Cell adhesion molecule contactin‐associated protein 3 is expressed in the mouse basal ganglia during early postnatal stages

Hirata, Haruna; Umemori, Juzoh; Yoshioka, Hiroki; Koide, Tsuyoshi; Watanabe, Kazutada; Shimoda, Yasushi

doi:10.1002/jnr.23670

Cited by 10 publications

(12 citation statements)

References 42 publications

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“…Caspr3 is highly expressed in postnatal developmental stages in the basal ganglia, such as the striatum, nucleus accumbens, external segment of the globus pallidus, and substantia nigra [ 12 ]. In postnatal stages, cell adhesion molecules play important roles in developmental events such as myelinations and synaptogenesis throughout the brain [ 5 – 7 , 25 – 27 ].…”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that neural maturation was observed for morphological and physiological characteristics in the striatum during the second postnatal week [ 28 – 31 ]. Although Nissl staining in histological analyses showed that Caspr3 KO mice have normal morphological structures in the basal ganglia [ 12 ], it is possible that undetectable changes in neural maturation might be caused by the lack of Caspr3 during postnatal development. Given that the protein product CASPR3 is localized in striatonigral fibers [ 12 ], it will be important to determine whether Caspr3 KO mice have normal circuit formation in the basal ganglia.…”

Section: Discussionmentioning

confidence: 99%

“…Collectively, these reports suggest that Caspr3 is associated with the transportation of NR2B, contributing to motor learning in the rotarod task. However, it remains unclear whether Caspr3 is localized in the synapses, even though punctate signals from Caspr3 were detected throughout the basal ganglia, cortex, and hippocampus [ 12 ]. Caspr3-positive signals did not overlap with presynaptic markers such as VGluT1, VGAT, and GAD67, in these brain regions on postnatal day 7, although this is still early in the process of synaptogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…We previously generated Caspr3-knockout (KO) mice and monoclonal antibodies against Caspr3, and have reported that Caspr3 is expressed abundantly between the first and second postnatal weeks in mouse basal ganglia, including the striatum, external segment of the globus pallidus, subthalamic nucleus, and substantia nigra [ 12 ]. In the striatum, the primary input nucleus of the basal ganglia, Caspr3 was shown to be expressed in cholinergic interneurons and a subpopulation of striatal projection neurons.…”

Section: Introductionmentioning

confidence: 99%

“…In the striatum, the primary input nucleus of the basal ganglia, Caspr3 was shown to be expressed in cholinergic interneurons and a subpopulation of striatal projection neurons. However, Caspr3 KO mice have no gross abnormalities in the basal ganglia, as shown by Nissl staining [ 12 ]. Given that the basal ganglia have very complicated structures and are involved in motor control and learning, their dysfunction causes movement disorders such as Parkinson’s disease, Huntington’s disease, attention deficit hyperactivity disorder, and hemiballism [ 13 – 16 ].…”

Section: Introductionmentioning

confidence: 99%

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Caspr3-Deficient Mice Exhibit Low Motor Learning during the Early Phase of the Accelerated Rotarod Task

et al. 2016

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Caspr3 (Contactin-associated protein-like 3, Cntnap3) is a neural cell adhesion molecule belonging to the Caspr family. We have recently shown that Caspr3 is expressed abundantly between the first and second postnatal weeks in the mouse basal ganglia, including the striatum, external segment of the globus pallidus, subthalamic nucleus, and substantia nigra. However, its physiological role remains largely unknown. In this study, we conducted a series of behavioral analyses on Capsr3-knockout (KO) mice and equivalent wild-type (WT) mice to investigate the role of Caspr3 in brain function. No significant differences were observed in most behavioral traits between Caspr3-KO and WT mice, but we found that Caspr3-KO mice performed poorly during the early phase of the accelerated rotarod task in which latency to falling off a rod rotating with increasing velocity was examined. In the late phase, the performance of the Caspr3-KO mice caught up to the level of WT mice, suggesting that the deletion of Caspr3 caused a delay in motor learning. We then examined changes in neural activity after training on the accelerated rotarod by conducting immunohistochemistry using antibody to c-Fos, an indirect marker for neuronal activity. Experience of the accelerated rotarod task caused increases in the number of c-Fos-positive cells in the dorsal striatum, cerebellum, and motor cortex in both Caspr3-KO and WT mice, but the number of c-Fos-positive cells was significantly lower in the dorsal striatum of Caspr3-KO mice than in that of WT mice. The expression of c-Fos in the ventral striatum of Caspr3-KO and WT mice was not altered by the training. Our findings suggest that reduced activation of neural cells in the dorsal striatum in Caspr3-KO mice leads to a decline in motor learning in the accelerated rotarod task.

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