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T Katafuchi

Publications and source records attributed to T Katafuchi.

At least 37 records · Page 2Linked to original sources
PubMed1997

Interleukin-6 inhibits long-term potentiation in rat hippocampal slices.

The effects of recombinant human interleukin-6 (rhIL-6) on long-term potentiation (LTP) induced in the Schaffer collateral/commissural-CA1 pathway were examined using rat hippocampal slices. Field excitatory postsynaptic potential was recorded in the stratum radiatum of the CA1 region. Ten-min applications of rhIL-6 (50-2000 U/ml), started 5 min before the tetanus, significantly inhibited the induction of LTP, and in high doses of rhIL-6 also inhibited short-term potentiation (over 200 U/ml) and post-tetanic potentiation (over 500 U/ml). The effects of rhIL-6 (500 U/ml) were completely abolished by the preincubation of the slices with monoclonal anti-IL-6 receptor antibody (16 microg/ml) for 2 h. Heat-inactivated rhIL-6 had no effect on the synaptic potentiation. RhIL-6 affected neither the previously established LTP nor the basal synaptic transmission. These findings indicated that rhIL-6 modulated synaptic potentiation through the IL-6 receptor-mediated process in the hippocampus, probably by affecting post- and presynaptic sites in the CA1 region. The possible mechanisms of the IL-6-induced suppression of the synaptic potentiation were discussed.

Action Potentials↗
PubMed1997

Tissue distribution and localization of natriuretic peptide receptor subtypes in stroke-prone spontaneously hypertensive rats.

OBJECTIVE: To investigate tissue distribution and localization of the natriuretic peptide receptor (NPR) subtypes' messenger RNA (mRNA) and to compare their expression between stroke-prone spontaneously hypertensive rats (SHR-SP) and Wistar-Kyoto (WKY) rats. METHODS: Total RNA was extracted from organs of SHR-SP and WKY rats aged 13 weeks. The mRNA level was examined by RNase protection assay. The localization of the transcripts was determined by in-situ hybridization. RESULTS: In SHR-SP aged 13 weeks, NPR-A was expressed most abundantly in the adrenal gland, lung and aorta, in that order. NPR-B was expressed highly in the uterus and ovary, and also in the lung, adrenal, and brain. NPR-C was expressed predominantly in the atrium and mesentery, less so in the lung, vein, and kidney. In the adrenal gland, NPR-A was expressed mainly in zona glomerulosa cells. In the atrium, NPR-C was expressed throughout the wall. In the mesentery, NPR-C mRNA was detected mainly in adipocytes. In the kidney, NPR-C was found predominantly in podocytes. Whereas the levels of expression of NPR subtypes in most tissues examined did not differ between SHR-SP and WKY rats, the NPR-C mRNA level was significantly greater in the kidneys of SHR-SP than it was in those of WKY rats. CONCLUSIONS: These results indicated that each NPR subtype had a distinct tissue distribution pattern and that the expression of NPR-C in the kidneys of SHR-SP was greater than that in the kidneys of WKY rats.

Animals↗
PubMed1997

Impaired left ventricular myocardial metabolism in patients with pulmonary hypertension detected by radionuclide imaging.

To assess whether left ventricular myocardial metabolism is affected by the presence of right ventricular pressure overload, we performed 123I-beta-methyl-iodophenyl pentadecanoic acid (123I-BMIPP) and 99Tc(m)-sestamibi (99Tc(m)-MIBI) single photon emission tomography in 24 patients with pulmonary hypertension and in 10 control subjects. The left ventricle was divided into six regions using a short-axis tomogram at the mid-ventricular level. The relative regional uptake (RRU, %) was determined for each region as the ratio of the regional uptake per pixel to the maximum uptake in the six regions. Right heart catheterization was performed to obtain mean pulmonary arterial pressure. 123I-BMIPP uptake in the septum and the adjacent myocardium of the left ventricle was lower in patients with pulmonary hypertension than in control subjects (septal RRU, 75 +/- 6 vs 85 +/- 4%; anteroseptal RRU, 76 +/- 6 vs 86 +/- 3%; posteroseptal RRU, 75 +/- 4 vs 84 +/- 4%; P < 0.001). The reduction in 99Tc(m)-MIBI uptake was confined to the septum in patients with pulmonary hypertension (79 +/- 5 vs 85 +/- 5%; P < 0.05). Interestingly, the septal RRU of 123I-BMIPP and the sum of the septal, anteroseptal and posteroseptal RRUs of 123I-BMIPP were negatively correlated with mean pulmonary arterial pressure (r = -0.70 and -0.55, respectively; P < 0.01). In conclusion, myocardial metabolism in the interventricular septum and the adjacent regions of the left ventricle may be impaired in proportion to the degree of pulmonary hypertension.

