Acute administration of delta (9)-tetrahydrocannabinol (THC), the major active compound in marijuana, also increases ERK phosphorylation in the dorsal striatum, in ways that parallel effects of stimulants. Unlike stimulants, THC increases ERK phosphorylation in the cerebellum as well.24,25 ERK phosphorylation is also increased by acute administration of opiates. Morphine increases p-ERK in the VTA18 and cerebral cortex.26 In general, stimulants, cannabinoids, and opiates increase p-ERK levels in a distinctive pattern that includes the NAc, lateral bed nucleus of the stria terminalis, central amygdala, and deep layers of the prefrontal cortex.14 Inhibition of MEK prevents these drug-induced increases in p-ERK.20,25
