Abstract
The long-term effects of perinatal Δ 9-tetrahydrocannabinol (Δ 9-THC) exposure – from gestational day (GD) 15 to postnatal day (PND) 9 – on hippocampal glutamatergic neurotransmission were studied in slices from the 40-day-old offspring of Δ 9-THC exposed (Δ 9-THC-rats) and vehicle-exposed (control) dams. Basal and in K+-evoked endogenous hippocampal glutamate outflow were both significantly decreased in Δ 9-THC-rats. The effect of short Δ 9-THC exposure (0.1 μM) on K +-evoked glutamate release disclosed a loss of the stimulatory effect of Δ 9-THC on hippocampal glutamate release in Δ 9-THC-rats, but not in controls. In addition, l-[ 3H]-glutamate uptake was significantly lower in hippocampal slices from Δ 9-THC-rats, where a significant decrease in glutamate transporter 1 (GLT1) and glutamate/aspartate transporter (GLAST) protein was also detected. Collectively, these data demonstrate that perinatal exposure to cannabinoids induces long-term impairment in hippocampal glutamatergic neurotransmission that persist into adolescence.
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