{Reference Type}: Journal Article
{Title}: Pituitary adenylate cyclase-activating polypeptide deficient mice show length abnormalities of the axon initial segment.
{Author}: Iwahashi M;Yoshimura T;Harigai W;Takuma K;Hashimoto H;Katayama T;Hayata-Takano A;
{Journal}: J Pharmacol Sci
{Volume}: 153
{Issue}: 3
{Year}: 2023 Nov
{Factor}: 3.578
{DOI}: 10.1016/j.jphs.2023.08.006
{Abstract}: We previously found that pituitary adenylate cyclase-activating polypeptide (PACAP)-deficient (PACAP-/-) mice exhibit dendritic spine morphology impairment and neurodevelopmental disorder (NDD)-like behaviors such as hyperactivity, increased novelty-seeking behavior, and deficient pre-pulse inhibition. Recent studies have indicated that rodent models of NDDs (e.g., attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder) show abnormalities in the axon initial segment (AIS). Here, we revealed that PACAP-/- mice exhibited a longer AIS length in layer 2/3 pyramidal neurons of the primary somatosensory barrel field compared with wild-type control mice. Further, we previously showed that a single injection of atomoxetine, an ADHD drug, improved hyperactivity in PACAP-/- mice. In this study, we found that repeated treatments of atomoxetine significantly improved AIS abnormality along with hyperactivity in PACAP-/- mice. These results suggest that AIS abnormalities are associated with NDDs-like behaviors in PACAP-/- mice. Thus, improvement in AIS abnormalities will be a novel drug therapy for NDDs.