Aquaporin 9 changes in pyramidal cells before and is expressed in astrocytes after delayed neuronal death in the ischemic hippocampal CA1 region of the gerbil

✍ Scribed by In Koo Hwang; Ki-Yeon Yoo; Hua Li; Bong-Hee Lee; Hong-Won Suh; Young-Guen Kwon; Moo Ho Won

• Publisher: John Wiley and Sons
• Year: 2007
• Tongue: English
• Weight: 781 KB
• Volume: 85
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.21381

✦ Synopsis

Abstract

In the present study, we observed changes of aquaporin 9 (AQP9) in the hippocampus induced by 5 min of ischemia in gerbils. In sham‐operated animals, weak AQP9 immunoreactivity was detected in the stratum pyramidale of the hippocampus. AQP9 immunoreactivity, and its protein level in the CA1 region began to increase significantly at 6 hr and peaked 24 hr after ischemia. In the CA2/3 region, AQP9 immunoreactivity significantly increased at 12 hr after ischemia. Thereafter, AQP9 immunoreactivity in the hippocampus decreased continuously with time. From 4 days after ischemia, AQP9 immunoreactivity in the CA1 region was expressed and increased in glial components in the strata oriens and radiatum. Based on double‐immunofluorescence staining, many AQP9‐immunoreactive glial cells in the CA1 region were identified as astrocytes. In a reverse transcription‐polymerase chain reaction study, AQP9 mRNA levels significantly increased in the CA1 region at 6 hr after ischemia, and thereafter AQP9 mRNA levels decreased with time after ischemia. In addition, the water content in the gerbil hippocampus was highest 3 hr after ischemia/reperfusion; thereafter, water content in the ischemic hippocampus was higher than that in the sham‐operated group. This result shows how AQP9 in the gerbil hippocampus changes in neurons and is expressed in astrocytes before and after delayed neuronal death, respectively, after ischemia. These results indicate that changes in AQP9 in ischemic CA1 pyramidal cells may be related to delayed neuronal death and that the expression of AQP9 in astrocytes is related to gliosis in the CA1 region after transient forebrain ischemia. © 2007 Wiley‐Liss, Inc.