Ketamine and amphetamine both enhance synaptic transmission in the amygdala-nucleus accumbens pathway but with different time-courses

Excitatory glutamatergic fibers from limbic structures, such as the hippocampus and the basolateral amygdala, are known to converge on the same neurons in the nucleus accumbens. We have recently shown that ketamine, at a dose (25 mg/kg) that produces psychosis-like behaviors in rats, decreases glutamatergic transmission between the hippocampus and the nucleus accumbens. Here we investigated whether ketamine also affects glutamatergic transmission between the basolateral amygdala and the nucleus accumbens. We also studied the effects of amphetamine (1.5 mg/kg), known to evoke psychosis-like behaviors in rats. We found that each drug produced a long-lasting (at least 30 min) potentiation of synaptic efficacy in the projection from the basolateral amygdala to the nucleus accumbens. However, while this synaptic potentiation developed shortly after ketamine injection (within 4 min), it occurred after a 30-min delay in rats injected with amphetamine. These data reveal, in freely behaving rats, that ketamine has a more rapid and powerful effect on projection targets of the basolateral amygdala than does amphetamine.