Electron-phonon thermodynamic potential and magnetism of a metal.
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Journal Article↗
Biomedical subjects
C Tanaka
Publications and source records attributed to C Tanaka.
Immunohistochemical localization of gamma-aminobutyric acid- and aspartate-containing neurons in the rat deep cerebellar nuclei.
The immunohistochemical localization of gamma-aminobutyric acid (GABA)- and aspartate-containing neurons was evidenced in the rat deep cerebellar nuclei, using purified antisera to GABA and aspartate, respectively. Most GABA-containing neurons had small cell bodies and were scattered unevenly throughout the deep cerebellar nuclei. The medial cerebellar nucleus had a few GABA-containing cell bodies and interpositus and lateral nuclei contained many GABA-containing cell bodies. GABA-containing terminals were distributed throughout the nuclei. A large number of various-sized aspartate-containing cells were present in the deep cerebellar nuclei and most of these cells were large or medium-size. Aspartate-containing cells in the medial, interpositus and lateral nucleus were surrounded by GABA-like immunoreactive terminals, thereby suggesting the modulation of aspartate-containing neurons by GABA-ergic fibers from Purkinje cells.
Animals↗
Possible roles of protein kinase C in neurotransmission.
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Animals↗
The investigation of experimental brain tumours using 31P-MRS and 1H-MRI.
In vivo 31P-magnetic resonance spectra (MRS) were obtained by the surface coil method from rat glioma, human glioblastoma, and human neuroblastoma inoculated subcutaneously in CD Fisher rats and hamsters, and the effects of chemotherapy, photoradiation therapy, and radiofrequency hyperthermia as well as 60Co-irradiation were evaluated by sequentially observing spectral changes. In the 31P-spectra of tumour tissue, the nucleoside triphosphate (NTP), phosphomonoesters (PME) peaks were high and the phosphocreatine peak was low compared to those of normal brain. When the antitumour agents were given and were effective, NTP peaks decreased, and inorganic phosphate increased remarkably within several hours after the treatment. 1H-magnetic resonance imaging (MRI) were also obtained in some cases. Necrotic regions was detected by the 1H-MRI as image changes which appeared later than those detected by MRS. It proved practical to monitor the effect of therapy by employing either 31P-MRS or 1H-MRI. However, the image changes which demonstrated the effect of the therapy used closely resembled those changes which occurred with the onset of necrosis in tumour tissue during tumour growth. Several problems for future application of these techniques to human brain tumours are also mentioned.
Animals↗
Pathophysiological investigation of experimental cerebral ischaemia using in vivo 31P-NMR spectroscopy and 1H-MRI.
The cerebral energy metabolism and brain oedema were investigated in three experimental cerebral ischaemia models using 31P-NMR spectroscopy (MRS) and 1H-NMR imaging (MRI) in the same subject animal. These measurements were performed also in experimental brain oedema models and the findings were compared with each other. 31P-MRS showed an ischaemic pattern in all of the cerebral ischaemia models, that is, ATP and PCr peaks decreased, and the Pi peak increased and shifted to a higher resonant frequency. However, 31P-MRS did not show any remarkable change in the brain oedema models. On the other hand, 1H-MRI clearly demonstrated brain oedema in the brain oedema model. In the cerebral ischaemia models, 1H-MRI findings differed depending upon the type of model, namely the most marked brain oedema was detected in the unilateral middle cerebral arterial occlusion model and no marked change was detected in the temporary four vessel occlusion model. It was thought that this difference depended on the severity of the ischaemic insult. Accordingly, the fundamental pathophysiological problem of cerebral ischaemia was the energy metabolism disturbance with the brain oedema being associated with this disturbance but occurring secondarily. However, in the brain oedema model the main pathological change was the increase in tissue water.
Animals↗
Molecular heterogeneity and differential expression of multiple protein kinase C subspecies in central nervous tissue.
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Animals↗
Uptake of 99Tcm-MDP in lung metastasis from osteosarcoma: clinical and animal studies.
Bone scintigraphy was performed in 17 patients with previously known lung metastases of osteosarcoma. 99Tcm-MDP uptake was observed in all primary bone lesions but lung metastatic lesions were positive in only six patients (35%). 99Tcm-MDP uptake by lung metastases was significantly correlated with bone and osteoid formation in the metastatic lesions and preoperative serum ALPase values. These clinical observations were confirmed by using nude mice transplanted with human lung metastatic osteosarcoma. 99Tcm-MDP scintigraphy appears to be useful for detecting lung metastases of osteosarcoma only in a selected group of patients.
Adolescent↗
The family of protein kinase C: its molecular heterogeneity and differential expression.
