Effects of Prenatal Exposure to Methamphetamine on the Development of the Rat Retina

Abstract

In recent years there has been growing use of methamphetamine (METH) by pregnant women, resulting in an increasing number of children exposed prenatally to this drug of abuse. METH is known to be potentially neurotoxic to human adults, but there is minimal information with respect to the consequences of such exposure to the fetus. The purpose of this study was to ascertain external parameters of animal development, as well as neurochemical and immunohistochemical alterations at three key points of retinal development (postnatal day [PND] 7, 14, and 30). Rats of the Wistar strain were used in this experimental model. Pregnant females received a dose of 5 mg/kg body weight per day of METH-HCl in 0.9% saline, from gestational day (GD) 8 to 22. The control group to be used was pair fed and saline injected. Litters were randomly culled at PND 1 to 8 pups. Analysis of maternal body weight gain during pregnancy showed that females treated with METH had lower body weights than control-treated females. The body weight on PND 1, showed that animals treated with METH prenatally had smaller body weights than the control-treated animals and also that females weighed less than males. Prenatal exposure to METH did not alter the retinal levels of 3,4-dihydroxyphenylacetic acid (DOPAC) in the male group and the level of dopamine (DA) in both female and male groups when compared with their respective pair fed control groups during the first month of life. Correlating with the neurochemical data, no obvious changes on the localization of TH immunoreactivity in the rat retina at PND 7, 14, and 30 could be detected between control and METH-treated animals. Thus, exposure to METH disrupted this pattern in a gender-dependent manner. These data confirm previous observation that developing rats are protected against the adult type of METH-induced neurotoxicity. Therefore, conventional markers used for adult animals appear to be unsatisfactory to demarcate boundaries of the PND 1 to 30 critical periods.