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Biomedical subjects

C Tanaka

Publications and source records attributed to C Tanaka.

At least 361 records · Page 20Linked to original sources
PubMed1984

3H-ACh release from guinea pig gallbladder evoked by GABA through the bicuculline-sensitive GABA receptor.

We investigated the effect of GABA on the spontaneous efflux of 3H-acetylcholine (ACh) from the isolated guinea pig gallbladder loaded with 3H-choline. Application of GABA (10(-5) M) caused a significant increase in the fractional rate of tritium efflux. This GABA-evoked efflux of ACh was inhibited by the perfusion of tetrodotoxin (10(-6) M) and Ca-free medium. Nipecotic acid (10(-4) M) did not affect the GABA-evoked release of ACh, indicating that ACh was not released by the entry of GABA into cholinergic nerve terminals. Bicuculline (10(-6) M) and furosemide (10(-6) M), the chloride ion channel blocker, inhibited the GABA-evoked ACh release. The application of muscimol (10(-5) M), but not baclofen (10(-5) M) also produced an increase in the fractional rate of ACh release. Thus, the GABA receptors involved in the increase of ACh release are bicuculline-sensitive. The GABA-evoked release of ACh was not altered by the perfusion with hexamethonium (10(-5) M), thus indicating the presence of GABA receptors on the postganglionic cholinergic neurons. These findings suggest that bicuculline-sensitive GABA receptors probably coupled to a Cl- ionophore are present on postganglionic cholinergic neurons and are involved in the increase of ACh release in guinea pig gallbladder.

Acetylcholine↗
PubMed1984

Measurements of in vivo energy metabolism in experimental cerebral ischaemia using 31P-NMR for the evaluation of protective effects of perfluorochemicals and glycerol.

Effects of perfluorochemical (PFC) and glycerol on energy metabolism in cerebral ischaemia were examined by the sequential measurements of in vivo 31P-NMR spectrum using topical magnetic resonance (TMR). Experimental cerebral ischaemia was induced in forty-five Wistar rats by a four-vessel occlusion method. The 31P-NMR spectrum and the EEG were monitored during preischaemic and ischaemic periods and after circulation was restored for various periods up to 240 min. There were several peaks in the 31P-NMR spectrum of the preischaemic rat brain; beta-ATP, alpha-ATP, gamma-ATP, phosphocreatine (PCr), phosphodiesters, inorganic phosphate (Pi) and sugar phosphate. As soon as the ischaemia was induced, PCr and ATP decreased and Pi increased. The chemical shift of the increased Pi peak decreased, showing acidosis of the brain tissue. After circulation was restored following the 30 min ischaemia, recovery of the 31P-NMR spectrum occurred within 30 min in all sixteen untreated rats. Recovery of the 31P-NMR spectrum was induced by recirculation only in half of the six rats in the untreated 60 min ischaemia group. None of the six rats in the untreated group showed recovery of the spectrum after 120 min ischaemia. When 20% Fluosol-DA was administered at a dose of 20 ml/kg before the induction of ischaemia, all eight rats showed recovery of the spectrum after 120 min ischaemia. Moreover, four of six rats treated with both PFC and glycerol showed temporary recovery even after 240 min ischaemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1984

Neuronal GABA release and GABA inhibition of ACh release in guinea pig urinary bladder.

gamma-Aminobutyric acid (GABA) and glutamate decarboxylase (GAD) are present in the urinary bladder of guinea pigs, and the possible correlation in regional distribution between GABA, GAD, and the number of vesical ganglion cells was studied. Electrical stimulation of the bladder strips produced an increase in the calcium-dependent and tetrodotoxin-sensitive [3H]GABA release and contractions in the strips preloaded with [3H]GABA. Nicotine, acetylcholine chloride (ACh), and hexamethonium did not significantly alter the release of [3H]GABA. Bicuculline significantly enhanced [3H]ACh release and cholinergic components of contractions evoked by electrical stimulation of the bladder strips preloaded with [3H]choline, thereby suggesting that this compound antagonizes the effect of endogenous GABA released during stimulation. GABA and muscimol but not baclofen reduced both the [3H]ACh release and contractions evoked by nicotine. These effects of GABA were antagonized by bicuculline and furosemide but not by alpha- and beta-adrenergic blockers. These findings suggest that GABA may be a noncholinergic nonadrenergic inhibitory neurotransmitter in the urinary bladder. The motility of the urinary bladder is thus inhibited by reducing the release of ACh from the postganglionic cholinergic neurons through bicuculline-sensitive GABA receptors probably associated with the chloride ion channel.

Acetylcholine↗
PubMed1983

Correspondency between different affinity states and target size of the bovine striatal D2 dopamine receptor.

