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S Mochida

Publications and source records attributed to S Mochida.

101 records · Page 6Linked to original sources
PubMed1988

Secondary late components of the muscarinic postsynaptic potentials, in rabbit superior cervical ganglion.

The well known muscarinic slow excitatory polysynaptic potential (s-EPSP) of rabbit superior cervical ganglion (SCG) peaking at about 1-2 s and lasting 5-10 s, is immediately followed by an abrupt change in slope to a longer, lower depolarizing phase. A brief dip in the level of depolarization (DP) often separates the two depolarizing phases. The secondary phase of s-EPSP rises to its own peak at about 25 s; total duration 60-120 s. With repetition of orthodromic volleys secondary s-EPSP builds up more gradually than initial s-EPSP, but more rapidly than slow-slow (ss-) EPSP. The later 'secondary' depolarizing phase along with the antecedent 'dip in DP' are, like the 'initial' s-EPSP, eliminated by a muscarinic antagonist, quinuclinidyl benzilate hydrochloride (QNB). This distinguishes secondary s-EPSP from the even slower rising non-cholinergic ss-EPSP. The ss-EPSP, although relatively small in the responses to the usual 3-pulse test stimuli, rises to an extraordinary amplitude (equal to the compound action potential) during a 10 s-120 s train of pulses. Gallamine blocked most of the slow IPSP component in test responses but not initial or secondary s-EPSP. A preganglionic conditioning train (10/s for 2 min) induced a long-term-enhancement (LTE) of secondary s-EPSP lasting greater than 3 h, with maximum postconditioning percentage increases greater than for initial s-EPSP. Also enhanced was the dip in DP, now forming a deeper notch between initial and secondary s-EPSPs; this attains a maximum at about 30 min postconditioning but thereafter progressively loses the enhancement by about 90 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Cyclic GMP-dependent protein kinase and phosphorylation of the endogenous substrate proteins in the rabbit superior cervical ganglion.

When the homogenate of rabbit superior cervical ganglia (SCG) was incubated in the presence of [gamma-32P]ATP and Mg2+, two specific proteins were strongly labeled. Their apparent molecular weights were 90,000 and 54,000, respectively. The phosphorylation of the latter was significantly stimulated by 10-50 nM cyclic GMP but to a lesser extent by cyclic AMP, whereas that of the former was not stimulated significantly by either of the cyclic nucleotides. The purified protein kinase inhibitor from rabbit skeletal muscle did not inhibit the phosphorylation. These results indicated that the observed phosphorylation of 54K protein was dependent on cyclic GMP but not on cyclic AMP. When intact SCG was incubated in the presence of 32Pi, phosphorylation of 90K protein was stimulated by cyclic GMP, dibutyryl cyclic GMP, and 8-bromo-cyclic GMP (10 microM), whereas phosphorylation of 54K protein was not significantly stimulated by any of these substances. The present demonstration of endogenous cyclic GMP-dependent protein kinase activity and its endogenous substrate proteins raises a possibility that the physiological actions of cyclic GMP in SCG are mediated by the phosphorylation of these proteins.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1987

Stimulation of adenylate cyclase in relation to dopamine-induced long-term enhancement (LTE) of muscarinic depolarization in the rabbit superior cervical ganglion.

Dopamine (DA) induction of the long-term enhancement (LTE) of the slow muscarinic depolarizing response to methacholine (MCh), equivalent to the slow EPSP (S-EPSP), was previously found to be mimicked by exogenous cyclic AMP (cAMP) in the rabbit superior cervical ganglion (SCG). DA-induced LTE of the S-EPSP was shown to be depressed by some DA antagonists. We now show that DA (15 microM), its analog, 2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene (ADTN), and a D2 receptor antagonist, metoclopramide, each can induce both LTE of MCh depolarization and an increase in ganglionic cAMP. Conversely, antagonists of DA-induced LTE also depress DA-induced rises in cAMP; these antagonists include haloperidol (1 microM), both (+) and (-) enantiomers of butaclamol (0.7-7 microM), flupenthixol (1 microM), and (+)-R-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-o l (SCH-23390) (7 microM). The selective D2 antagonists sulpiride (10 microM) and domperidone (10 microM) affect neither DA action. Alpha-2 adrenergic agonists (alpha-methyl-norepinephrine and clonidine) produce no LTE; alpha-antagonist dihydroergotamine (35 microM) does not affect either DA action, although it can completely block the hyperpolarizing response to DA or other catecholamines. Beta-antagonist propranolol (5 microM) partially depresses DA-induced rises in cAMP but has no effect on the DA-induced LTE. (Butaclamol and propranolol in combination can completely block the cAMP rise induced by DA.) Beta-agonist isoproterenol can induce appreciable LTE of MCh depolarization, but this LTE is not depressed by propranolol (10 microM). Isoproterenol can elicit a substantial rise in cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1986

Activation of M2 muscarinic receptors causes an alteration of action potentials by modulation of Ca entry in isolated sympathetic neurons of rabbits.