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Animals↗
Structural heterogeneity regarding local Shwartzman activity of lipid A.
The relation of chemical structure to local Shwartzman activity of lipid A preparations purified by thin-layer chromatography from five bacterial strains was examined. Two lipid A fractions from E. coli F515--Ec-A2 and Ec-A3--exhibited strong activity, similar to that of previous synthetic E. coli-type lipid A (compound 506 or LA-15-PP). The Ec-A3 fraction contained a component that appeared to be structurally identical to compound 506, and the main component of Ec-A2 fraction was structurally similar to compound 506 except that it carried a 3-hydroxytetradecanoyl group at the C-3' position of the backbone in place of a 3-tetradecanoyloxytetradecanoyl group. Free lipid A (12 C) and purified lipid A fractions, Ec-A2 (12 C) and Ec-A3 (12 C), respectively, obtained from bacteria grown at 12 C, exhibited activity comparable to Ec-A2 or Ec-A3. In these preparations, a large part of the 3-dodecanoyloxytetradecanoyl group might be replaced by 3-hexadecenoyloxytetradecanoyl group. Salmonella minnesota R595 free lipid A also contained at least two active lipid A components as seen in E. coli lipid A, but the third component corresponding to the synthetic Salmonella-type lipid A (compound 516 or LA-16-PP) exhibited low activity. A lipid A fraction, Cv-A4 from Chromobacterium violaceum IFO 12614, which was proposed to have two acyloxyacyl groups at the C-2 and C-2' positions with other acyl groups, exhibited weaker activity than the free lipid A or LPS. The purified lipid A fractions from Pseudomonas diminuta JCM 2788 and Pseudomonas vesicularis JCM 1477 contained an unusual backbone with 2,3-diamino-2,3-dideoxy-D-glucose disaccharide phosphomonoester, and these lipid A (Pd-A3 and Pv-A3) exhibited strong activity comparable to the E. coli lipid A. Thus, the present results show that the local Shwartzman reaction can be expressed by partly different lipid A structures in both hydrophilic backbone and fatty acyl residues; when they have the same backbone the potency varies markedly depending on the structure of the acyl residues.
Animals↗
Inhibition by cyclic AMP of phorbol ester-potentiated norepinephrine release from guinea pig brain cortical synaptosomes.
The involvement of Ca2+/phospholipid-dependent protein kinase (protein kinase C, PKC) and cyclic AMP-dependent protein kinase in the K+-evoked release of norepinephrine (NE) was studied using guinea pig brain cortical synaptosomes preloaded with [3H]NE. 12-O-Tetradecanoylphorbol-13-acetate (TPA), a potent activator of PKC, enhanced the K+-evoked release of [3H]NE, in a concentration-dependent manner, but with no effect on the spontaneous outflow and uptake of [3H]NE in the synaptosomes. The apparent affinity of the evoked release for added calcium but not the maximally evoked release was increased by TPA (10(-7) M). Inhibitors of PKC, polymyxin B, and a more potent inhibitor, staurosporine, counteracted the TPA-induced potentiation of the evoked release. Both forskolin and dibutyryl cyclic AMP (DBcAMP) enhanced the evoked release, but reduced the TPA-potentiated NE release. A novel inhibitor of cyclic AMP-dependent protein kinase, KT5720, blocked both the forskolin-induced increase in the evoked release and its inhibition of TPA-induced potentiation in the evoked release, thereby suggesting that forskolin or DBcAMP counteracts the Ca2+-dependent release of NE by activating cyclic AMP-dependent protein kinase. These results suggest that the activation of PKC potentiates the evoked release of NE and that the activation of cyclic AMP-dependent protein kinase acts negatively on the PKC-activated exocytotic neurotransmitter release process in brain synaptosomes of the guinea pig.
Alkaloids↗
Regulation of [3H]GABA release from strips of guinea pig urinary bladder.
The presence of receptors that regulate the release of gamma-aminobutyric acid (GABA) was studied in strips of the guinea pig urinary bladder. GABA (10(-8)-10(-5) M) and muscimol (10(-8)-10(-5) M), but not baclofen (10(-5) M), reduced the Ca2+-dependent, tetrodotoxin-resistant release of [3H]GABA evoked by high K+ from the urinary bladder strips preloaded with [3H]GABA. The inhibitory effect of muscimol was antagonized by bicuculline and potentiated by diazepam, clonazepam, and pentobarbital sodium. The potentiating effect of clonazepam was antagonized by Ro 15-1788. Acetylcholine (ACh) inhibited the high K+-evoked release of [3H]GABA. The inhibitory effect of ACh was antagonized by atropine sulfate and pirenzepine but not by hexamethonium. Norepinephrine (NE) inhibited the evoked release of [3H]GABA. The inhibitory effect of NE was mimicked by clonidine, but not by phenylephrine, and was antagonized by yohimbine but not by prazosin. These results provide evidence that the release of GABA from strips of guinea pig urinary bladder is regulated via the bicuculline-sensitive GABAA receptor, M1-muscarinic, and alpha 2-adrenergic receptors.
