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Potential mechanisms for phencyclidine/ketamine-induced brain structural alterations and behavioral consequences
Cheng Wang1, Amy Inselman2, Shuliang Liu1
1Division of Neurotoxicology, National Center for Toxicological Research/U.S. Food & Drug Administration, Jefferson, AR, United States.
Neurotoxicology
|December 9, 2019
Summary
Recreational drugs like PCP and ketamine may harm the central nervous system (CNS) by disrupting glutamate neurotransmission and reducing polysialic acid neural cell adhesion molecule (PSA-NCAM) levels, potentially leading to addiction.
Area of Science:
- Neuroscience
- Neuropharmacology
- Developmental Neuroscience
Background:
- Recreational drug use (PCP, ketamine) is linked to CNS structural abnormalities.
- These drugs interfere with neurotransmission, particularly glutamate.
- This may cause neuronal loss, synaptic changes, and disrupted neural networks.
Purpose of the Study:
- To review the relationship between PCP/ketamine-induced cortical neuron loss and reduced striatal polysialic acid neural cell adhesion molecule (PSA-NCAM).
- To explore changes in striatal synaptogenesis during development.
- To discuss PSA-NCAM regulation and its role in synaptic protein expression.
Main Methods:
- Literature review of preclinical and clinical studies.
- Analysis of neurobiological mechanisms underlying drug-induced neurotoxicity.
- Examination of the role of PSA-NCAM in neural development and plasticity.
Main Results:
- PCP/ketamine may reduce cortical neurons and striatal PSA-NCAM levels.
- This reduction can compromise subcortical area development, including the nucleus accumbens.
- Disrupted cortico-striatal communication and synaptogenesis are implicated.
Conclusions:
- PCP/ketamine-induced neurotoxicity affects cortico-striatal pathways.
- Reduced PSA-NCAM may impair synaptogenesis and contribute to addiction.
- Interruption of neural communication underlies drug-induced behavioral changes.
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