(−) Deprenyl Attenuates Aluminium Induced Neurotoxicity in Primary Cortical Cultures

Abstract

The role of (−) deprenyl in offering neuroprotection to cortical neurons exposed to Aluminium chloride (AlCl₃) was examined. Primary cortical cultures derived from newborn rats were exposed to AlCl₃on 6th dayin vitro, at 100, 200, 400, 600, 800 and 1000 μM concentrations of AlCl₃. After 48 h of AlCl₃exposure, many nerve cell bodies were swollen; a beading of neurites and a disruption of the neuritic network were also observed suggesting neurodegeneration. Lactate dehydrogenase (LDH) efflux increased in a dose-dependent manner (59–120%). (−) Deprenyl co-exposure at concentrations of 10⁻⁷, 10⁻⁸and 10⁻⁹M significantly attenuated both the morphological alterations and the LDH efflux induced by AlCl₃. Thisin vitrostudy has demonstrated that (−) deprenyl can protect neurons from aluminium induced neurotoxicity.