Shin-ichi Muramatsu

TL;DR: The neuronal mechanism of dyskinesia of the contralateral forelimb produced by microinjection of picrotoxin into the caudoputaminal unit (CPU) was analyzed electrophysiologically and it is proposed that the primary origin of the dyskinisia is the CPU and that the inhibitory CPU efferent, as well as the nigrothalamic, pathway plays a basic role in the manifestation of the Dyskineia.

TL;DR: Results indicate that Shati/Nat8l in the NAc, but not in the dS, plays an important suppressive role in the behavioral responses to METH by controlling the dopaminergic system via activation of group II mGluRs.

TL;DR: An AADC deficient mouse model is generated, in which compensatory regulation allowed the mice to survive to adulthood and will be useful both for developing gene therapies for A ADC deficiency and for designing treatments for diseases associated with neurotransmitter deficiency.

TL;DR: Pathological hyperechogenic alterations in the SN in patients with iRBD may suggest the existence of preclinical SN dysfunction as determined by FMT-PET.

TL;DR: The findings suggest that TDP-43 regulates cellular exocytosis mediated by L-type voltage-dependent calcium channels and thus plays an important role in the early phase of insulin secretion by pancreatic islets, and is implicated in not only the selective loss of motor neurons but also in glucose intolerance due to impaired insulin secretion at an early stage of ALS.