講演者：Dr. Yutaka Yoshida
Assistant Professor
Division of Developmental Biology, Cincinnati Children's Hospital Medical Center
タイトル：Neural circuit formation in corticospinal motor systems
日時：2014年10月21日（火） 17:00〜
場所：大阪大学 吹田キャンパス ナノバイオロジー棟 3階セミナー室
要旨：
【要旨】 Corticospinal neurons, connecting between the sensorimotor cortex and the spinal cord, are the key conveyers of motor instructions controlling voluntary movement. Despite their critical roles in motor controls, little is known about how corticospinal circuits are formed during development. In my presentation, I would like to introduce the following two projects.
1) "How do corticospinal neurons elaborate specific neural circuits to control different groups of muscles?" To examine the patterns of corticospinal connections with groups of spinal motor neurons supplying functionally related (synergistic or antagonistic) muscles, we use trans-synaptic retrograde pseudorabies viruses (PRVs) in mice. Following intramuscular injection, PRVs are retrogradely transported from the muscle to the sensorimotor cortex. Our preliminary data using two colors of PRVs reveal that synaptic refinement of cortico-muscle circuitry during adolescence involves only corticospinal neurons that connect with antagonistic muscle pairs. We further find that non-apoptotic Bax/Bak1-caspase pathway is required for the synaptic refinement. Moreover, defects in synaptic refinement of antagonistic cortico-muscle circuitry in the absence of Bax/Bak1-caspase pathway cause impaired skilled movements. Thus, our data suggest that Bax/Bak1-caspase pathway-mediated synaptic refinement of cortico-muscle circuits is required for skilled movements.
2) "How does Sema6D-PlexA1 signaling-mediated synapse elimination contribute to formation and function of corticospinal circuits?" We find that during early postnatal development, corticospinal axons transiently form synapses with spinal neurons, and these synapses are eliminated by postnatal day 14. However, these synapses are not eliminated in mice lacking the receptor PlexA1. Moreover, PlexA1 mutants exhibit disrupted skilled movements. Therefore, appropriate corticospinal circuits and skilled motor behavior require proper corticospinal synapse elimination regulated by Sema6D-PlexA1 signaling.
Assistant Professor
Division of Developmental Biology, Cincinnati Children's Hospital Medical Center
タイトル：Neural circuit formation in corticospinal motor systems
日時：2014年10月21日（火） 17:00〜
場所：大阪大学 吹田キャンパス ナノバイオロジー棟 3階セミナー室
要旨：
【要旨】 Corticospinal neurons, connecting between the sensorimotor cortex and the spinal cord, are the key conveyers of motor instructions controlling voluntary movement. Despite their critical roles in motor controls, little is known about how corticospinal circuits are formed during development. In my presentation, I would like to introduce the following two projects.
1) "How do corticospinal neurons elaborate specific neural circuits to control different groups of muscles?" To examine the patterns of corticospinal connections with groups of spinal motor neurons supplying functionally related (synergistic or antagonistic) muscles, we use trans-synaptic retrograde pseudorabies viruses (PRVs) in mice. Following intramuscular injection, PRVs are retrogradely transported from the muscle to the sensorimotor cortex. Our preliminary data using two colors of PRVs reveal that synaptic refinement of cortico-muscle circuitry during adolescence involves only corticospinal neurons that connect with antagonistic muscle pairs. We further find that non-apoptotic Bax/Bak1-caspase pathway is required for the synaptic refinement. Moreover, defects in synaptic refinement of antagonistic cortico-muscle circuitry in the absence of Bax/Bak1-caspase pathway cause impaired skilled movements. Thus, our data suggest that Bax/Bak1-caspase pathway-mediated synaptic refinement of cortico-muscle circuits is required for skilled movements.
2) "How does Sema6D-PlexA1 signaling-mediated synapse elimination contribute to formation and function of corticospinal circuits?" We find that during early postnatal development, corticospinal axons transiently form synapses with spinal neurons, and these synapses are eliminated by postnatal day 14. However, these synapses are not eliminated in mice lacking the receptor PlexA1. Moreover, PlexA1 mutants exhibit disrupted skilled movements. Therefore, appropriate corticospinal circuits and skilled motor behavior require proper corticospinal synapse elimination regulated by Sema6D-PlexA1 signaling.