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Biomedical subjects

C Tanaka

Publications and source records attributed to C Tanaka.

At least 289 records · Page 16Linked to original sources
PubMed1988

Distinct cellular expression of beta I- and beta II-subspecies of protein kinase C in rat cerebellum.

Immunohistochemical and biochemical studies with subspecies-specific antibodies have revealed that beta I- and beta II-subspecies of protein kinase C, which result from alternative splicing of a single RNA transcript, show different regional expression in rat CNS. In the cerebellar cortex, beta I-subspecies is localized mainly in the granular layer, whereas beta II-subspecies is found predominantly in the molecular layer, most apparently in the presynaptic nerve endings that terminate at Purkinje cells. These distribution patterns are in sharp contrast to that of gamma-subspecies, which is most abundant within the Purkinje cells. The different patterns of expression imply that the multiple subspecies of protein kinase C may each have a specific function in modulating the neuronal activity of particular cell types.

Amino Acid Sequence↗
PubMed1988

Distribution of protein kinase C-like immunoreactive neurons in rat brain.

Distribution of protein kinase C in the CNS of rat is presented based on immunohistochemical analysis with monoclonal antibodies against this protein kinase. Protein kinase C-like immunoreactivity was discretely localized and associated with neurons. Most, if not all, glial cells were not significantly stained. The greatest density of the immunoreactive material was seen in the following regions: the olfactory bulb (external plexiform layer), olfactory tuberculum, anterior olfactory nucleus, cerebral cortex (layers I and IV), pyriform cortex, hippocampus (strata radiatum and oriens), amygdaloid complex (central and basolateral nuclei), cerebellar cortex (molecular layer), dorsal cochlear nucleus, nucleus spinal tract of the trigeminal nerve, and dorsal horn of the spinal cord (substantia gelatinosa). Image analysis revealed that the regional distribution of the protein kinase C-like immunoreaction generally agreed with that of phorbol ester-binding sites. Immunoreactive perikarya were found in the following areas: the cerebral cortex (layers V and VI), caudate putamen, hippocampus, thalamus, amygdaloid complex, medial and lateral geniculate nucleus, superior colliculus, cerebellar cortex, nucleus spinal tract of the trigeminal nerve, dorsal cochlear nucleus, and dorsal horn of the spinal cord. Intense protein kinase C-like immunoreactivity in the neuron was observed both in the membrane and cytoplasm of the perikarya, dendrites, axons, and axon terminals, while weak immunoreaction was seen in the nuclei but almost never in the nucleoles. A map of protein kinase C-containing neurons was constructed. Such an uneven distribution in the brain suggests that this enzyme may play roles in controlling neuronal function in the areas noted.

Animals↗
PubMed1988

Postnatal development of a brain-specific subspecies of protein kinase C in rat.

Protein kinase C in the developing rat brain was investigated by a biochemical assay and by light-microscopic immunocytochemistry. The protein kinase was resolved on hydroxyapatite column chromatography into 3 fractions, designated types I, II, and III. Type I, with structure encoded by a gamma-sequence, was not detected early postnatally, maintained a low level of activity during the first week, which increased gradually, and reached its maximum around postnatal day 28. This type of enzyme was expressed specifically in nervous tissues, and was not found in any other tissues thus far tested. Type II enzyme activity, a mixture of the 2 subspecies encoded by the beta I- and beta II-sequences, was found at birth, increased rapidly, and reached a plateau level between postnatal days 14 and 28. This type was the predominant subspecies of protein kinase C in the brain. Type III, its structure encoded by the alpha-sequence, was also detected at birth, and reached its maximum level on postnatal day 7. Immunocytochemical studies with a monoclonal antibody, which recognized preferentially the type I enzyme, visualized the developmental pattern of type I subspecies in the Purkinje cell, a typical cell having a large quantity of type I protein kinase C.

Aging↗
PubMed1988

Use of silicone elastomer for improvement of intestinal clamp.