Activation of muscarinic receptors caused an alteration of the configuration of action potentials in the isolated sympathetic ganglion cells of rabbits, e.g. elimination of the shoulder in the falling phase and depression of the afterspike-hyperpolarization and after-depolarization. The responsible receptors appeared to be of the M2-type since the above changes by the low concentration (greater than or equal to 10 nM) of muscarinic agonists were potently antagonized by AF-DX 116. Similar changes were induced by removing the external Ca2+ and no more changes were produced by further application of muscarinic agonists in the absence of external Ca2+. The action potential in sympathetic neurons is thus shown to be modulated via the M2 receptor possibly by regulating the Ca entry.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1986

Effects of Ca antagonists on the action potential and their relationship to the muscarinic ACh actions in isolated sympathetic neurons of rabbits.

Muscarinically induced depressions of the shoulder in the falling phase as well as the after-spike-hyperpolarization and -depolarization of the action potential in the isolated sympathetic neurons of rabbits were mimicked by a novel peptide Ca channel blocker, omega-conotoxin (synthetic; 0.1-0.5 microM). Cobalt ions (0.1-2 mM) showed bidirectional effects on the shoulder, an early depression followed by a later prolongation, while they consistently induced depressions of other components. Organic Ca channel blockers, verapamil and D-600 (1-50 microM) and nifedipine (0.1-1 microM) appeared to have other effects as they rather caused a prolongation of the falling phase that was shortened by further application of acetylcholine.

Action Potentials↗
PubMed1986

Three types of muscarinic conductance changes in sympathetic neurons discriminately evoked by the different concentrations of acetylcholine.

Three different types of changes in membrane conductance were induced in isolated mammalian sympathetic neurons by the muscarinic actions of acetylcholine at different levels of concentration. These include a voltage-independent increase and two decreases, voltage-dependent and -independent, respectively. Muscarinic receptors in sympathetic neurons are thus shown to be coupled to multiple ionic channels, even within a single cell, and controlled by the different concentrations of a neurotransmitter.

Acetylcholine↗
PubMed1986

Multiple muscarinic responses directly evoked in isolated neurones dissociated from rabbit sympathetic ganglia.

Single sympathetic neurones, enzymatically isolated from the superior cervical ganglia of adult rabbits and maintained in culture medium, responded directly to DL-muscarine with a variety of electrical responses. The falling phase of the action potential was markedly accelerated while the late portion of the after-spike hyperpolarization was depressed. These changes occurred before any detectable change in membrane potential. The slow depolarizing changes in membrane potential induced by muscarine were associated with different changes in membrane conductance: a voltage-independent increase, a decrease at the levels of membrane potential positive to about -70 mV and a voltage-independent decrease. Muscarine can produce these multiple membrane changes often within the same cell, suggesting that the different effects are not due to heterogeneous cell types.

Animals↗
PubMed1985

Synaptic long-term enhancement (LTE) induced by a heterosynaptic neural input.

The slow excitatory postsynaptic potential (s-EPSP) response of cat stellate ganglion can be enhanced for hours (long term enhancement, LTE) following a conditioning preganglionic train of low frequency pulses, even when test s-EPSPs are elicited by an unconditioned input line. This provides another model for associational alterations of synaptic efficacy.

Animals↗
PubMedDate not supplied

Magnetic resonance imaging in chronic liver disease evaluated in relation to hepatic fibrosis--clinical and experimental results.

In 21 patients with chronic liver disease, the ratio of liver to muscle signal intensity on T1-weighted images was negatively correlated with the progression of hepatic fibrosis defined according to findings by laparoscopy and liver biopsy, and differentiated six patients with early chronic hepatitis from eight with liver cirrhosis. On T2-weighted images, the number of low intensity nodules comparable in size to regenerating nodules surrounded by connective tissues showed a positive correlation with stage. When hepatic fibrosis with no necrosis or fat infiltration was induced in rats, T2 values were positively correlated with hepatic hydroxyproline content, though there was no such correlation for T1 values. These results suggest that MR imaging may be useful for determining the progression of hepatic fibrosis in chronic liver disease. T2 values may directly reflect hepatic fibrosis.

Adult↗
PubMedDate not supplied

Computed tomography density of gallbladder stones may aid in predicting the rate of stone fragmentation with extracorporeal lithotripsy.

Thirty-six patients with gallbladder stone(s), 21 with solitary stone and 15 with multiple stones up to five in number, were treated by a single session of extracorporeal shock wave lithotripsy. In eight patients (group A), stones were gradually fragmented from the surface, producing fine powderlike fragments which made residual stones invisible, leading to reduced therapeutic efficacy. In 13 patients (group B), residual stones remained visible up to 2,400 shocks, though they showed similar fragments. Such fragments did not appear throughout treatment in 14 patients (group C). Computed tomography (CT) attenuation number, when the region of interest was settled on the whole stone, increased in the order of group A, B, and C. When the distribution of CT density on stones was analyzed, the density was diffusely lower than 50 HU in all patients in group A, higher than 50 HU only on the surface in all patients except for two in group B, and diffusely higher than 50 HU in all patients except for one in group C. CT findings may be useful for predicting the fragmentation mode of gallbladder stones by extracorporeal shock wave lithotripsy.

Adult↗