclinical models.
View Article and Find Full Text PDFBrain Res
January 2025
Cognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences, Islamic Azad University, Tehran, Iran; Department of Physiology, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. Electronic address:
The present research examined the possible role of α-2 adrenergic receptor drugs (clonidine, selective α-2 adrenergic receptor agonist, and yohimbine, competitive α-2 adrenoreceptor antagonist,) on the effect of arachidonylcyclopropylamide (ACPA), a cannabinoid CB1 receptor agonist, in non-acute restraint stress (NARS) and acute restraint stress (ARS) mice. The animals were unilaterally implanted with a cannula in the left lateral ventricle. ARS was carried out by movement restraint at a period of 4 h.
View Article and Find Full Text PDFMetabolism
January 2025
Department of Endocrinology, the Second Affiliated Hospital, Chongqing Medical University, Chongqing, China. Electronic address:
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