Changes in brain catecholamine mechanisms following perinatal exposure to marihuana.

Adult female rats received daily oral doses of a crude marihuana extract (CME; equivalent to 20 mg/kg delta 9-THC) throughout gestation and lactation. The offspring were sacrificed at 10, 20, 40 or 60 days postpartum and tissue samples of cerebral cortex and striatum were dissected and assayed for alpha 1-adrenergic and D2-dopaminergic receptors, respectively, and tyrosine hydroxylase activity. The body weight at birth and 10 days of age was reduced as was brain weight at 10 and 60 days of age in offspring exposed to CME. Perinatal exposure to CME reduced the binding capacity (Bmax) of D2 receptors in the striatum of 10 and 20-day-old offspring. The Bmax for alpha 1 receptors in the cerebral cortex was not altered at any age. Tyrosine hydroxylase activity was significantly decreased in the striatum of 20 and 40-day-old offspring exposed to CME. The results indicate that chronic perinatal exposure to CME can selectively alter the development of specific catecholamine mechanisms in rat brain.