Target size analysis of the D2 dopamine receptor in the bovine striatum revealed the presence of two populations of this receptor, in terms of apparent molecular size. The size of large target was approximately 150 X 10(4) daltons, while that of small target was 11 X 10(4) daltons. The antagonist [3H]spiperone labeled both large and small sized D2 receptors, while agonist [3H]n-propylapomorphine (NPA) labeled only the former. In addition, the apparent molecular size of a functional unit for the GTP effect was calculated to be 150 X 10(4) daltons, such appearing to be identical to that of large target sized D2 dopamine receptors. Therefore, the large sized D2 receptor, probably an oligomeric complex consisting of D2 receptor recognition protein and guanine nucleotide regulatory protein, has a high affinity for both agonist and antagonist, while the small sized receptor, probably a monomeric or dimeric receptor recognition protein, has a high affinity for only the antagonist.

Acetylcholinesterase↗
PubMed1983

Labeled norepinephrine uptake and release in rat globus pallidus.

The uptake and release of [3H]norepinephrine [( 3H]NE) were investigated using isolated rat globus pallidus slices to determine the possible neurotransmitter role of this catecholamine. The uptake into these slices was linear for the first 10 min. Kinetic analysis indicated two components of NE accumulation, one representing a high (Km1 2.9 X 10(-7) M and Vmax1 1.4 pmol/mg/10 min) and other a low (Km2 1.6 X 10(-6) M and Vmax2 5 pmol/mg/10 min) affinity uptake system. Desmethylimipramine at a concentration of 10(-5) M reduced the high affinity uptake of [3H]NE by 25% of the control values. Electrical stimulation of the slices increased the efflux of [3H]NE and its metabolites from tissues preloaded with [3H]NE, in a current- and frequency-dependent fashion. The release of [3H]NE and its metabolites induced by electrical stimulation (1 mA, 20 Hz, 1 ms for 2 min) was inhibited by tetrodotoxin (10(-6) M), and by a calcium-free medium containing EGTA (10(-4) M) or medium with a high magnesium-concentration (2 X 10(-2) M). These findings provide strong evidence for the neurotransmitter role of NE, in these tissues.

Animals↗
PubMed1983

The glycoprotein nature of solubilized muscarinic acetylcholine receptors from bovine cerebral cortex.

Muscarinic acetylcholine receptors were solubilized from bovine cerebral cortex with 3-[(3-cholamidopropyl)-dimethylammonio]-1-propane sulfonate. The so-obtained receptors could be precipitated by Wheat Germ (73%), Concanavalin A (55%), Lens Culinaris (36%) and Ricinus Communis (26%), but not by Peanut, Dolichus Biflorus and Ulex Europaeus. On Wheat Germ- and Concanavalin A-affinity chromatography, the solubilized muscarinic receptors were retained on both columns and subsequently eluted with N-acetylglucosamine and alpha-methyl-D-mannoside, respectively. A high concentration (100 micrograms/ml) of Wheat Germ or Concanavalin A did not interfere with Z-[3H]quinuclidinyl benzilate binding, thereby suggesting that the lectin binding sites are not directly involved in the receptor binding function. These solubilized muscarinic receptors are postulated to contain carbohydrate residues, N-acetyl-glucosamine, mannose and galactose, as glycoprotein.

Acetylcholine↗
PubMed1983

Selective decrease in the affinity of D2 dopamine receptor for agonist induced by islet-activating protein, pertussis toxin, associated with ADP-ribosylation of the specific membrane protein of bovine striatum.

When the crude synaptic membrane preparations from bovine striatum were treated with islet-activating protein (IAP), one of the pertussis toxins, a protein with a molecular weight of about 40,000 was ADP-ribosylated. In parallel with this ADP-ribosylation, there was a decrease in D2 dopamine receptor affinity for agonist, while the affinity for antagonist remained unaltered. Addition of GTP to nontreated membranes also resulted in a decrease in the affinity of D2 receptor for agonist, and there was no further reduction of affinity for agonist with addition of GTP to the IAP-treated membranes. As IAP specifically acts on the guanine nucleotide regulatory protein which mediates the inhibition of adenylate cyclase activity (Ni), our findings indicate a possible molecular interaction between the brain D2 dopamine receptor and Ni.

Adenosine Diphosphate Ribose↗
PubMed1983

Regulation of the solubilized bovine cerebral cortex muscarinic receptor by GTP and Na+.

