Neuroglobin expression in the rat suprachiasmatic nucleus: Colocalization, innervation, and response to light
Neuroglobin (Ngb) is a myoglobin‐like (Mb) heme‐globin, belonging the globin family located only in neuronal tissue of the central nervous system. Ngb has been shown to be upregulated in and to protect neurons from hypoxic and ischemic injury, but the function of Ngb—in particular how Ngb may protec...
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Veröffentlicht in: | Journal of comparative neurology (1911) 2010-05, Vol.518 (9), p.1556-1569 |
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Sprache: | eng |
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Zusammenfassung: | Neuroglobin (Ngb) is a myoglobin‐like (Mb) heme‐globin, belonging the globin family located only in neuronal tissue of the central nervous system. Ngb has been shown to be upregulated in and to protect neurons from hypoxic and ischemic injury, but the function of Ngb—in particular how Ngb may protect neurons—remains largely elusive. We have previously described the localization of Ngb in the rat brain and found it to be expressed in areas primarily involved in sleep/wake, circadian, and food regulation. The present study was undertaken, using immunohistochemistry, to characterize the localization, colocalization, innervation, and response to light of Ngb‐immunoreactive (IR) cells in the rat suprachiasmatic nucleus (SCN). Our results demonstrate that the majority of Ngb‐expressing neurons in the SCN belong to a cell group not previously characterized by neurotransmitter content; only a small portion was found to co‐store GRP in the ventral SCN. Furthermore, some Ngb‐containing neurons were responsive to light stimulation at late night evaluated by the induction of cFOS and only a few cells were found to express the core clock gene PER1 during the 24‐hour light/dark cycle. The Ngb‐containing cells received input from neuropeptide Y (NPY)‐containing nerve fibers of the geniticulo‐hypothalamic tract (GHT), whereas no direct input from the eye or the midbrain raphe system was demonstrated. The results indicate that the Ngb could be involved in both photic and nonphotic entrainment via input from the GHT. J. Comp. Neurol. 518:1556–1569, 2010. © 2009 Wiley‐Liss, Inc. |
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ISSN: | 0021-9967 1096-9861 |
DOI: | 10.1002/cne.22290 |