Biomedical subjects

M Satoh

Publications and source records attributed to M Satoh.

At least 487 records · Page 27Linked to original sources

PubMed1995

Scratching behavior induced by pruritogenic but not algesiogenic agents in mice.

We compared the behavioral effects of treatment with pruritogenic and algesiogenic agents in mice. The animals were given subcutaneous injections of pruritogenic agents, compound 48/80 (3-100 micrograms), substance P (10-300 micrograms) and histamine (3-300 micrograms), and algesiogenic agents, capsaicin (30 and 100 micrograms) and dilute formalin (5 mg of formaldehyde), into the rostral back, and scratching of the injected site by the hind paws was counted. Compound 48/80 and substance P dose dependently elicited the scratching behavior, but histamine, capsaicin and dilute formalin were without significant effects at the doses examined. These results suggest that compound 48/80- and substance P-induced scratching of the injected site is due to itch, but not to pain. The data did not provide support for the idea that histamine produces itch in the mouse.

Animals↗

PubMed1995

A subtype of opioid kappa-receptor is coupled to inhibition of Gi1-mediated phospholipase C activity in the guinea pig cerebellum.

PLC activity was stimulated either by 1-100 microM of GTP or by 100-3,000 microM Ca2+ in lysed synaptosomal membranes of the guinea pig cerebellum. The kappa-opioid receptor agonist selectively inhibited the PLC activity stimulated by 100 microM GTP, but not by 100-3,000 microM Ca2+. Pretreatment of membranes with PTX abolished such a kappa-agonist-induced inhibition of PLC activity. The reconstitution of Gi1, but not of Go purified from porcine brains with PTX-treated membranes showed a complete recovery of the kappa-agonist-inhibition of PLC activity. These findings suggest that a novel subtype kappa-receptor mediates inhibition of PLC through inhibiting the intrinsic activity of PTX-substrate G-proteins.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1995

Gz coupling to the rat kappa-opioid receptor.

We have expressed the cloned rat kappa-opioid receptor in human embryonic kidney 293 cells and studied the ability of kappa-selective ligands to inhibit adenylyl cyclase. In transfected 293 cells, activation of the kappa-opioid receptor by U50,488 and the dynorphins resulted in the inhibition of cAMP accumulation. The inhibitory response was sensitive to pertussis toxin and highly selective for kappa-agonists; neither mu- nor delta-opioids were able to activate the kappa-opioid receptor. Upon co-transfection with the alpha subunit of Gz, inhibition of cAMP accumulation by kappa-agonist became refractory to pertussis toxin, indicating that the kappa-opioid receptor can couple to both G(i) and Gz proteins.

Adenylate Cyclase Toxin↗

PubMed1995

Immunocytochemical localization of mu-opioid receptor in the rat caudate-putamen.

A guinea pig antibody against a C-terminal peptide of rat mu-opioid receptor (MOR) was produced to examine the distribution of MOR in the rat caudate-putamen (CP). The anti-peptide antibody recognized a protein of M(r) 69,000 in Triton X-100 extract of rat brain and in the membrane fraction of MOR-expressing culture cells. Intense MOR-like immunoreactivity (LI) was observed in island-like areas of the CP. Some MOR-LI was located on the cell bodies and dendrites of CP neurons. Double immunofluorescence study revealed that the intensely MOR-immunoreactive areas showed weak calbindin-LI, surrounded by intensely calbindin-positive regions. The results indicate that MOR-LI is enriched in the 'patches' of the neostriatal mosaic compartmentation.

Animals↗

PubMed1995

DAMGO, a mu-opioid receptor selective agonist, distinguishes between mu- and delta-opioid receptors around their first extracellular loops.

The structural basis of mu-opioid receptor (OPR) for the specificity in its ligand binding was investigated using chimeric mu/delta-OPRs. Replacement of the region around the first extracellular loop of delta-OPR with the corresponding region of mu-OPR gave the resultant chimeric receptor the similar affinity to DAMGO compared with the native mu-OPR. The reciprocal replacement deprived the high affinity to DAMGO from mu-OPR. These results indicate that the difference(s) in the structure around the first extracellular loop is critical for DAMGO to distinguish between mu- and delta-OPRs. Furthermore, displacement studies revealed that this region is partly involved in the discrimination between mu- and delta-OPRs by other peptidic mu-selective ligands, such as dermorphin, morphiceptin and CTOP, but not by non-peptidic ligands, such as morphine and naloxone.

Amino Acid Sequence↗

PubMed1995

Metabolism of 2-thiobenzothiazoles in the rat. Urinary, fecal and biliary metabolites of 2-benzothiazyl sulfenamides.

