Chronological alterations of calbindin D-28k immunoreactivity in the gerbil main olfactory bulb after ischemic insult

• Published in: Brain research 2003-05, Vol.971 (2), p.250-254
• Main Authors: Hwang, In Koo, Kang, Tae-Cheon, Lee, Jae Chul, Park, Seung-Kook, An, Sung Jin, Lee, In Se, Lee, Yoon-Bok, Sohn, Heon-Soo, Kang, Jung Hoon, Choi, Soo Young, Won, Moo Ho
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Brain Ischemia - metabolism; Calbindin D-28k; Calbindins; Cell damage; Disease Models, Animal; Gerbil; Gerbillinae; Immunohistochemistry; Immunohistochemistry - methods; Main olfactory bulb; Male; Medical sciences; Neurology; Olfactory Bulb - metabolism; Olfactory Bulb - pathology; Reperfusion Injury - metabolism; Reperfusion Injury - pathology; S100 Calcium Binding Protein G - metabolism; Time Factors; Transient forebrain ischemia; Vascular diseases and vascular malformations of the nervous system
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(03)02480-6

We investigated spatial and temporal alterations of calbindin D-28k (CB) immunoreactivity in the gerbil main olfactory bulb after transient ischemia–reperfusion. In sham-operated animals, CB-immunoreactive (IR) neurons were found in the periglomerular layer, external plexiform layer and granule cell layer. At 1–4 days after ischemic insult, the number of CB-IR neurons significantly increased. This result suggests that the increased CB may buffer the intracellular calcium at an early time point after the ischemic insult. In contrast, 10–30 days after the ischemic insult, the number of CB-IR neurons significantly decreased as compared to sham-operated animals. This result suggests that a malfunction in olfactory process may have occurred in the olfactory bulb at a later time point after the ischemic insult.