Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Genetic ablation of orexin neurons in mice results in narcolepsy, hypophagia, and obesity.

Neuron | May 7, 2001

http://www.ncbi.nlm.nih.gov/pubmed/11394998

Orexins (hypocretins) are a pair of neuropeptides implicated in energy homeostasis and arousal. Recent reports suggest that loss of orexin-containing neurons occurs in human patients with narcolepsy. We generated transgenic mice in which orexin-containing neurons are ablated by orexinergic-specific expression of a truncated Machado-Joseph disease gene product (ataxin-3) with an expanded polyglutamine stretch. These mice showed a phenotype strikingly similar to human narcolepsy, including behavioral arrests, premature entry into rapid eye movement (REM) sleep, poorly consolidated sleep patterns, and a late-onset obesity, despite eating less than nontransgenic littermates. These results provide evidence that orexin-containing neurons play important roles in regulating vigilance states and energy homeostasis. Orexin/ataxin-3 mice provide a valuable model for studying the pathophysiology and treatment of narcolepsy.

Pubmed ID: 11394998 RIS Download

Mesh terms: Animals | Carrier Proteins | Eating Disorders | Female | Humans | Hypothalamus | Intracellular Signaling Peptides and Proteins | Machado-Joseph Disease | Male | Mice | Mice, Inbred C57BL | Mice, Inbred DBA | Mice, Transgenic | Narcolepsy | Nerve Tissue Proteins | Neurons | Neuropeptides | Neurotransmitter Agents | Nuclear Proteins | Obesity | Peptides | Repressor Proteins | Sequence Deletion | Sleep Stages | Sleep, REM | Transcription Factors

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

None

Mouse Genome Informatics (Data, Gene Annotation)

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.