Abstract
Glutamatergic neurotransmission is critical both for neurogenesis and mature functioning of the central nervous system (CNS), and is thought to be one target for toluene-induced damage. It has been reported that toluene antagonizes the function of N-methyl-D-aspartate (NMDA) receptor. In this study, we examined the effect that neonatal toluene exposure has on NMDA receptor in cerebellar granule neurons. Sprague-Dawley rats were treated with 0, 200, 500, and 1000 mg/kg of toluene by intraperitoneal injection from postnatal day (PN) 4 to 7. After culture under toluene-free condition, Ca2+ signaling in response to glutamate and NMDA was measured using fura-2 Ca2+ imaging for up to 14 days. Toluene exposure dose-dependently reduced glutamate/glycine and NMDA/glycine induced Ca2+ signaling in culture cerebellar granule neurons at DIV5 (day in vitro), and the effects were gradually recovered. The effects of toluene exposure on NMDA-stimulated Ca2+ signals in response to NMDA receptor inhibitors were also compared. The results indicated that neonatal toluene exposure can induce long-term but reversible changes in NMDA-induced Ca2+ signaling pathway. Such changes could be involved in the impairment of CNS function and development observed in fetal solvent syndrome.
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