Developmental differences in neural damage following trimethyl-tin as demonstrated with GFAP immunohistochemistry.

Abstract

Long-Evans rat pups received intraperitoneal (i.p.) injections of trimethyl-tin (TMT) 6 mg/kg hydroxide or saline on postnatal day (PND) 10 or PND 18 and were sacrificed for immunohistochemical staining for glial fibrillary acidic protein (GFAP) on PND 12, 18, 20, or 25. After dosing with TMT on PND 10 there was a transient increase in GFAP immunoreactivity (IR) in the amygdala, piriform, and entorhinal cortex 2 days post-dosing (PND 12) and a persistent increase in GFAP IR in the hippocampus and cingulate cortex up to two weeks post-dosing. Following dosing with TMT on PND 18 there was a delayed (PND 25) increase in GFAP IR in the amygdala, hippocampus, cingulate, piriform, and entorhinal cortex. In addition, increases in GFAP IR were observed in the neocortex 7 days post-dosing, which was not observed following earlier postnatal dosing. The regions in which gliosis and loss of Nissl-staining were consistent for the different time points of TMT treatment were the amygdala, hippocampus, cingulate, piriform, and entorhinal cortex. The present findings indicate the GFAP immunohistochemistry can be used to reveal regional effects of developmental neurotoxicant exposure during early stages of development.