Acetylcholine↗
[3H]GBR-12935 binding sites in human striatal membranes: binding characteristics and changes in parkinsonians and schizophrenics.
The binding of the diphenyl-substituted piperazine derivative, [3H]GBR-12935, a selective dopamine uptake inhibitor, to the post-mortem human putamen was studied. Inhibition curves by dopamine uptake inhibitors suggested the existence of two populations of [3H]GBR-12935 binding sites: one is potently inhibited by mazindol and/or nomifensine, and the second binding site is benztropine- and/or GBR 12909-sensitive. In the human putamen, [3H]GBR-12935 labeled both these two distinct binding sites. The [3H]GBR-12935 binding displaced by mazindol was enriched in the mouse and rat striatum, but not in the cultured mouse neuroblastoma cell N1E-115. The mazindol-sensitive [3H]GBR-12935 binding site increased in the presence of sodium and markedly decreased in the putamen from parkinsonians (45% of controls). On the other hand, the [3H]GBR-12935 binding displaced by benztropine showed no sodium-dependent increase and was not decreased in the putamen from parkinsonians. In the putamen from schizophrenics, the [3H]GBR-12935 binding did not significantly change in the density, while that displaced by mazindol tended to increase. It is concluded that in the human putamen, [3H]GBR-12935 binds to two distinct sites. One site is partially sodium-dependent and appears to be associated with a high-affinity dopamine uptake system on dopaminergic nerve terminals. The second binding site shows no sodium-dependency and may be associated with a nondopaminergic and/or extraneuronal DA uptake system.
Aged↗
GABAA receptor but not muscarinic receptor density was decreased in the brain of patients with Parkinson's disease.
The activity of glutamic acid decarboxylase (GAD) and choline acetyltransferase (ChAT) as presynaptic markers of gamma-aminobutyric acid (GABA)- and acetylcholine (ACh)-containing neurons, and the binding of [3H]muscimol and [3H]quinuclidinyl benzilate ([3H]QNB) as postsynaptic ones were measured in autopsied samples of the caudate nucleus, putamen, pallidum, substantia nigra and the cerebral cortex from L-dopa-treated patients with Stage V (terminally bedridden) patients with Parkinson's Disease (PD). In PD, GAD activities were significantly reduced in the caudate nucleus and substantia nigra relative to normal controls, but were normal when the values from protracted terminal illness (PTI) cases were used as the controls. ChAT activities were reduced in all regions studied. These reductions in GAD and ChAT activities were not accompanied by a concomitant increase in the density of GABAA or muscarinic receptors. GABAA receptor densities were significantly decreased in both the cortical and subcortical brain regions, while muscarinic receptor densities remained unchanged. We suggest that the decreased density of GABAA receptor in PD brains reflects degeneration of neurons on which the receptor is localized, i.e., degeneration of ascending monoaminergic neurons including nigral dopamine (DA) neurons.
Aged↗
Role of protein kinase C in the vesicular release of acetylcholine and norepinephrine from enteric neurons of the guinea pig small intestine.
The involvement of protein kinase C in the release of [3H]acetylcholine (ACh) and [3H]norepinephrine (NE) was studied in strips of guinea pig small intestine. 12-O-tetradecanoyl phorbol 13-acetate (TPA), but not 4 alpha-phorbol-12,13-didecanoate (4 alpha-PDD) potentiated the A23187-evoked release of [3H]ACh and [3H]NE from the strips of small intestine preloaded with [3H]choline and [3H]NE, and the potentiating effect of TPA was inhibited by polymyxin B. High K+-evoked releases of [3H]ACh and [3H]NE in the presence of tetrodotoxin were also potentiated by TPA. These TPA-induced potentiations of the evoked release were greater at a low concentration of external Ca2+ (0.5 mM) than at a high concentration (2 mM). Ouabain induced the release of these neurotransmitters both in the absence and presence of the low concentration of external Ca2+. The ouabain-evoked release was not altered by TPA. These results indicate that the activation of protein kinase C potentiates the vesicular release of ACh and NE at low Ca2+ concentration from the nerve terminals of enteric neurons in the guinea pig small intestine.