Adult↗
PubMed1997

AV3V neurons that send axons to hypothalamic nuclei respond to the systemic injection of IL-1beta.

The single neuron activity in the anteroventral region of the third ventricle (AV3V) was extracellularly recorded in urethan and alpha-chloralose anesthetized rats. Electrical stimulation of the medial preoptic area (mPOA) and the paraventricular nucleus (PVN) revealed a reciprocal neural connection between the AV3V and these hypothalamic nuclei with an ipsilateral preponderance. All the AV3V neurons, which were antidromically activated by the stimulation of the mPOA or the PVN, altered their activity after the systemic injection of interleukin (IL)-1beta. On the other hand, only about 60% of the AV3V neurons that showed orthodromic responses were affected by IL-1beta. In seven of nine AV3V neurons that were electrophysiologically identified to send their axons to the mPOA or the PVN, the recombinant human IL-1beta-induced excitation and inhibition were attenuated by a local application of sodium salicylate through multibarreled micropipettes. These results suggest that the AV3V neurons alter their activity in response to the blood-borne IL-1beta, at least in part, through a local synthesis of prostanoids and then send the information to the mPOA and PVN.

Animals↗
PubMed1997

Differential effects of tumor necrosis factor-alpha and -beta on rat ventromedial hypothalamic neurons in vitro.

The effects of tumor necrosis factor (TNF)-alpha and -beta on the spontaneous firing rate of ventromedial hypothalamic (VMH) neurons were examined in rat brain slice preparations. Of 89 neurons, 36 (40%) showed a decrease in the firing rate to -78.2 +/- 4.0% (n = 36, mean +/- SE) of the preapplication level after a bath application of 20 ng/ml (approximately 1.2 nM) of TNF-alpha. This response to TNF-alpha still persisted in a low-Ca2+, high-Mg2+ medium. Six (7%) of the 89 neurons were excited and 47 (53%) were unaffected by TNF-alpha. The inhibitory responses induced by TNF-alpha were abolished in a solution that contained sodium salicylate (1.9 x 10(-8)M). In contrast, TNF-beta at a dose of 20 ng/ml (approximately 1.1 nM) increased the firing rate to +39.2 +/- 6.5% (n = 11) of the preapplication level in 11 (24.5%) of 45 VMH neurons. Two of the 45 neurons (4.5%) were inhibited and 32 (71%) were unaffected by TNF-beta. The threshold concentration of TNF-alpha to alter the VMH neuron activity was lower than that of TNF-beta. Heat-inactivated TNFs were without effect. These findings suggest that TNF-alpha and -beta act as neuromodulators in the VMH, at least partly through prostaglandin synthesis, and differentially modulate the VMH neuron activity.

Animals↗
PubMed1997

Role of natriuretic peptide receptor type C in Dahl salt-sensitive hypertensive rats.

The natriuretic peptide system is suggested to be involved in the pathogenesis of salt-sensitive hypertension; a recent report indicated that disruption of the atrial natriuretic peptide precursor gene caused salt-sensitive hypertension. However, natriuretic peptide receptor (NPR)-A knockout mice did not show enhanced salt sensitivity of blood pressure. The aim of the present study was to investigate the role of NPR-C, the other receptor for atrial natriuretic peptide, in increased salt sensitivity of blood pressure. Dahl salt-sensitive (DS) and salt-resistant (DR) rats were placed on a 0.3% or 8% NaCl diet for 4 weeks. Blood pressure was elevated by salt loading only in DS rats. RNase protection assay demonstrated that NPR-C transcript level in the kidney was reduced by chronic salt loading in both DR and DS rats, whereas expression of NPR-A and NPR-B was not altered. The reduction of NPR-C mRNA in response to salt loading was enhanced in DS compared with DR rats. In situ hybridization indicated that the salt-induced NPR-C change was attributed mainly to suppressed expression of NPR-C in the podocytes. NPR-C gene expression was regulated by salt loading in a tissue-specific manner; the marked decrease in NPR-C mRNA by salt loading was seen only in the kidney. These data suggest that the exaggerated salt-induced reduction of NPR-C in the kidney of DS rats may play an important role in the pathogenesis of salt hypertension in this animal, possibly related to impaired renal sodium excretion.

Animals↗
PubMed1997

Gene expression of endothelial type isoform of nitric oxide synthase in various tissues of stroke-prone spontaneously hypertensive rats.