An intestinal clamp was improved by application of a silicone elastomer measuring 3, 4 and 5 millimeters in thickness to the nip surfaces to reduce nip force or to make pressure distribution more uniform. For the 1 kilogram weight, the output from the pressure sensor, which was placed on the blade, was decreased as the thickness of the silicone elastomer was increased. Pressures loaded on central and marginal regions of the large intestine were more than seven times greater than that on the mesenteric region with use of a conventional clamp. In contrast, pressures on all of the mesenteric, central and marginal regions were relatively low and uniform with use of clamps equipped with silicone elastomer. These results indicate that the clamp equipped with the silicone elastomer damages tissues only to a small extent because of the dispersion effect of the pressure and the uniformity of the pressure distribution.

Anastomosis, Surgical↗
PubMed1987

Specific stimulation of steroid 5 alpha-reductase solubilized from rat liver microsomes by endogenous phosphatidylserine.

Dilauroylphosphatidylcholine caused a marked increase in progesterone 5 alpha-reductase activity solubilized from rat liver microsomes, whereas naturally occurring phosphatidylcholines from biological sources as well as dioleoylphosphatidylcholine had not effect on the activity. Therefore, the stimulatory effect of phospholipids normally found in rat liver microsomes was examined. The lipid extracts were prepared from the fraction which was freed from 5 alpha-reductase activity by DEAE-cellulose chromatography, and found to exhibit a strong stimulatory effect. The lipid extracts were then separated into phosphatidylserine, phosphatidylcholine and phosphatidylethanolamine by chromatography on silicic acid column and preparative thin-layer plate. Among these endogenous phospholipids, only phosphatidylserine stimulated the 5 alpha-reductase, suggesting that the lipid requirement is specific for phosphatidylserine in steroid 5 alpha-reductase from liver microsomes.

Animals↗
PubMed1987

Molecular cloning and cDNA structure of the regulatory subunit of type I cAMP-dependent protein kinase from rat brain.

Complementary DNA (cDNA) clones encoding the regulatory subunit of the type I cAMP-dependent protein kinase (R-I) were isolated by screening of rat brain cDNA libraries. A 1.5-kilobase (kb) cDNA insert containing the entire coding region was sequenced and full amino acid sequence has been deduced from the nucleotide sequence. The clone encodes for a protein of 380 amino acids that shows 97% homology to the bovine R-I subunit. Northern blot analysis demonstrated two major mRNA species (2.8 and 4.4 kb in size) in rat brain and liver.

Amino Acid Sequence↗
PubMed1987

Immunohistochemical localization of gamma-aminobutyric acid- and aspartate-containing neurons in the guinea pig vestibular nuclei.

The immunohistochemical distributions of gamma-aminobutyric acid (GABA)- and aspartate-containing neurons were studied in the guinea pig vestibular nuclei using purified antisera to GABA and aspartate, respectively. Most GABA-containing neurons had small cell bodies and were scattered throughout all regions of the vestibular nuclei. The largest number of these cells was found in the medial nucleus. Intraventricular injection of colchicine markedly increased GABA-like immunoreactivity in these cell bodies. GABA-containing terminals were distributed throughout all 4 subdivisions of the nuclei, with the richest localization found around the floor of the fourth ventricle. Various sized aspartate-containing neurons were noted in the vestibular nuclei and small cells were present in the superior, medial and lateral nucleus. Medium-sized cells were observed throughout the vestibular nuclei. Giant cells in the lateral nucleus also contained aspartate and were surrounded by GABA-like immunoreactive terminals, thereby suggesting the modulation of aspartate-containing neurons by GABAergic fibers from Purkinje cells.

Animals↗
PubMed1987

Pseudomonas diminuta LPS with a new endotoxic lipid A structure.

