Recently, cannabinoids have been implicated in a variety of positive brain developmental processes but at the same time have been thought to be associated with deleterious effects after acute exogenous exposure. In humans, maternal use of Cannibis sativa (marijuana) during pregnancy is associated with cognitive deficits in the offspring (1). In animals, deficits in glutamatergic transmission, abnormal learning in adulthood, and apoptosis in developing brain have been described with exogenous exposure (2–4). Like many systems that have been implicated in this type of duality (glutamatergic systems, e.g.), these compounds may behave differently in physiologic and endogenously derived circumstances, but when administered exogenously during critical periods, may result in adverse effects.

The endocannabinoids, anandamide (AEA) and 2-arachidonoylglycerol (2-AG), are arachadonic acid derivatives that signal through Gi-protein coupled receptors, mainly CB1 and CB2. They are important modulators of a variety of CNS developmental functions including synaptic transmission, neurogenesis, migration and proliferation (5). Complex physiologic functions such as control of movement, appetite, thermoregulation, nociception, motivation and memory are assumed to be modulated by these compounds (6). The CB1 receptors are found on neurons and are responsible for the psychoactive properties attributed to these compounds while the CB2 receptors are found primarily on lymphoid cells but are also seen on brain endothelial cells and glia. Acting through the CB2 receptor, endocannabinoids may be immunomodulatory with effects both within and outside of the CNS (7).

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