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N Hikawa

Publications and source records attributed to N Hikawa.

23 records · Page 2Linked to original sources

Effect of neurotransmitters on axoplasmic transport: acetylcholine effect on superior cervical ganglion cells.

The effect of acetylcholine (ACh) on particle movements along axons of cultured superior cervical ganglion cells was analyzed with a computer-assisted video-enhanced differential interference contrast microscope system. ACh suppressed the axoplasmic transport reversibly in both anterograde and retrograde directions. A muscarinic agonist, arecoline, mimicked the ACh effect, but nicotine did not. An experiment with the Ca(2+)-indicator dye, fura-2, revealed that ACh suppressed the transport without any change of intracellular Ca2+ concentration. ACh also suppressed the axoplasmic transport in Ca(2+)-free medium. Islet-activating protein (IAP), pertussis toxin, blocked the ACh effect. These results indicate that ACh activates muscarinic receptors and suppresses fast axoplasmic transport through the activation of IAP-sensitive GTP-binding protein, irrespective of Ca2+ ions.

Acetylcholine↗

Increase in intracellular calcium induced by stimulating histamine H1 receptors in macrophage-like P388D1 cells.

The addition of histamine to macrophage-like P388D1 cells resulted in a dose-dependent increase in intracellular calcium [Ca2+]i measured by fura-2 in single cells. The maximum level of [Ca2+]i was obtained by addition of 1 x 10(-4) M histamine. The increase was primarily due to release from the intracellular store. The addition of an H1 specific antagonist pyrilamine before histamine treatment inhibited the increase reversibly, while an H2 specific antagonist cimetidine had no inhibitory effect. Histamine also resulted in a dose-dependent increase in cGMP but not in cAMP. These data suggest the existence of histamine H1 receptors in these cells and histamine may have some biological effect on the function of macrophages via [Ca2+]i and cGMP as the second messengers.

Animals↗

Axoplasmic transport of mitochondria in cultured dorsal root ganglion cells.

The movements of individual mitochondria in cultured mouse dorsal root ganglion cells were directly observed by using fluorescent staining with rhodamine 123 in combination with video microscopic techniques. This gives greater spatial and temporal resolution and much higher specificity than possible by conventional methods. The instantaneous velocities were 0.55 +/- 0.11 microns/s anterograde and 0.60 +/- 0.10 microns/s retrograde. Movement of the mitochondria was in fits and starts, and some reversed direction. The number of mitochondria moving retrogradely was 1.5-1.9 times greater than the number moving anterogradely. The average length of mitochondria moving retrogradely was 2.8 microns and of mitochondria moving anterogradely was 4.1 microns. These results suggest that mitochondria increase their numbers by division in the nerve fiber terminal.

Animals↗

Introduction of macromolecules into primary cultured neuronal cells by fusion with erythrocyte ghosts.

The macromolecules were injected into primary cultured neuronal cells by fusion with human erythrocyte ghosts containing macromolecules. The injection efficiency was about 30% and 80% of the cells extended neurites like normal neuronal cells. In order to succeed in this method, phytohaemagglutinin E and polyethylene glycol 1000 were essential, and monolayer culture cells were used.

Cell Fusion↗

Analysis of hen egg white lysozyme (HEL)-specific delayed type hypersensitivity hybridomas.

Hen egg white lysozyme (HEL) specific delayed type hypersensitivity hybridomas (TDTH hybridomas) were established by fusing HEL specific C3H/HeN (H-2k haplotype) TDTH with BW5147 thymoma cells. TDTH hybridomas, which had Lyt-1+2- and Thy-1.2 antigens on their surfaces, were injected into mouse footpads with HEL antigens, and foot pad swellings were measured 24 h later. Mice with I-Ak haplotype showed strong responses, and their swellings were reduced by anti-I-Ak specific monoclonal antibodies, which suggests that the activity of the hybridomas is restricted by I-Ak. However, TDTH hybridomas did not modulate HEL specific T-cell proliferation responses.

Animals↗