Lipid A that contains mainly 2,3-diamino-2,3-dideoxy-D-glucose, phosphate and fatty acids in the molar ratio 2:1:5-6 was found in Pseudomonas diminuta lipopolysaccharide. The lipid A was considered to have a diamino-sugar disaccharide structure that carries a nonglycosidic phosphomonoester group and amide-bound acyloxyacyl and 3-hydroxy fatty acyl groups. The lipopolysaccharide exhibited endotoxic activities including lethal toxicity, pyrogenicity, local Shwartzman activity, body weight-decreasing toxicity and Limulus activity. The free lipid A was also endotoxic.

Animals↗
PubMed1987

[3H]muscimol binding sites increased in autopsied brains of chronic schizophrenics.

[3H]muscimol binding and glutamic acid decarboxylase (GAD) activity in the prefrontal cortex and caudate nucleus of autopsied brains from 19 chronic schizophrenics and 17 control subjects were investigated. In the schizophrenics, saturation analysis with varying concentrations of [3H]muscimol revealed an increase in the number of GABAA receptors, but there was no significant difference in the affinity. In addition, the enhancement of [3H]muscimol binding by diazepam was significantly greater in schizophrenics than in controls. GAD activity did not differ between controls and schizophrenics. The possibility that GABAergic mechanisms might play a role in case of chronic schizophrenia should be given further attention.

Adult↗
PubMed1987

Immunohistochemical localization of gamma-aminobutyric acid (GABA) in the rat pancreas.

The localization of gamma-aminobutyric acid (GABA) in rat pancreas was investigated using antiserum raised against GABA conjugated to bovine serum albumin with glutaraldehyde. Immunoreactive cells were only found in the center of the pancreatic islets, and these cells were surrounded by nonimmunoreactive cells. When two serial sections of rat pancreas were consecutively stained with GABA antiserum and with antibodies against insulin, both antisera stained the same population of endocrine cells within the islets. In rats pretreated with streptozotocin, a B-cell toxin, we observed a marked decrease in the number of cells exhibiting GABA-like immunoreactivity. These observations indicate that GABA is present in the B cells of rat pancreatic islets.

Animals↗
PubMed1987

Enteric gamma-aminobutyric acid-containing neurons and the relevance to motility of the cat colon.

gamma-Aminobutyric acid (GABA)-containing neurons were identified and the functional relevance in the motility of the colon was studied. Autoradiography of the cat colon treated with [3H]GABA demonstrated scattered neurons in the myenteric plexus selectively labeled with [3H]GABA. Electrical transmural stimulation of the isolated cat colon led to an increase in the Ca2+-dependent, tetrodotoxin-sensitive release of endogenous GABA. gamma-Aminobutyric acid increased the amplitude of rhythmic contractions of the circular muscle of the colon and also the release of acetylcholine, which was Ca2+-dependent and tetrodotoxin-sensitive. Scopolamine inhibited the GABA-evoked rhythmic contractions, without effect on the evoked release of acetylcholine. Bicuculline and furosemide reduced the amplitude of spontaneous rhythmic contractions and the tone, which was reversed by GABA. These results suggest that GABA-containing neurons are involved in the control of motility of the cat colon, due to the stimulation of cholinergic neurons.

Acetylcholine↗
PubMed1987

Relation of growth process to spatial patterns of electric potential and enzyme activity in bean roots.

The electric spatial pattern and invertase activity distribution in growing roots of azuki bean (Phaseolus chrysanthos) have been studied. The electric potential near the surface along the root showed a banding pattern with a spatial period of about 2 cm. It was found that the enzyme activity has a peak around 3-7 mm from the root tip, in good agreement with the position of the first peak of the electric potential, which is located a little behind the elongation zone. An inhomogeneous distribution of ATP content was also detected along the root. Experiments on the electric isolation of the elongation zone from the mature zone and acidification treatment showed that H+ is transported from the mature-side to elongation-side regions, causing tip elongation through an acid-growth mechanism. Both acidification and electric disturbance on growing roots affected growth significantly. Simultaneous measurements of electric potential and enzyme activity clearly showed a good correlation between these two quantities and growth speed. From an analogy with the Characean banding, the spatio-temporal organization via the cell membrane in electric potential and enzyme activity can be regarded as a dissipative structure arising far from equilibrium. These experimental results can be interpreted with a new mechanism that the dissipative structure is formed spontaneously along the whole root, accompanied by energy metabolism, to make H+ flow into the root tip.