The muscarinic acetylcholine receptor was solubilized, in a sensitive form for GTP and Na+, from bovine cerebral cortex using a zwitterionic detergent 3-[(3-cholamidopropyl)-dimethylammonio]-1-propane sulfonate. The solubilized muscarinic receptor displayed characteristics as follows: (1) high affinity to nanomolar concentration of Z-[3H]quinuclidinyl benzilate; (2) muscarinic agonists and antagonists had similar inhibitory potencies as on the membrane-bound receptor; (3) without Na+, GTP did not significantly alter the binding affinity of muscarinic agonists and antagonists; (4) GTP in the presence of Na+, selectively decreased the affinity of muscarinic agonists, carbamylcholine and oxotremoline, but not the antagonist binding affinity; (5) Na+ in the absence or presence of GTP, reduced both muscarinic agonist and antagonist affinities.

Animals↗
PubMed1983

GABA evoked ACH release from isolated guinea pig ileum.

To identify the target cells of GABAergic neurons located in the myenteric plexus, the action of gamma-aminobutyric acid (GABA) on the release of acetylcholine (ACh) and on the contractions was studied using the isolated guinea pig ileum. GABA evoked a release of 3H-ACh from the contracting ileum, under conditions of loading with 3H-choline. As both the GABA-evoked release of 3H-ACh and the contractions were inhibited by bicuculline, tetrodotoxin and furosemide, but not by hexamethonium, this release seems to be evoked through GABA receptors which are bicuculline sensitive and associated with the Cl- ion channel.

Acetylcholine↗
PubMed1983

Adrenergic and cholinergic receptors in human nasal mucosa in cases of nasal allergy.

We have demonstrated for the first time alpha-1 adrenergic, beta-adrenergic, and muscarinic cholinergic receptors in human nasal mucosa obtained from patients with nasal allergy or sinusitis. Using the radioligand 3H-prazosin, 3H-dihydroalprenolol (3H-DHA) and 3H-quinaclidinyl benzilate (3H-QNB), we determined the receptor densities (Bmax) and affinities (KD) of alpha-1, beta, and muscarinic receptors. There was an increased number of muscarinic receptors and a decreased number of alpha-1, beta receptors in patients with nasal allergy but not in those with sinusitis. Binding affinities (KD) of alpha-1, beta, and muscarinic receptors were unchanged in all patients with nasal allergy and sinusitis. Disorders of the autonomic nerve receptors appear to play a definite role in pathology of nasal allergy.

Adult↗
PubMed1983

Solubilization of D2 dopamine receptor coupled to guanine nucleotide regulatory protein from bovine striatum.

D2 dopamine receptor from bovine striatum was solubilized in a form sensitive to guanine nucleotides, by means of a zwitterionic detergent, 3-[(3-cholamidopropyl)-dimethylammonio]-1-propane sulfonate (CHAPS). The presence of sodium ion markedly increased the solubilization yield. Treatment of the membranes with 10 mM CHAPS and 0.72 M NaCl solubilized 26% of the stereospecific [3H]spiperone binding sites in the original membrane preparations. The solubilized [3H]spiperone binding sites possessed characteristics of the D2 dopamine receptor: (a) localization of the site in the striatum but not in the cerebellum; (b) high affinity to nanomolar concentrations of [3H]spiperone; (c) displacement of [3H]spiperone binding by nanomolar concentrations of neuroleptics, but only by micromolar concentrations of dopamine and apomorphine; (d) equal activity of various dopamine agonists and antagonists in the soluble and membrane preparations. Guanine nucleotides decreased the affinity of the solubilized D2 dopamine receptor for dopamine agonists, but not for antagonists. The solubilized receptor complex was eluted in Sepharose CL-4B column chromatography as a large molecule, with a Stokes radius of approximately 90 A. These results indicate that the complex between the D2 dopamine receptor and GTP binding protein remains intact throughout the solubilization procedure.

Animals↗
PubMed1983

GABA, glutamic acid decarboxylase, and GABA transaminase levels in the myenteric plexus in the intestine of humans and other mammals.

Regional distribution of endogenous gamma-aminobutyric acid (GABA), its synthesizing enzyme, glutamic acid decarboxylase (GAD), and metabolic enzyme, GABA transaminase (GABA-T), were determined in the intestinal tract of guinea pigs and cats and the findings compared with the number of ganglion cells in Auerbach's plexus. There were positive correlations among the GABA contents and the numbers of neural cells of the plexus. The precise localization of GABA and GAD in individual layers (mucosa, circular and longitudinal muscles, and Auerbach's plexus) in the human and cat colon was also determined. The endogenous GABA contents and GAD activity were the highest in Auerbach's plexus in tissues of both species. These results indicate that GABA is synthesized and localized in Auerbach's plexus and probably plays a significant role in the enteric nervous system.

4-Aminobutyrate Transaminase↗