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Biomedical subjects

S Uchida

Publications and source records attributed to S Uchida.

At least 307 records · Page 17Linked to original sources
PubMed1993

Extracellular release of acetylcholine, noradrenaline and serotonin increases in the cerebral cortex during walking in conscious rats.

The effect of walking on the extracellular release of acetylcholine (ACh), noradrenaline (NA) and serotonin (5-HT) in the parietal lobe of the cerebral cortex was examined in conscious rats using the microdialysis technique. Walking at the speed of 2.3 m/min for 5 min produced significant increases in ACh, NA and 5-HT release in the cerebral cortical extracellular space. The increase in ACh release was the most prominent among the transmitters examined. It is suggested that the increased release of ACh in the cerebral cortex may contribute at least partly to the increases in the cerebral cortical blood flow during walking.

Acetylcholine↗
PubMed1993

Mouse brain opioid receptor identification by direct ultraviolet photoaffinity labeling.

[3H]Morphine, PL-017[prolyl-3,4-3H,D-prolyl,3,4-3H] ([3H]PL-017) and enkephalin-(2-D-penicillamine,5-D-penicillamine)[tyrosyl-2,6-3H] ([3H]DPDPE) were directly cross-linked to mouse brain opiate receptors by an ultraviolet (254 nm) irradiation procedure. [3H]Morphine preferentially and specifically labeled a 58 kDa protein. The labeling of this protein was suppressed by the addition of excess naloxone. Dithiothreitol reduced the irreversible binding of [3H]morphine and [3H]PL-017 to the receptor protein. In the acid hydrolysate of [3H]DPDPE-labeled opiate receptors, dityrosine, was detected. These results suggest that the [3H]tyrosine residue of [3H]DPDPE covalently bound the tyrosine residue of delta-opioid receptors. The direct UV-photoaffinity labeling method using commercially available radioactive opiates described here should be a useful tool for characterization and purification of the opiate receptors.

Affinity Labels↗
PubMed1993

Muscarinic receptors stimulate Ca2+ influx via phospholipase A2 pathway in ileal smooth muscles.

Receptor-mediated changes in intracellular Ca2+ in ileal longitudinal smooth muscles of guinea pig were studied. Stimulation of muscarinic receptors by carbachol induced both Ca(2+)-influx through plasma membranes and Ca(2+)-release from intracellular stores. Pretreatment of the muscle with an inhibitor of phospholipase A2 abolished the Ca2+ influx but not the Ca(2+)-release, whereas an inhibitor of phospholipase C showed opposite effects. The inhibitors of cyclooxygenase and lipoxygenase enhanced the muscarinic receptor-induced Ca(2+)-influx. Addition of arachidonic acid mimic the receptor-induced Ca(2+)-influx. Treatment of muscles with pertussis toxin abolished the receptor-induced release of arachidonic acid as well as Ca(2+)-influx, but was less effective on the IP3 formation and the Ca(2+)-release. Taken together, our results suggest that phospholipase A2 but not phospholipase C pathway is involved in the muscarinic receptor-induced Ca(2+)-influx in ileal smooth muscle.

Animals↗
PubMed1993

Tissue expression of mRNA of chloride channel from MDCK cells and its regulation by protein kinases.

A new chloride channel has recently been identified by expression cloning (Paulmichl, M., et al. Nature 356: 238). To date there is no information available on the distribution of this channel in mammalian tissues. We cloned rat homologue of this Cl channel and found 92% identity in deduced amino-acid sequence. We studied the tissue distribution of its mRNA and regulation by protein kinases. Its mRNA was expressed in all 17 bovine tissues we studied, most abundantly in the brain. In the kidney, it was expressed more in the medulla than cortex. Dehydration up to 5 days did not change its mRNA level in the rat kidney. Both phorbol myristate acetate (PMA) and forskolin down regulated its expression in MDCK cells, suggesting that both PKC and PKA modulated its expression. The physiological role of this chloride channel remains to be clarified.

Amino Acid Sequence↗
PubMed1993

Molecular cloning of a chloride channel that is regulated by dehydration and expressed predominantly in kidney medulla.

Complementary DNA encoding a rat kidney chloride channel (CIC-K1) was isolated by a polymerase chain reaction (PCR) cloning strategy. We designed degenerate primers, based on the regions where previously cloned chloride channels (CIC-0, -1, and -2) possess significant amino acid identity, and performed reverse transcription PCR with whole kidney mRNA. The 686-amino acid protein encoded by CIC-K1 is about 40% identical to the previously cloned chloride channels and has a similar hydropathy profile. Expression of CIC-K1 in Xenopus oocytes induced Cl- currents that activate instantaneously upon hyperpolarization and depolarization, and displayed a slightly outwardly rectifying current-voltage relationship. The message for CIC-K1 was 2.4 kilobases and was found predominantly in kidney, especially in the inner medulla. Reverse transcription PCR technique using micro-dissected nephron segments revealed that the main site of expression in kidney was the thin ascending limb of Henle's loop, which has the highest Cl- permeability among the nephron segments and is thought to be involved in a counter-current system for urine concentration in the inner medulla. The abundance of CIC-K1 mRNA in kidney increased about 4-fold as rats became dehydrated by deprivation of water for 5 days. The site of expression and the regulation by dehydration suggest that CIC-K1 function may be important in urinary concentrating mechanisms.

Amino Acid Sequence↗