Excessive testosterone treatment and castration induce reactive astrocytes and fos immunoreactivity in suprachiasmatic nucleus of mice.
The suprachiasmatic nucleus (SCN) has long been recognized as the central mammalian circadian pacemaker that controls behavioral and physiological processes. The role of the SCN in circadian rhythms has been the subject of a wide range of physiological and behavioral studies, although the influence of homeostasis rhythms (such as fluctuating hormone levels) on the SCN of the hypothalamus is not entirely clear. The present study was undertaken to examine the morphological interactions between astroglial and neuronal elements in the SCN of mice after either a short-term excessive testosterone treatment (ETT) or castration, using glial fibrillary acidic protein (GFAP), and immediate early gene c-fos as well as calbindin-D28k (CB) immunohistochemistry. Both ETT and castration resulted in a significant increase in the accumulation of reactive astrocytes and Fos-imunoreactivity (IR), especially in the dorsomedial (DM) sub-region of the SCN. However, CB-IR neurons in the examined brain regions showed little change. These findings indicate that the DM sub-region of the SCN may be a possible center of hormonal regulation via a hypothalamic neuroendocrine circuit, and that a non-photic stimuli mechanism might play a role in circadian rhythm regulation.
Satriotomo
Irawan
I
Department of Anatomy and Neurobiology, Faculty of Medicine, Kagawa University, 1750-1, Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan. irawan@kms.ac.jp
Miki
Takanori
T
Gonzalez
Daniel
D
Matsumoto
Yoshiki
Y
Li
Hong-Peng
HP
Gu
He
H
Takeuchi
Yoshiki
Y
D000818:Animals; D001253:Astrocytes / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism*; D001931:Brain Mapping; D064092:Calbindin 1; D064026:Calbindins; D002369:Castration; D002940:Circadian Rhythm / Q000502:physiology; D005904:Glial Fibrillary Acidic Protein / Q000187:drug effects / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D009490:Neurosecretory Systems / Q000502:physiology; D016761:Oncogene Proteins v-fos / Q000187:drug effects / Q000378:metabolism*; D064030:S100 Calcium Binding Protein G / Q000187:drug effects / Q000378:metabolism; D013493:Suprachiasmatic Nucleus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D013739:Testosterone / Q000172:deficiency / Q000494:pharmacology
C576499:Calb1 protein, mouse; D064092:Calbindin 1; D064026:Calbindins; D005904:Glial Fibrillary Acidic Protein; D016761:Oncogene Proteins v-fos; D064030:S100 Calcium Binding Protein G; D013739:Testosterone