Journal Article↗
PubMed1987

D2-dopamine receptor-mediated inhibition of intracellular Ca2+ mobilization and release of acetylcholine from guinea-pig neostriatal slices.

The effect of dopamine receptor activation on electrically- or high K+ (30 mM)-evoked neurotransmitter release and rise in intracellular Ca2+ concentration was investigated using slices of guinea-pig neostriatum. A specific D2-dopamine receptor agonist, LY-171555 (a laevorotatory enantiomer of LY-141865: N-propyl tricyclic pyrazole) at 10(-6) M inhibited electrical stimulation- and high K+-evoked release of [3H]-acetylcholine ([3H]-ACh) to 47.7 +/- 6.0% and 54.1 +/- 5.0% of control, respectively. The maximal inhibition by LY-171555 at 10(-5) M was 54.8 +/- 5.1% reduction of the control. The half-maximal effective concentration (EC50) of LY-171555 for the inhibition of [3H]-ACh release was 2.3 X 10(-7) M. A specific D2-dopamine receptor antagonist, (-)-sulpiride (10(-7) M) reversed the inhibition of [3H]-ACh release induced by LY-171555. A specific D1-dopamine receptor agonist, SK&F 38393 (2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-benzazepine) (10(-5) M) had no effect on the release of [3H]-ACh. LY-171555 (10(-6) M) also inhibited the high K+-evoked endogenous glutamate release, by 47% of control. This inhibitory effect was reversed by (-)-sulpiride (10(-7) M). We used a fluorescent, highly selective Ca2+ indicator, 'quin 2' to measure intracellular free Ca2+ concentrations ([Ca2+]i). Electrical stimulation of slices preloaded with quin 2 led to an elevation of relative fluorescence intensity and this response was reduced by the removal of Ca2+ from the bathing medium. These results indicate that the enhanced elevation in fluorescence intensity in the quin 2-loaded slices reflects the increase of intracellular free Ca2+ concentration, [Ca2+]i. The mixed D1- and D2-receptor agonist, apomorphine and LY-171555 inhibited the increase of [Ca2+]i induced by electrical stimulation or high K+ medium, in a concentration-dependent manner, while SK&F 38393 did not affect the increase of [Ca2+]i. The maximal inhibitory effect of LY-171555 at 3 X 10(-5) M was 35 +/- 3% reduction in control values. The inhibitory effect of LY-171555 was antagonized by (-)-sulpiride (10(-7) M). There was a high correlation (r = 0.997, P less than 0.05) between the D 2-receptor-mediated inhibition of the stimulated rise of [Ca2+]i and [3H]-ACh release. When the slices were superfused with the Ca2+-free medium containing EGTA (10(-4) M) for 5 min, the rise in [Ca2+]i was markedly suppressed to 18.0% of control by LY-171555 (10(-6) M). These data indicate that activation of the D2-dopamine receptor suppresses the elevation of [Ca2+]i induced by depolarizing stimuli. This may be due to inhibition of mobilization of Ca2+ from the intracellullar store. We propose that the D2-receptor-mediated inhibition of transmitter release is probably due to a reduction in intracellular Ca2+ mobilization.

Acetylcholine↗
PubMed1987

Release of gamma-aminobutyric acid and acetylcholine by neurotensin in guinea-pig ileum.

