Schizophrenia (SCZ) is a complex neuropsychiatric disorder marked by significant disruptions in brain function, including dopamine (DA) dysregulation in the ventral tegmental area (VTA), which is driven by hyperexcitability in the ventral hippocampus (vHipp). Current antipsychotic treatments primarily address positive symptoms of SCZ, but are limited in reducing vHipp hyperexcitability. Phosphodiesterase 10A (PDE10A) inhibition has emerged as a novel therapeutic strategy to treat multiple symptom classes of SCZ. Our study examines the effects of THPP-1, a PDE10A inhibitor, on DA dysregulation and vHipp activity in rats. This is investigated using a well-established neurodevelopmental rodent model of SCZ induced by prenatal exposure to methylazoxymethanol acetate (MAM) injection on gestational day 17 (20 mg/kg, i.p). Adult male offspring of pregnant MAM-treated or Saline-treated rats were administered acute (3 mg/kg, i.p.) doses of THPP-1. Electrophysiological recordings were used to assess changes in DA neuron activity in the VTA and pyramidal neuron activity in the vHipp. Our findings indicate that acute THPP-1 administration reduced the abnormal, elevated number of spontaneously active DA neurons only in MAM-offspring rats (p<0.05, F_1,24=9.2, two-way ANOVA) without affecting the average firing rate and spikes in burst of DA neurons (p>0.05, Kruskal-Wallis). The saline-offspring rats were unaffected by THPP-1 treatment in all measures. In the vHipp, THPP-1 did not alter the number of spontaneously active pyramidal neurons (p>0.05, two-way ANOVA) and spikes in burst (p>0.05, Kruskal-Wallis). THPP-1 was also unable to decrease the enhanced firing rate of pyramidal neurons observed in MAM rats (p>0.05, Kruskal-Wallis). Our results demonstrate that THPP-1, a PDE10A inhibitor, normalizes the hyperdopaminergic state in the MAM phenotype but does not normalize vHipp hyperexcitability. Therefore, THPP-1 may modulate a different brain circuit to mitigate the VTA hyperdopaminergic state in the MAM model of SCZ.