- Prenatal cocaine exposure attenuates cocaine-conditioned place preference, implicating disrupted spatial memory and altered drug reward processing.
- PCE impairs long-term synaptic plasticity in the dorsal hippocampus, producing spatial memory deficits that drive CPP attenuation.
- Ventral hippocampal plasticity is largely spared; acute cocaine increases presynaptic plasticity regardless of prenatal history.
Brain Res. 2026 Nov 6:150628. doi: 10.1016/j.brainres.2026.150628. Online ahead of print.
ABSTRACT
Prenatal cocaine exposure (PCE) severely affects brain development, psychology, and behavior in exposed offspring, while altering their susceptibility to drug addiction. however, the mechanisms underlying PCE-induced changes in cocaine-conditioned place preference (CPP) remain unclear. This study demonstrates that PCE attenuates cocaine-induced CPP, a process involving spatial memory and drug reward. We also investigated the dorsal hippocampus (dH), which is closely associated with spatial memory, and the ventral hippocampus (vH), which is linked to motivational reward mechanisms. Results indicate that PCE impairs long-term synaptic plasticity in the dH, suggesting that spatial memory deficits contribute to the attenuation of CPP. In contrast, PCE did not significantly inhibit synaptic plasticity in the vH, indicating that while the vH contributes to addiction susceptibility, it is less affected by prenatal exposure. Notably, acute cocaine exposure increased presynaptic plasticity in the vH regardless of prenatal history. These findings suggest that synaptic impairment in the dH drives spatial memory deficits in PCE offspring, while the vH retains sensitivity to acute drug challenge. This study elucidates the cellular mechanisms underlying PCE-induced cognitive changes and guides future molecular investigations.
PMID:42994772 | DOI:10.1016/j.brainres.2026.150628
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