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Yoshio Hata

Publications and source records attributed to Yoshio Hata.

8 recordsLinked to original sources

Experience-driven axon retraction without binocular imbalance in developing visual cortex.

Refinement of the neural circuit during brain maturation is regulated by experience-driven neural activity. In the mammalian visual cortex, monocular visual deprivation (MD) in the early postnatal life causes a significant loss of cortical responses to a deprived eye and the retraction of input axons serving the deprived eye. A competitive interaction between inputs serving both eyes has been supposed to underlie the effects of MD because the loss of cortical response is much weaker when both eyes are deprived of vision. Also, the input axons do not retract after binocular deprivation. Here, we report that uncorrelated activity between presynaptic and postsynaptic neurons can solely lead to the retraction of geniculocortical axons in the absence of activity imbalance between two inputs. We analyzed the morphology of geniculocortical axons in a pharmacologically inhibited visual cortex of animals with normal vision and of binocularly deprived animals. In the normal vision animals, the axonal arbors in the inhibited cortex showed robust retraction. On the other hand, the arbors in binocularly deprived animals remained mostly intact. These results suggest that a homosynaptic associative mechanism, rather than a heterosynaptic competition between inputs, may play an important role in experience-driven axon retraction.

Animals↗

Substrate specificity of a chimera made from Xenopus SGLT1-like protein and rabbit SGLT1.

To characterize the sugar translocation pathway of Na(+)/glucose cotransporter type 1 (SGLT1), a chimera was made by substituting the extracellular loop between transmembrane domain (TM) 12 and TM13 of Xenopus SGLT1-like protein (xSGLT1L) with the homologous region of rabbit SGLT1. The chimera was expressed in Xenopus oocytes and its transport activity was measured by the two-microelectrode voltage-clamp method. The substrate specificity of the chimera was different from those of xSGLT1L and SGLT1. In addition the chimera's apparent Michaelis-Menten constant (K(m)) for myo-inositol, 0.06 mM, was about one fourth of that of xSGLT1L, 0.25 mM, while the chimera's apparent K(m) for d-glucose, 0.8 mM, was about one eighth of that of xSGLT1L, 6.3 mM. Our results suggest that the extracellular loop between TM12 and TM13 participates in the sugar transport of SGLT1.

Amino Acid Sequence↗

Recovery of binocular responses after brief monocular deprivation in kittens.

Monocular deprivation induces a rapid ocular dominance change in the developing visual cortex. The early phase of the change is supposed to be labile and stabilized later by consolidation processes. To test the stability of early ocular dominance change, we examined whether binocular responses of cortical neurons can recover after a brief monocular deprivation in anesthetized and paralyzed kittens in which ocular dominance plasticity does not operate. After the 24-h monocular deprivation, most cortical neurons lost their responses to the deprived eye. The deprived eye responses, however, recovered following 2-3 days interval under anesthetized and paralyzed conditions. Visual stimulation did not facilitate the recovery. These results suggest that the early phase of ocular dominance plasticity is labile and declines passively.

Anesthesia↗

[A case where herbal medicine sho-seiryu-to induced interstitial pneumonitis].

A 67-year-old man, treated for years for hypertension, presented with a persistent dry cough and dyspnea 10 days after the administration of drugs including Sho-seiryu-to against the common cold. Chest X-ray and CT scans revealed diffuse reticular shadows in both lung fields. Under a suspected diagnosis of drug-induced pneumonia or a complex of bacterial and interstitial pneumonia, Sho-seiryu-to was discontinued and antibiotics started. After several days, chest X-ray reticular shadows developed and hypoxia worsened. Subsequently the patient received Prednisolone. Two days later his symptoms and findings markedly improved. Drug lymphocyte stimulation tests for Sho-seiryu-to using peripheral lymphocyte were positive and other drugs were negative. Chest CT showed the reversed halo sign in right middle zone, which was relatively specific to the cryptogenic organizing pneumonia. On the basis of clinical history and these findings, we diagnosed a drug-induced interstitial pneumonia caused by the herbal medicine Sho-seiryu-to. To our knowledge, this is the first case of Sho-seiryu-to induced interstitial pneumonia to be reported.

Aged↗

Long-term depression is not induced by low-frequency stimulation in rat visual cortex in vivo: a possible preventing role of endogenous brain-derived neurotrophic factor.

Low-frequency stimulation (LFS) at 1 Hz for 15 min is an effective protocol to induce homosynaptic long-term depression (LTD) in visual cortical slices. It is reported that LFS becomes ineffective when brain-derived neurotrophic factor (BDNF) is applied to slices. It is not known, however, whether such a protocol induces LTD in visual cortex in vivo, and whether endogenous BDNF has the same or similar action. To address these questions, we recorded field potentials of rat visual cortex evoked by stimulation of lateral geniculate nucleus, white matter, or cortical layer IV. We found that LFS did not induce LTD of cortical responses in vivo. To test the possibility that spontaneous activity from retinas would interfere with the induction of LTD, both eyes were removed or inactivated by tetrodotoxin. LTD was not induced in these conditions either. To test whether the difference in temperature between the two preparations is a factor for the discrepancy, the temperature of slices was increased from 31 to 37 degrees C. LTD was induced in slices at either temperature. Then, we hypothesized that endogenous BNDF and its receptors, TrkB, prevent the induction of LTD. To test this, we infused the cortex with an inhibitor of Trk receptor tyrosine kinases, anti-TrkB IgG1, anti-BDNF, and anti-neurotrophin 4/5 antibodies. LTD was induced when the BDNF-TrkB system was blocked. In slices, the level of phosphorylation of Trks was found to decrease with time. These results indicate that activation of TrkB signal pathway prevents LFS from inducing synaptic depression in visual cortex in vivo.