Metabolic fates of 2-benzothiazyl sulfenamides, N-oxydiethylene-2-benzothiazyl sulfenamide and N-cyclohexyl-2-benzothiazyl sulfenamide in rats were studied using tracer technique. These compounds given orally to rats were excreted rapidly in the urine and feces. Five urinary metabolites, 2-mercaptobenzothiazole (MBT), its three conjugates, mercapturate, glucuronide and sulfate, and 2,2'-dibenzothiazyl disulfide (BTDS) were confirmed. Furthermore, BTDS was found as a fecal metabolite. The sulfenamides were partly transformed in the stomach to BTDS, which was predominantly excreted into the feces. In the liver, the sulfenamides were mainly transformed to MBT and its conjugates. The S-glucuronide and S-sulfate conjugates were predominantly excreted into the bile. Mechanisms were discussed concerning the metabolite formation of sulfenamide derivatives in vivo and in vitro.

Animals↗

PubMed1995

Opioidergic inhibition of capsaicin-evoked release of glutamate from rat spinal dorsal horn slices.

We investigated the effects of opioid agonists on the capsaicin-evoked release of glutamate from nociceptive primary afferent fibers of the rat (6-8 weeks) using a fluorometric on-line continuous monitoring system for glutamate. In the presence of 0.3 microM tetrodotoxin, the application of 3 microM capsaicin to spinal dorsal horn slices produced an evoked glutamate release (55.9 +/- 4.02 pmol.mg-1 protein, n = 15). DAMGO ([D-Ala2,N-Me-Phe4,Gly5-ol]enkephalin; 0.3-10 microM) and morphine (1-30 microM), mu-opioid agonists, produced a concentration-dependent reduction (approximately 85 and approximately 77% reduction, respectively) in the capsaicin (3 microM)-evoked release of glutamate. These inhibitory effects were significantly antagonized by naloxone (1 microM). DPDPE ([D-Pen2,5]enkephalin; 1-10 microM), a delta-opioid agonist, also reduced the capsaicin-evoked release in a concentration-dependent manner (approximately 59% reduction). Naltrindole (1 microM), a selective delta-antagonist, significantly antagonized the inhibitory effect of DPDPE (10 microM). In contrast, neither U-50,488H (1-10 microM) nor U-69,593 (10 microM), kappa-opioid agonists, had any effects on the evoked release of glutamate. These results suggest that mu-, and delta-opioid agonists modulate pain transmission in the spinal dorsal horn, at least in part, by inhibiting the release of glutamate from capsaicin-sensitive primary afferents.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1995

Isoproterenol augments ATP-evoked Cl- secretion across canine tracheal epithelium.

Using an Ussing chamber, both the posterior epithelial membrane and cultured epithelial cell monolayers from canine trachea were used for measurements of potential difference (PD) and short circuit current (SCC). Conductance (G) was calculated as the ratio SCC/PD. Adenosine (10(-5) to 10(-3) M) failed to produce any significant increases in PD and SCC. ATP (10(-6) to 10(-4) M) produced a significant transient increase in SCC in a dose-dependent fashion, reaching a peak value within 3 min after stimulation. Isoproterenol (ISOP) at 10(-8) M itself did not significantly alter the SCC value. In both the epithelial membrane and cultured epithelial cells treated with amiloride, however, pretreatment with 10(-8) M ISOP significantly augmented the ATP-induced SCC rise, whereas G did not significantly change. These findings indicate that beta-adrenergic stimulation augments Cl- secretion induced by P2-receptor stimulation in airway epithelial cells.

Action Potentials↗

PubMed1995

Molecular pharmacology of the opioid receptors.

Opioid receptors are the primary sites of actions of opiates and endogenous opioid peptides, which have a wide variety of pharmacological and physiological effects. The opioid receptors are classified into at least three subtypes, mu, delta, and kappa, and their cDNAs have been cloned. In this review, we describe the molecular cloning of opioid receptor gene family and studies of the structure-function relationships, modes of coupling to second messenger systems, pharmacological effects of antisense oligonucleotides, and anatomical distribution of opioid receptor mRNAs.

Amino Acid Sequence↗

PubMed1995

Participation of cAMP and cAMP-dependent protein kinase in beta-adrenoceptor-mediated interleukin-1 beta mRNA induction in cultured microglia.

