Circadian effects on basal and stress-induced Fos-like immunoreactivity (IR) in the paraventricular nucleus of the hypothalamus (PVN), the habenula (Hab) and the posterior paraventricular nucleus of the thalamus (PVN-Thal) were examined. Stress induced a significant increase in the number of Fos-like IR cells within all 3 brain regions. In the Hab, expression was localized specifically to the medial region of the lateral Hab. No differences between the effects of daytime vs nighttime stress on numbers of Fos-like IR cells in the PVN and PVP-Thal were observed. Significantly fewer Fos-like IR cells were observed, however, in the lateral habenula of nighttime vs daytime non-stressed controls, resulting in a significantly greater percentage increase in Fos-like IR in the lateral habenula following nighttime vs daytime stress.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/0006-8993(91)91559-j | DOI Listing |
Elife
January 2025
Department of Medicine, Division of Endocrinology, Albert Einstein College of Medicine, Bronx, United States.
It has been well documented that cold is an enhancer of lipid metabolism in peripheral tissues, yet its effect on central nervous system lipid dynamics is underexplored. It is well recognized that cold acclimations enhance adipocyte functions, including white adipose tissue lipid lipolysis and beiging, and brown adipose tissue thermogenesis in mammals. However, it remains unclear whether and how lipid metabolism in the brain is also under the control of ambient temperature.
View Article and Find Full Text PDFArch Endocrinol Metab
January 2025
Universidade de Campinas Centro de Pesquisa em Obesidade e Comorbidades CampinasSP Brasil Centro de Pesquisa em Obesidade e Comorbidades, Universidade de Campinas, Campinas, SP, Brasil.
The hypothalamus is a master regulator of energy balance in the body. First-order hypothalamic neurons localized in the arcuate nucleus sense systemic signals that indicate the energy stores in the body. Through distinct projections, arcuate nucleus neurons communicate with second-order neurons, which are mostly localized in the paraventricular nucleus and in the lateral hypothalamus.
View Article and Find Full Text PDFCell Res
January 2025
Department of Endocrinology, Endocrinology Research Center, Xiangya Hospital of Central South University, Changsha, Hunan, China.
Sleep deficiency is associated with obesity, but the mechanisms underlying this connection remain unclear. Here, we identify a sleep-inducible hypothalamic protein hormone in humans and mice that suppresses obesity. This hormone is cleaved from reticulocalbin-2 (RCN2), and we name it Raptin.
View Article and Find Full Text PDFUnlabelled: Motivated behaviors are regulated by distributed forebrain networks. Traditional approaches have often focused on individual brain regions and connections that do not capture the topographic organization of forebrain connectivity. We performed co-injections of anterograde and retrograde tract tracers in rats to provide novel high-spatial resolution evidence of topographic connections that elaborate a previously identified closed-loop forebrain circuit implicated in affective and motivational processes.
View Article and Find Full Text PDFVitam Horm
January 2025
Department of Chemical Physiology and Biochemistry, Oregon Health & Science University, Portland, OR, United States. Electronic address:
The balance between food intake and energy expenditure is precisely regulated to maintain adipose stores. Leptin, which is produced in and released from adipose in direct proportion to its size, is a major contributor to this control and initiates its homeostatic responses largely via binding to leptin receptors (LepR) in the hypothalamus. Decreases in hypothalamic LepR binding signals starvation, leading to hunger and reduced energy expenditure, whereas increases in hypothalamic LepR binding can suppress food intake and increase energy expenditure.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!