Although the etiology of neurodevelopmental mental disorders remains obscure, 
converging lines of evidence using animal modeling suggest a critical role for 
activity-dependent neurodevelopmental processes during neonatal life. Here, we 
report the behavioral effects of a novel technique designed to induce targeted, 
transient disruption of activity-dependent processes in early development via 
reduction of calcium-mediated neurotransmitter release. We examined the 
post-pubertal behavioral effects of neonatal (postnatal day 7) medial prefrontal 
cortex infusion of either vehicle or N-type and P/Q-type presynaptic 
voltage-dependent calcium channel blockers (omega-conotoxins MVIIA and MVIIC 
respectively; 6.8 and 45 pmol infused respectively) in rat pups. In a test of 
amphetamine-induced behavioral sensitization, neonatal omega-conotoxin MVIIA 
treatment significantly increased locomotion following repeated amphetamine 
injections (1.5 mg/kg i.p.) and significantly decreased locomotion following 
repeated saline injections relative to animals treated neonatally with vehicle. 
However, there was no effect of conotoxin treatment on the long-term expression 
of amphetamine sensitization. Neonatal treatment with omega-conotoxins had no 
effect on the other behaviors assayed, namely, acoustic startle response, 
prepulse inhibition of startle, novelty- and amphetamine-induced (1.5 mg/kg 
i.p.) locomotion, and anxiety-like behavior in the elevated plus-maze. These 
data confirm that transient, region-specific disruption of synaptic transmission 
during early development can have long-term effects on behaviors relevant to 
neurodevelopmental mental disorders.