Animals↗

Imaging of calcineurin activated by long-term depression-inducing synaptic inputs in living neurons of rat visual cortex.

Long-term depression (LTD) of synaptic transmission is induced by low-frequency stimulation (LFS) of afferents lasting for a long time, typically for 10-15 min, in neocortical and hippocampal slices. It is suggested that calcineurin, Ca2+/calmodulin-dependent protein phosphatase, plays a role in the induction of LTD, based on the results that pharmacological or genetic manipulation of calcineurin activity interfered in its induction. However, questions as to why it takes so long to induce LTD and in which compartment of neurons calcineurin is activated remain unanswered. With a fluorescent indicator for calcineurin activity, we visualized the spatiotemporal pattern of its activation in living neurons in layer II/III of visual cortical slices of rats during the LFS of layer IV that induced LTD of synaptic responses. During LFS, the fluorescence intensity gradually increased with a latency of a few minutes in dendrites and soma of neurons, and remained increased during the whole observation period (10-25 min) after LFS. The onset latency of the increase in the soma was slower than that in the distal dendritic region. The LFS-induced rise in fluorescence was not observed in neurons which were loaded with inhibitors of calcineurin, indicating that the intensity of fluorescence reflects calcineurin activity. Control stimulation at 0.05 Hz and theta-burst stimulation did not significantly change the intensity of fluorescence. Only LFS-type inputs effectively activate calcineurin in postsynaptic neurons in an augmenting manner, and such a time-consuming activation of calcineurin may be a reason why long-lasting LFS is necessary for the induction of LTD.

Animals↗

NT-4 protein is localized in neuronal cells in the brain stem as well as the dorsal root ganglion of embryonic and adult rats.

We have newly established a sensitive, two-site enzyme immunoassay system for neurotrophin-4 (NT-4) and investigated its tissue distribution in the rat nervous system. The minimal limit of detection of the assay is 0.3 pg/0.2 mL of assay mixture. Concentrations of NT-4 were found to be extremely low in all brain regions, irrespective of the animal age, the highest level being found in the brain stem of 40-day-old rats, at 0.12 ng/g wet weight. NT-4 levels in young adult rats were significantly lower in the thalamus and higher in the olfactory bulb, neocortex, hypothalamus and brain stem than respective levels in 1-week-old rats. NT-4 immunoreactivity was strong in large neurons of the red nucleus and pontine reticular nucleus as well as the locus coeruleus, and moderate in cells in the mesencephalic trigeminal nucleus and interstitial nucleus of the medial longitudinal fasciculus. In the rat embryo, stong staining of NT-4 was detected in cells of regions corresponding to the midbrain/pons from E11.5 through E15.5. The intensity was decreased after E13.5 when the cytoplasm of cells in the medulla oblongata, fibers of the cerebellar primordium, and both cells and fibers of the dorsal root ganglion were also stained. Concentrations of NT-4 were detected in regions including the hindbrain and the dorsal root ganglion. Immunoblotting of NT-4-immunoreactive proteins extracted from these two regions revealed a band corresponding to mature NT-4 with a molecular mass of approximately 14 kDa. Kainic acid and another glutamte agonist, (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid did not affect NT-4 levels in the hippocampus. The present results show NT-4 to be localized in very limited brain cells and fibers from the embyonic period through to the young adult, suggesting specific roles in brain functions.

Age Factors↗

Chronic electrical stimulation of afferents from one eye changes ocular dominance of visual cortical neurons in kittens.

Binocular visual responsiveness of neurons in visual cortex of the cat can be changed by monocular visual deprivation in the critical period of postnatal development. It is hypothesized that afferents from each eye compete with one another for synaptic connections with cortical neurons so that less active afferents from the deprived eye fail to maintain the connections. This hypothesis predicts that an increase in inputs from one eye instead of decrease due to deprivation should also change binocular responsiveness of cortical neurons. However, the hypothesis has not successfully been tested with experimental activation of afferents from one eye. In the present study, we activated one of the optic nerves by chronic electrical stimulation of theta-burst type in behaving kittens for 2 days. After such a monocular activation, visual cortical neurons showed a significant ocular dominance shift in favor of the electrically activated eye, although neurons in the activated and nonactivated layers of the dorsal lateral geniculate nucleus had no biased visual responses. Also, we found no detectable difference between activated and nonactivated eye responses of cortical neurons in other response properties such as orientation selectivity. These results support the hypothesis that the balance between activities of both afferents is critical for formation or consolidation of each eye-specific pathway.

Animals↗