We previously reported evidence of beta-adrenoceptor-mediated induction of IL-1 beta mRNA in the rat hypothalamus. The present in vitro studies using northern blot analysis showed that the beta-adrenoceptor agonist isoproterenol (1 x 10(-8) to 1 x 10(-5) M) caused a marked induction of IL-1 beta mRNA in microglia, but not in astrocytes. This induction was remarkably suppressed by pretreatment of cells with the beta-adrenoceptor antagonist propranolol. These phenomena were confirmed by in situ hybridization with digoxigenin-labelled IL-1 beta RNA probe. Furthermore, dibutyryl cyclicAMP (dbcAMP) (5 x 10(-4) and 5 x 10(-5) M) markedly induced IL-1 beta mRNA in microglia. The intracellular level of cAMP in microglia was elevated in a dose-dependent manner when they were treated with isoproterenol, and this elevation was completely blocked by propranolol. The induction of IL-1 beta mRNA by either isoproterenol or dbcAMP was strongly inhibited by a cAMP-dependent protein kinase inhibitor, H8. These results, taken together, suggest that (1) microglia primarily induce IL-1 beta mRNA by stimulation of beta-adrenoceptors, and (2) cAMP and cAMP-dependent protein kinase presumably participate in a signal transduction mechanism involved in the induction of IL-1 beta mRNA via beta-adrenoceptors.

Adrenergic beta-Agonists↗

PubMed1995

Molecular biology of the opioid receptors: structures, functions and distributions.

Opiates like morphine and endogenous opioid peptides exert their pharmacological and physiological effects through binding to their endogenous receptors, opioid receptors. The opioid receptors are classified into at least three types, mu-, delta- and kappa-types. Recently, cDNAs of the opioid receptors have been cloned and have greatly advanced our understanding of their structure, function and expression. This review focuses on the recent advances in the studies on opioid receptors using the cloned cDNAs. We describe the molecular cloning of the opioid receptor gene family and studies of the structure-function relationships, modes of coupling to second messenger systems, pharmacological effects of antisense oligonucleotide and anatomical distributions of opioid receptors.

Animals↗

PubMed1995

Double in situ hybridization study on coexistence of mu-, delta- and kappa-opioid receptor mRNAs with preprotachykinin A mRNA in the rat dorsal root ganglia.

Coexistence of the mRNA for each subtype of opioid receptor (OPR) with the mRNA for preprotachykinin A (PPTA), a precursor protein of substance P (SP), in the rat dorsal root ganglia was examined by double in situ hybridization technique. About 90% and 30% of PPTA mRNA-positive neurons expressed mu- and kappa-OPR mRNAs at high level, respectively. However, only about 3% of PPTA mRNA-positive neurons expressed delta-OPR mRNA at high level. These results suggest that mu- and kappa-OPRs exist on most of and a part of the primary afferent terminals containing SP, respectively. On the other hand, among the neurons which highly expressed mu-, delta- or kappa-OPR mRNA, PPTA mRNA was not expressed in about 58%, 95% or 24% of those neurons, respectively. These findings suggest the possibility that OPRs co-exist with other neurotransmitters and/or neuromodulators than SP in the primary afferent neurons.

Animals↗

PubMed1995

Transient expression of FGF receptor-4 mRNA in the rat cerebellum during postnatal development.

The fibroblast growth factor (FGF) receptor-4 mRNA in the adult rat brain is expressed preferentially in the medial habenular nucleus. In this paper, we examined the expression of FGFR-4 mRNA in the brain during postnatal development. Interestingly, in addition to the persistent expression of FGFR-4 mRNA in the medial habenular nucleus, FGFR-4 mRNA was transiently expressed in the proliferative zone of the external granule layer of the developing cerebellum. The localization and transient expression of FGFR-4 mRNA in the developing cerebellum suggest that FGFR-4 mRNA was expressed by proliferative granule cells. The present findings indicate that FGFR-4 in the brain has an important role in the postnatal development of the cerebellar cortex.

Animals↗

PubMed1995

Immunocytochemical localization of motilin-containing cells in the rabbit gastrointestinal tract.

Motilin-immunopositive cells (Mo cells) are known to be present in the upper small intestine of various species, including man. However, whether Mo cells are present in the rabbit gastrointestinal tract remained to be elucidated. Therefore, this study was designed to investigate the distribution of Mo cells in the rabbit gastrointestinal tract by the avidin-biotin-peroxidase complex method using a new anti-motilin serum (CPV2) raised in chickens. The results of an enzyme-linked immunosorbent assay suggested that this antiserum recognized the C-terminal region of the motilin molecule. Motilin-immunopositive cells were found in the epithelia of the crypts and villi throughout the rabbit gastrointestinal tract from the gastric antrum to the distal colon, but no immunostaining occurred in the gastric body. Morphometric analysis revealed that Mo cells were localized preferentially in the upper small intestine, as reported for other species, and the cell densities (cells/mm2, mean +/- SE) were: gastric antrum (0.41 +/- 0.16), duodenum (8.2 +/- 0.8), jejunum (1.9 +/- 0.5), ileum (0.62 +/- 0.14), cecum (0.19 +/- 0.05), proximal colon (0.13 +/- 0.03), and distal colon (0.39 +/- 0.18). Our results demonstrated conclusively that Mo cells exist in the rabbit gastrointestinal tract and showed for the first time their regional distribution. Furthermore, our new chicken antiserum would appear to be a useful tool for the determination of plasma motilin concentrations by radioimmunoassay and for the immunoneutralization of endogenous motilin in the rabbit.

