Hitoshi Komuro

Stage-specific control of neuronal migration by somatostatin.

Intrinsic program for migration of cerebellar granule cells in vitro.

Cellular and molecular mechanisms of cerebellar granule cell migration.

Completion of neuronal migration regulated by loss of Ca(2+) transients.

Ca2+ transients control CNS neuronal migration.

Reversal of neuronal migration in a mouse model of fetal alcohol syndrome by controlling second-messenger signalings.

Glutamate stimulates oligodendrocyte progenitor migration mediated via an alphav integrin/myelin proteolipid protein complex.

How does alcohol impair neuronal migration?

Neurotrophic effects of PACAP in the cerebellar cortex.

Cerebellar granule cell migration and the effects of alcohol.

Autonomous turning of cerebellar granule cells in vitro by intrinsic programs.

Four distinct phases of basket/stellate cell migration after entering their final destination (the molecular layer) in the developing cerebellum.

Role of PACAP in controlling granule cell migration.

Demyelination increases axonal stationary mitochondrial size and the speed of axonal mitochondrial transport.

Myelination and axonal electrical activity modulate the distribution and motility of mitochondria at CNS nodes of Ranvier.

Pituitary adenylate cyclase-activating polypeptide (PACAP) stimulates the expression and the release of tissue plasminogen activator (tPA) in neuronal cells: involvement of tPA in the neuroprotective effect of PACAP.

Light stimuli control neuronal migration by altering of insulin-like growth factor 1 (IGF-1) signaling.

Rescue of neuronal migration deficits in a mouse model of fetal Minamata disease by increasing neuronal Ca2+ spike frequency.

Cortical-layer-specific effects of PACAP and tPA on interneuron migration during post-natal development of the cerebellum.

Mitochondrial immobilization mediated by syntaphilin facilitates survival of demyelinated axons.

The role of calcium and cyclic nucleotide signaling in cerebellar granule cell migration under normal and pathological conditions.

Mitochondrial fission augments capsaicin-induced axonal degeneration.