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Hypocretin/orexin neuronal loss increases adult neurogenesis

Arias-Carrion O, Hernandez-Martinez H, Drucker-Colin R (2007) Hypocretin/orexin neuronal loss increases adult neurogenesis. Neuroscience 2007 Abstracts 456.14/C7. Society for Neuroscience, San Diego, CA.

Summary: Adult neurogenesis in the subventricular zone (SVZ) is subjected to physiological regulation and can be modified by brain injuries. The sleep disorder narcolepsy may now be considered a neurodegenerative disease, as there is a massive reduction in the number of neurons containing the neuropeptide, hypocretin (HCRT). In the present study, we investigate the relationship between hypocretin neuronal loss and adult neurogenesis. The neurotoxin, hypocretin-2-saporin (HCRT2-SAP), was administered bilaterally to the lateral hypothalamus (LH) to lesion HCRT neurons. Five weeks after HCRT2-SAP administration a loss of HCRT-ir neurons into LH was produced. In normal animals, a high density of HCRT-ir fibers was found in the septum and was poor in the corpus callosum and striatum. These densities decreased in lesioned animals. To label dividing cells, we used 5-bromo-2′-deoxyuridine (BrdU). BrdU was injected twice daily during days 10-14 after lesion, saline or control procedure. Animals were killed at 3 weeks after the last BrdU injection. Experimental depletion of HCRT in rats increases precursor cell proliferation in the SVZ and subependimal layer of 3rd ventricle. However, we don’t find BrdU/HCRT double-labeled cells in the subependimal zone or LH. These observations suggest that the HCRT is a negative factor in adult neurogenesis.

Related Products: Orexin-B-SAP (Cat. #IT-20)

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