Acetylcholine↗
Novel type of monoclonal antibodies against cyclic GMP and application to immunocytochemistry of the rat brain.
A novel type of monoclonal antibodies against cyclic GMP were produced to study the immunocytochemical distribution of cyclic GMP in the rat brain. Cyclic GMP conjugated to bovine serum albumin with glutaraldehyde was used as an immunogen, and monoclonal antibodies were produced. The one monoclonal antibody which did not crossreact against other nucleotides was applied to the immunocytochemistry of the rat brain. Cyclic GMP immunoreactivities were distributed unevenly in the rat brain. The cerebellar cortex, hippocampus and cerebral cortex contained a high degree of cyclic GMP immunoreactivity, while most of the white matter was not stained. In the cerebellar cortex, stellate cells and Golgi cells showed intense immunoreactivities, but granule cells showed weak immunoreactivities. Approximately 60-80% of the Purkinje cells showed intense immunoreactivities, while the remaining ones showed only weak staining. The pyramidal cells in the cerebral cortex and hippocampus also showed intense immunostaining. Some glial cells adjacent to the Purkinje cells also stained. The nuclei of cyclic GMP-immunoreactive cells were not stained. These immunocytochemical distributions of cyclic GMP are in fairly good agreement with reported the biochemical data and the immunocytochemical distribution of guanylate cyclase. These monoclonal antibodies should be helpful for elucidating the physiological role of cyclic GMP in the brain.
Animals↗
Benzodiazepines and barbiturate potentiate the pre- and postsynaptic gamma-aminobutyric acid (GABA)A receptor-mediated response in the enteric nervous system of guinea pig small intestine.
To determine whether or not presynaptic gamma-aminobutyric acid (GABA) receptors regulate the release of GABA, we examined properties of the presynaptic GABA receptor and compared the findings within the case of the postsynaptic GABA receptor, using the longitudinal muscle with myenteric plexus (L-M) preparation of guinea pig small intestine. Muscimol, but not baclofen, reduced the Ca++-dependent release of [3H]GABA evoked by high K+ in the presence of tetrodotoxin from L-M preparation of the small intestine preloaded with [3H]GABA. Bicuculline, picrotoxin and furosemide antagonized the effect of muscimol. Diazepam, clonazepam and pentobarbital potentiated the muscimol-induced inhibition of high K+-evoked release of [3H]GABA. The potentiating effect of clonazepam was antagonized by Ro 15-1788. Muscimol induced a Ca++-dependent and tetrodotoxin-sensitive release of [3H]acetylcholine from L-M preparation preloaded with [3H]choline. The effect of muscimol was antagonized by bicuculline, picrotoxin and furosemide. Diazepam, clonazepam and pentobarbital potentiated the muscimol-evoked release of [3H]ACh. The potentiation of muscimol effect by clonazepam was inhibited by Ro 15-1788. These results indicate that both the GABA autoreceptor and postsynaptic receptor may possess the same property which is related to benzodiazepine and barbiturate binding sites in the enteric nervous system of the guinea pig small intestine. The benzodiazepine binding site seems to be of central type.
Acetylcholine↗
Structure-activity relationship of aldose reductase inhibitors based on X-ray crystal structures of oxazolecarbamate derivatives.
In order to elucidate the key atoms and/or stereostructures necessary for the inhibitory emergence of aldose reductase, crystal structure determinations were carried out for 11 oxazolecarbamate analogues, which have similar chemical and physicochemical properties but different inhibitory activities. The molecular conformations, revealed by X-ray analyses, were also ascertained to be energetically stable from theoretical conformational energy calculations. A surprising degree of conformational similarity was observed for the potent inhibitors. The analyses of the quantitative structure--activity relationships showed that the molecular conformation and the dipole moment, as well as the hydrophobicity at the oxazole C5-site, were important for high activity.
Aldehyde Reductase↗
Electron microscopic localization of type I protein kinase C in rat Purkinje cells.
A monoclonal antibody against protein kinase C (PKC) was used for immunocytochemical studies of the type I PKC encoded by gamma-cDNA sequence (gamma-subspecies) in rat Purkinje cells. Dense gamma-subspecies-like immunoreactivity was found on the cell membrane and in the cytoplasm except within cell organelles of the perikaryon, dendrites, axon, and axon terminals. The nucleus was also stained but less heavily, and the nucleoli remained unstained. Synaptic vesicles in the axon terminals were densely stained. The results suggest that gamma-subspecies might be functionally involved in modulation of nuclear function and of pre- and postsynaptic functions including transmitter release in the rat Purkinje cells.
Animals↗