Mice homozygous for the phosphodiesterase 10A (PDE10A) targeted mutation are viable and fertile with no gross abnormalities, although breeding homozygotes together produces reduced liter sizes. The targeted gene generates a truncated transcript. A small amount of functionally inactive protein is detected in striatum, cortex and cerebellum. Homozygous mice on the C57BL/6N genetic background (PDE10AC57) exhibit multiple behavioral abnormalities; decreased locomotor activity when placed in a novel environment, delayed acquisition of conditioned avoidance response, blunted response to the NMDA receptor antagonist MK-801 (but not PCP), altered locomotor responses to both amphetamine and methamphetamine, and increased striatal dopamine utilization. These PDE10AC57 mutant mice may be useful in neurobiological studies including metabolic inactivation of intracellular signal transduction pathways by cyclic phosphodiesterases (PDEs), regulation of information processing by basal ganglia circuitry, and striatal hypofunction or psychotic disease.

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These PDE10AC57 mutant mice are deficient in phosphodiesterase 10A activity, and may be useful in neurobiological studies including metabolic inactivation of intracellular signal transduction pathways by cyclic phosphodiesterases (PDEs), regulation of information processing by basal ganglia circuitry, and striatal hypofunction or psychotic disease.

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