Nesfatin-1/NUCB2 as a potential new element of sleep regulation in rats

Autor: Zita Kátai, Miklós Palkovits, Gyorgy Bagdy, Csaba Adori, Zsuzsanna Tóth, Szilvia Vas, Katalin Könczöl, Rege Sugárka Papp, Dorottya Pap
Jazyk: angličtina
Rok vydání: 2013
Předmět:
Central Nervous System
Male
Anatomy and Physiology
Gene Expression
lcsh:Medicine
Premovement neuronal activity
lcsh:Science
media_common
Slow-wave sleep
Clinical Neurophysiology
Neurons
Multidisciplinary
Neuronal Morphology
Neurochemistry
Electroencephalography
DNA-Binding Proteins
Hypothalamus
Homeostatic Mechanisms
Medicine
Wakefulness
medicine.symptom
Proto-Oncogene Proteins c-fos
Research Article
medicine.medical_specialty
media_common.quotation_subject
Rapid eye movement sleep
Neurophysiology
Sleep
REM
Nerve Tissue Proteins
In situ hybridization
Biology
Diagnostic Medicine
Internal medicine
medicine
Animals
Nucleobindins
Rats
Wistar
Injections
Intraventricular
Calcium-Binding Proteins
lcsh:R
Appetite
Rats
Sleep deprivation
Endocrinology
Cellular Neuroscience
Sleep Deprivation
lcsh:Q
Molecular Neuroscience
Physiological Processes
Sleep
Neuroscience
Zdroj: PLoS ONE, Vol 8, Iss 4, p e59809 (2013)
PLoS ONE
ISSN: 1932-6203
Popis: Study Objectives Millions suffer from sleep disorders that often accompany severe illnesses such as major depression; a leading psychiatric disorder characterized by appetite and rapid eye movement sleep (REMS) abnormalities. Melanin-concentrating hormone (MCH) and nesfatin-1/NUCB2 (nesfatin) are strongly co - expressed in the hypothalamus and are involved both in food intake regulation and depression. Since MCH was recognized earlier as a hypnogenic factor, we analyzed the potential role of nesfatin on vigilance. Design We subjected rats to a 72 h-long REMS deprivation using the classic flower pot method, followed by a 3 h-long ‘rebound sleep’. Nesfatin mRNA and protein expressions as well as neuronal activity (Fos) were measured by quantitative in situ hybridization technique, ELISA and immunohistochemistry, respectively, in ‘deprived’ and ‘rebound’ groups, relative to controls sacrificed at the same time. We also analyzed electroencephalogram of rats treated by intracerebroventricularly administered nesfatin-1, or saline. Results REMS deprivation downregulated the expression of nesfatin (mRNA and protein), however, enhanced REMS during ‘rebound’ reversed this to control levels. Additionally, increased transcriptional activity (Fos) was demonstrated in nesfatin neurons during ‘rebound’. Centrally administered nesfatin-1 at light on reduced REMS and intermediate stage of sleep, while increased passive wake for several hours and also caused a short-term increase in light slow wave sleep. Conclusions The data designate nesfatin as a potential new factor in sleep regulation, which fact can also be relevant in the better understanding of the role of nesfatin in the pathomechanism of depression.
Databáze: OpenAIRE
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