Animals↗

PubMed1995

Distribution of enteric neural peptide YY in the dog gastrointestinal tract.

Various regions of the dog gastrointestinal tract were investigated for the distribution of peptide YY (PYY) neurons using immunocytochemistry and radioimmunoassay. PYY neurons that encircled non-PYY-immunoreactive neurons were mainly observed in the myenteric plexus from the stomach to the colon. There was more PYY-like immunoreactivity in the muscle layer of the stomach and ileum than in the other intestines. The results of high performance liquid chromatography revealed that neural PYY-immunoreactive substance is identical to authentic PYY. PYY was not localized in the cholinergic neurons. These results indicate that PYY, as a neuropeptide, is involved in the regulation of gastrointestinal function.

Animals↗

PubMed1995

Influence of temperature and relative humidity on early bond strengths to dentine.

The effect of temperature and relative humidity (RH) on the early tensile bond strengths to bovine dentine of two bonding systems (Liner Bond System, and Scotchbond Multi-purpose), and an experimental system (KB-110) were tested. Two environmental conditions, room temperature (23 degrees C/50% RH) and oral temperature (30 degrees C/80% RH), were used in a controlled temperature and humidity chamber. Bond strengths were recorded immediately after, 10 min and 24 h following light curing. The tensile bond strengths did not vary between the two test conditions, but the mode of fracture was observed to change. The 30 degrees C/80% RH condition exhibited a slightly greater degree of adhesive type failures compared with the 23 degrees C/50% RH group. This was particularly so for the experimental system, indicating that different bonding systems may be more or less sensitive to changes in RH and temperature. Failures occurred partially or totally within the resin composite at the early test times, and it was concluded that the bond strengths of the systems tested tended to exceed the early cohesive strengths of the resin composite.

Adhesiveness↗

PubMed1995

Helix formation of poly (L-glutamic acid) in the presence of alkaline earth metal cations in aqueous alcohol solutions.

Effects of divalent counterions (Mg2+, Ca2+, Sr2+, Ba2+) on the helix formation of poly(L-glutamic acid) are investigated in aqueous alcohol (MeOH, EtOH, 2PrOH, tBuOH) solutions. To observe helix formation inherent to the divalent counterions, the chlorides were added to a poly(L-glutamate) having an inert monovalent counterion, tetrabutylammonium cation. Marked counterion- and alcohol-specificities were observed for the dependence of helix content, theta, on the alcohol content. The theta values for most Mg2+ and Ca2+ systems decreased with increasing alcohol content in a higher alcohol region, while those for Sr2+ and Ba2+ systems were almost constant. A specific helix stabilization was observed for mixed divalent counterion systems. These results are self-consistently interpreted by taking into account contact ion-pair formation between the counterions and the polymer charges on the coil conformation.

Alcohols↗

PubMed1995

Alpha 1A-adrenoceptor subtype effectively increases Ca(2+)-sensitivity for contraction in rabbit thoracic aorta.

1. Norepinephrine and phenylephrine increase cytosolic Ca2+ concentration ([Ca2+]i) and muscle tension, which shows positive correlation between [Ca2+]i and tension development. 2. The slopes of regression lines between [Ca2+]i and tension development for norepinephrine and phenylephrine in tissues treated with an irreversible alpha 1B-adrenoceptor selective blocking agent, 10(-4) M chloroethylclonidine, were significantly steeper than those with untreated tissues. 3. Myosin light chain kinase inhibitors, KT5926 (3 x 10(-6) M) and K252a (10(-6) M) more selectively reduced the contraction produced by norepinephrine (3 x 10(-7) M) than that produced by clonidine (3 x 10(-6) M). 4. In the chloroethylclonidine-treated tissues, KT5926 and K252a did not tend to affect the contraction induced by norepinephrine and clonidine. 5. These results suggest that the contractile response through the alpha 1A-adrenoceptor subtype causes a greater muscle tension than that through the alpha 1B-subtype at the same level of [Ca2+]i, and that the alpha 1A-adrenoceptor subtype mainly activates myosin light chain kinase independent pathways of contractile mechanisms in vascular smooth muscle of rabbit.

Adrenergic alpha-Agonists↗