Key result
PDE2A haploinsufficiency in mice increased exploratory behavior and was associated with upregulated nNOS expression in the striatum.
Why the study?
Neurological and neurochemical effects of PDE2A deficiency are poorly understood.
PDE2A haploinsufficiency in mice increases exploratory behavior and is associated with upregulated nNOS/NO/cGMP signaling in the striatum.
Answers are grounded in this paper and cite their sources.
PDE2A haploinsufficiency may alter exploratory behavior in mice; leaves open relevance to human neuropsychiatric disorders.
Phosphodiesterase 2 A (PDE2A) function is stimulated by cGMP to catabolize cAMP. However, neurological and neurochemical effects of PDE2A deficiency are poorly understood. To address this gap, we studied behavioral characteristics and cerebral morpho-chemical changes of adult male heterozygous C57BL/6-PDE2A+/- (HET), and wild type C57BL/6-PDE2A+/+ (WT) mice. Behavioral functions of mice were evaluated by a wide test battery. HET mice exhibited greater tendency to explore novel environments in comparison to WT mice, but spatial working memory, anxiety, and sociability were similar in adult HET and WT mice. In HET mice, PDE2A mRNA, PDE2A protein expression, and cGMP hydrolyzing enzymatic activity were consistently reduced by about 50 %. Consequently, the cyclic nucleotide levels were significantly increased in HET mice, but unexpectedly the mean percentage variation was higher for cGMP equal to 153.23 %, and lower for cAMP equal to 16.41 %. Therefore, to try to explain the preponderant increase of cGMP to cAMP we evaluated other PDE enzymes functionally related to PDE2A. Surprisingly, results were quite contradictory: in HET mice protein levels of the other dual-specificity enzyme PDE3A and PDE10A were reduced, whereas the expressions of PDE5A and PDE9A that selectively hydrolyze cGMP were increased. Therefore, we investigated the involvement of neuronal nitric oxide synthase (nNOS) expression, as determinant of a possible increased synthesis of NO/cGMP signaling. Interestingly, in HET mice the expression level of brain nNOS, measured by western blot and immune-histochemistry was significantly increased, particularly in interneurons from the striatum. In conclusion, the deficiency of PDE2A could be compensated in the striatum by upregulating nNOS/NO/cGMP pathway, which in turn likely upregulates PDE2A-dependent cAMP hydrolysis. The neuroanatomical correlation between striatal nNOS upregulation and the behavioral phenotype of increased exploratory behavior in HET mice is advanced.
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Rêgo et al. (2024) studied this question. PDE2A haploinsufficiency vs. Wild type (WT) mice was evaluated on Behavioral characteristics and cerebral morpho-chemical changes. PDE2A haploinsufficiency in mice increased exploratory behavior and was associated with upregulated nNOS expression in the striatum.
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