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M Koshimizu

Publications and source records attributed to M Koshimizu.

15 recordsLinked to original sources
PubMed1998

Identification of amino acid residues contributing to desensitization of the P2X2 receptor channel.

The P2X2 receptor (P2X2R) is a member of the ATP-gated ion channels that mediate Ca2+ entry in several tissues, including the brain, adrenal medulla, and pituitary. Alternative usage of cryptic splice sites in the primary P2X2R transcript accounts for the existence of several transcript types, one of which (P2X2-2R) encodes a functional channel. P2X2-2R lacks a stretch of cytoplasmic C-terminal amino acids (Val370-Gln438) and exhibits rapid and complete desensitization, whereas P2X2R desensitizes slowly and incompletely. The role of the C terminus in P2X2R desensitization was studied by generating several channel mutants and monitoring intracellular free Ca2+ changes in transfected single GT1-7 neurons. Deletion studies indicated that the Arg371-Ile391 segment of the P2X2R is required for sustained Ca2+ influx. To identify the important residues within this segment, three contiguous amino acids were sequentially changed to alanine. Only two of these replacement mutants, at Arg371-Thr372-Pro373 and Lys374-His375-Pro376, had an enhanced rate of desensitization. Single amino acid deletions in the P2X2R C terminus and a series of insertions of wild-type sequences into the corresponding spliced site identified four residues, Pro373-Lys374-His375-Pro376, required for sustained Ca2+ influx through agonist-occupied wild-type channels. Thus, it is likely that the Pro373-Pro376 sequence of P2X2R represents a functional motif that is critical for the development of the slow desensitization profile observed in these channels. Consequently, deletion of this motif by alternative splicing provides an effective mechanism for generating a channel with controlled Ca2+ influx.

Amino Acid Sequence↗
PubMed1997

The minimum alveolar concentration of sevoflurane in rats.

There are only limited data on sevoflurane minimum alveolar concentration (MAC) in rats. This study was designed to determine the minimum alveolar concentration value for sevoflurane in younger and older rats. Minimum alveolar concentration determination was performed in spontaneously breathing animals, 9-week-old rats (younger, n = 8) and more than 13-month-old rats (older, n = 8). Rats were instrumented with a silastic catheter in the abdominal aorta via the femoral artery to allow for arterial blood gas sampling. Subsequently, minimum alveolar concentration for sevoflurane was determined in 40 younger and 38 older rats. Minimum alveolar concentration for sevoflurane in younger rats was significantly higher than in the older rats (2.68 +/- 0.19 vs. 2.29 +/- 0.19, P < 0.001). Subgroup analysis indicated that minimum alveolar concentration for sevoflurane was not affected by the presence of an arterial catheter in the abdominal aorta (younger, 2.75 +/- 0.08 vs. 2.67 +/- 0.21; older, 2.23 +/- 0.19 vs. 2.30 +/- 0.18). Minimum alveolar concentration is profoundly affected by the age of the animal, but not by limited instrumentation.

Aging↗
PubMed1997

I.m. midazolam as premedication produces a concentration-dependent decrease in core temperature in male volunteers.

We tested the hypothesis that premedication with i.m. midazolam decreases core temperature dose-dependently. We studied six male volunteers, in random order, on 3 days: (1) no midazolam administration (control day), (2) midazolam 0.025 mg kg-1 i.m., (3) midazolam 0.075 mg kg-1 i.m. On the first day, subjects were maintained alert during a 30-min control period. On the second and third days, midazolam 0.025 or 0.075 mg kg-1 was administered i.m. Core temperatures were measured at the right tympanic membrane. Four adhesive skin surface probes were fixed on the chest, upper right arm, lateral calf and thigh. Finger tip perfusion was evaluated using forearm minus fingertip and calf minus toe, skin surface temperature gradients. Thirty minutes after midazolam i.m., the level of sedation in the volunteers was assessed. Peripheral venous blood was obtained immediately after the assessment of the level of sedation. Tympanic membrane temperatures after administration of midazolam 0.075 mg kg-1 i.m. were significantly lower than those on the control and midazolam 0.025 mg kg-1 i.m. days at 20 and 30 min. The decreases in tympanic membrane temperatures at 30 min after midazolam i.m. became larger as the volunteers were more deeply sedated. i.m. midazolam produced a concentration-dependent decrease in tympanic membrane temperature at 30 min after midazolam 0.025 and 0.075 mg kg-1 i.m. We conclude that midazolam impaired tonic thermoregulatory vasoconstriction, allowing core-to-peripheral heat redistribution in a dose-dependent manner after i.m. administration.

