Disruption of PPI is observed in schizophrenia patients and can be pharmacologically induced in rodents, making it a critical translational endpoint for antipsychotic drug screening.

What you will find in this case study:

MK-801-Induced PPI Deficits

The study evaluates PPI disruption following MK-801 treatment in Sprague-Dawley rats, a widely used NMDA receptor antagonist model that mirrors glutamatergic dysfunction in schizophrenia. Data are presented comparing PPI levels between control and MK-801-treated groups, illustrating the magnitude of sensorimotor gating impairment.

Amphetamine-Induced PPI Deficits

As a complementary model, the study examines PPI disruption induced by amphetamine, a dopamine-releasing agent that models the hyperdopaminergic state associated with psychotic symptoms. The results highlight the reduction in PPI following amphetamine administration, providing a clear reference for evaluating dopaminergic-targeting compounds.

Translational Relevance

By using two mechanistically distinct acute models (glutamatergic and dopaminergic), the case study demonstrates how PPI can be leveraged to assess candidate antipsychotics across different pathological pathways, supporting more comprehensive efficacy profiling.

Experimental Design & Key Endpoints

The overview outlines the study design, including dosing regimens, timing of PPI testing, and the specific startle/PPI parameters analyzed, offering a transparent view of the model's reliability and reproducibility.

Whether you are developing novel antipsychotics, validating model systems, or seeking a reliable CRO partner to conduct PPI studies with rigorous quality control, this case study provides concrete evidence of Ace Therapeutics' expertise in acute schizophrenia models.

Download the full case study to review the complete data and explore how our preclinical models can support your CNS drug development programs.

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