The release of gamma-aminobutyric acid (GABA) and acetylcholine (ACh) from the strips of guinea-pig ileum was investigated in the presence of neurotensin. Neurotensin evoked the release of [3H]-GABA from the strips preloaded with [3H]-GABA, and the evoked release was Ca2+-dependent and tetrodotoxin-sensitive. Hexamethonium, scopolamine, [D-Pro2,D-Trp7,9] substance P and pretreatment with substance P did not alter the neurotensin-evoked release of [3H]-GABA. Pretreatment with neurotensin inhibited the release of [3H]-GABA evoked by neurotensin but not by high K+, thereby indicating that neurotensin induced a specific desensitization of its own receptor. These observations indicate that neurotensin may stimulate the GABAergic neurone through its own receptor. Neurotensin evoked the release of [3H]-ACh from strips preloaded with [3H]-choline and this release was Ca2+-dependent and tetrodotoxin-sensitive. The evoked release of [3H]-ACh was not affected by hexamethonium, scopolamine and [D-Pro2,D-Trp7,9] substance P. Bicuculline partly inhibited the neurotensin-evoked release of [3H]-ACh; thus neurotensin seems to induce a release of ACh partly through the release of endogenous GABA. All this evidence indicates that neurotensin induces release of GABA as well as ACh from the myenteric neurones of the guinea-pig ileum.

Acetylcholine↗
PubMed1987

Distribution of beta-adrenoceptors associated with cAMP-generating system in cat colon.

The localization of beta-adrenoceptor associated with the adenosine 3',5'-cyclic monophosphate (cAMP)-generating system was determined by an assessment of the smooth muscle cell contractility and by assay of cAMP in individual layers of the cat colon. Isoproterenol inhibited the acetylcholine (ACh)-induced contractions of isolated longitudinal and circular muscle cells in a dose-dependent manner. The response of the longitudinal muscle cells to isoproterenol was double that seen in the circular muscle cells, and this inhibition was antagonized by sotalol. The basal content of cAMP was 3.42 pmol/mg protein in longitudinal muscle layers, 3.09 pmol/mg protein in circular muscle layers, and 2.75 pmol/mg protein in Auerbach's plexus. Isoproterenol produced a dose-dependent elevation of cAMP levels in longitudinal and circular muscle layers, which were antagonized by sotalol and potentiated by theophylline. By contrast, isoproterenol had no effect on cAMP in Auerbach's plexus. Phenylephrine did not alter the cAMP levels in any layer. Therefore, beta-adrenoceptors associated with the cAMP-generating system probably exist in the longitudinal and circular muscles of the cat colon.

Acetylcholine↗
PubMed1987

gamma-Aminobutyric acid stimulates acid secretion from the isolated guinea pig stomach.

gamma-Aminobutyric acid (GABA) content was measured, and the effect of GABA on acid secretion was studied using the everted preparation of isolated guinea pig stomachs. GABA contents in the mucosa layer and the remaining layer were 20-24 nmol/g tissue and 34-42 nmol/g tissue, respectively. GABA at 10(-6) to 3 X 10(-5) M induced acid secretion, and the maximum secretion was obtained at 3 X 10(-5) M, that is approximately 1.6-fold of the spontaneous secretion and approximately half of the amount secreted by histamine at 3 X 10(-4) M. The GABA-induced acid secretion was inhibited by bicuculline, scopolamine, pirenzepine, proglumide, and tetrodotoxin, but not by cimetidine. Muscimol (3 X 10 to 10(-5) M), but not baclofen, induced acid secretion in a concentration-dependent manner. The responses to GABA and muscimol were antagonized by bicuculline. Scopolamine and tetrodotoxin completely inhibited the acid secretion induced by low concentrations of GABA and muscimol and to some extent the response induced by high concentrations of muscimol. All these results indicate that GABA induces acid secretion via the A type of GABA receptor, probably located mainly on the cholinergic neurons and partially on the nonneuronal cells in the guinea pig stomach.

Animals↗