Adult↗
PubMed1995

Isoflurane and sevoflurane produce a dose-dependent reduction in the shivering threshold in rabbits.

All general anesthetics markedly impair thermoregulatory responses; nonetheless, sufficient hyperthermia or hypothermia will trigger most protective reflexes. Shivering, however, remains an exception among thermo-regulatory responses: it is common during postanesthetic recovery, but is rare at typical anesthetic concentrations. This observation suggests that general anesthesia impairs shivering far more than other thermoregulatory defenses. Accordingly, we tested the hypothesis that low concentrations of isoflurane and sevoflurane would virtually obliterate shivering. Japanese white rabbits were anesthetized with isoflurane or sevoflurane at end-tidal concentrations of 0.2, 0.3, and 0.4 minimum alveolar anesthetic concentration (MAC) (n = 6 in each group); the normal core temperature for these rabbits is approximately 39 degrees C. Core temperatures were subsequently reduced by a water-perfused thermode positioned in the colon. The core temperature triggering shivering identified the threshold for this response. Five of the six rabbits given 0.2 MAC isoflurane shivered at a mean core temperature of 36.3 +/- 0.3 degrees C (mean +/- SD), and one rabbit failed to shiver at a minimum core temperature of 35.0 degrees C. Four of the six rabbits given 0.3 MAC isoflurane shivered at a mean core temperature of 36.2 +/- 0.6 degrees C, and two of these rabbits failed to shiver at a minimum core temperature of 35.0 degrees C. However, no rabbit given 0.4 MAC isoflurane shivered, even at minimum core temperatures of 35.0 degrees C. All of the rabbits given 0.2 MAC sevoflurane shivered at a mean core temperature of 36.6 +/- 0.7 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1992

[Static perimetry and temporal aspects of the photopic electroretinogram in sector retinitis pigmentosa].

Six cases of sector retinitis pigmentosa were studied by automated static perimetry and photopic electroretinogram. Four cases out of six revealed elevated thresholds in the lower half of the visual field, which corresponded to the normally appearing upper eyeground. They also showed delayed implicit time on the photopic electroretinogram. These results show that sector retinitis pigmentosa is not necessarily a regional retinal dystrophy.

Aged↗
PubMed1987

Microelectrode depth study of the electroretinographic oscillatory potentials in the frog retina.

The depth profile of the electroretinographic oscillatory potentials was studied in the isolated frog retina. The intraretinal electrode was introduced from the receptor side, and the reference electrode was placed on the vitreal side. The electroretinogram, recorded either transretinally or with the electrode tip in the receptor layer, showed 4 to 10 oscillatory potential wavelets. As the electrode was advanced proximally, the wavelets disappeared as a function of retinal depth. The wavelets with longer peak latencies disappeared earlier, and only the first one or two wavelets could be identified when the electrode was in the inner plexiform layer. These findings indicate that the oscillatory potentials are generated between the inner and outer plexiform layers and that the earlier wavelets originate in the more proximal retina. The results are consistent with the notion that the oscillatory potentials are generated by synaptic feedback circuits.

Animals↗
PubMed1986

Microelectrode depth study of electroretinographic b- and d-waves in frog retina.

The depth profiles of the b- and d-waves of the electroretinogram were studied in the isolated frog retina placed with its receptor side up. The electrode was introduced into the retina from the receptor side and the reference electrode was placed on the vitreal side. The b-wave was maximum in amplitude in the receptor layer, and decreased as the electrode was advanced proximally from the outer plexiform layer until it disappeared at the inner limiting membrane. The b-wave in the inner plexiform layer was different from that in the distal portion of the inner nuclear layer in form and peak latency. The results suggested that the b-wave is generated in the layers between the inner limiting membrane and the outer plexiform layer, and that at least two processes are involved in the generation of the b-wave. The depth profile of the d-wave resembled that of the b-wave except in the receptor layer; it was recorded in the whole retinal layers as was the b-wave, and decreased as the electrode was advanced proximally until it disappeared at the inner limiting membrane. The peak latency of the d-wave was longer in the inner plexiform layer than in the distal portion of the inner nuclear layer. The results indicated that the d-wave consists of the off-response of the late receptor potential and the postsynaptic components, the latter being generated by a similar mechanism as the b-wave.

Animals↗