Nitric oxide (NO) has been suggested to play important roles in the pathophysiology of various cardiovascular diseases. This study tested the hypothesis that an attenuated biological action of NO in hypertension is attributed to a change in the gene expression of NO synthase (NOS), a key enzyme involved in NO formation. The expression level of mRNA of endothelial type NOS (NOS-III) was determined in stroke-prone spontaneously hypertensive rats (SHR-SP/Izm) and Wistar Kyoto rats (WKY/Izm) by ribonuclease protection assay using a partial clone as probe. NOS-III mRNA was expressed ubiquitously in various tissues of WKY/Izm and SHR-SP/Izm either at 5 wk or 13 wk of age. There was no significant difference in the tissue expression of NOS-III mRNA between the two strains at either age. The intensity and localization of the hybridization signal for NOS-III mRNA in the heart of SHR-SP/Izm did not differ from those in the heart of WKY/Izm. These results suggest that the attenuated biological action of NO implied in genetically hypertensive rats is not attributed to an abnormality at the level of NOS-III mRNA expression in the tissues, although lack of an increase in NOS-III gene expression, despite the hypertensive hemodynamic stress, may modify the blood pressure in hypertension.

Animals↗
PubMed1997

[Evaluation of the automatic quantification of left ventricular function using ECG gated 99mTc-MIBI myocardial SPECT].

We studied the accuracy of left ventricular (LV) volumes and ejection fraction (EF) derived from ECG gated 99mTc-sestamibi myocardial perfusion SPECT (G-SPECT) and the software for automatic data analysis (QGS program described by Germano G et al.). G-SPECT was performed in 29 patients with various cardiac diseases. LV end-diastolic and end-systolic volumes (LVEDV and LVESV), and LVEF determined by QGS program were compared to those by Simpson method in biplane left ventriculography (LVG). Interobserver reproducibility in measuring the G-SPECT parameters was excellent (LVEDV: r = 0.99, LVESV: r = 0.99, LVEF: r = 0.97). There was a good correlation between the values obtained from G-SPECT and LVG (LVEDV: r = 0.92, LVESV: r = 0.94, LVEF: r = 0.85), but G-SPECT tended to underestimate LVEDV and LVEF. In 17 patients with moderate to severe myocardial perfusion defects selected from the subjects, the correlation was maintained fairly high (LVEDV: r = 0.90, LVESV: r = 0.92, LVEF: r = 0.77). In conclusion, QGS program provides high accuracy and reproducibility in determining LV volumes and LVEF from G-SPECT.

Adult↗
PubMed1996

Effects of IL-1 beta on neuronal activities in the dorsal motor nucleus of the vagus in rat brain slices.

Effects of recombinant human interleukin-1 beta (IL-1 beta) on the neuronal activities in the rat dorsal motor nucleus of the vagus (DMV) were investigated by extra- and intracellular recordings in slice preparations. Twelve (52%) of 23 spontaneously firing neurons recorded extracellularly, 7 of which were electrophysiologically identified as vagal motoneurons, were inhibited by a bath application of IL-1 beta at a dose of either 5.8 x 10(-8) or 5.8 x 10(-8) M. The duration of the responses ranged widely from about 10 min to more than 2 h. Two (9%) of the 23 neurons were excited, whereas the remaining 9 (39%) were not affected by IL-1 beta. Of 42 DMV neurons recorded intracellularly, 19 (45%) showed a hyperpolarization following an application of 5.8 x 10(-8) M IL-1 beta, which still persisted in a TTX-containing solution. Two (5%) displayed depolarization and 21 (50%) were unaffected. The hyperpolarization in 16 of the 19 neurons (84%) ranged from -5 to -10 mV and lasted for more than 30 min without changing the input resistance. The IL-1 beta-induced hyperpolarization was completely blocked by concurrent perfusion with sodium salicylate. The remaining three neurons showed a short-lasting (5-14 min) hyperpolarization (ranging from -6 to -15 mV) with a decrease in the input resistance. These findings indicate that IL-1 beta mainly inhibits the vagal motoneurons in the DMV, at least partly through prostaglandin synthesis. This provides a mechanism that could account for the central action of IL-1 beta on visceral processes such as the inhibition of gastric acid secretion.

Animals↗
PubMed1996

Facilitatory effects of pituitary adenylate cyclase activating polypeptide (PACAP) on neurons in the magnocellular portion of the rat hypothalamic paraventricular nucleus (PVN) in vitro.

To establish the role of pituitary adenylate cyclase activating polypeptide (PACAP), a member of vasoactive intestinal polypeptide (VIP) family, as a neurotransmitter/neuromodulator in the central nervous system, the effects of PACAP38, PACAP27 and VIP on the single neuron activity in the magnocellular portion of the hypothalamic paraventricular nucleus (mg.PVN) were examined in rat brain slice preparations. Extracellular recordings were made from 111 neurons in the mg.PVN, which fired spontaneously at an average rate of 1.85 +/- 0.2 spikes/s (mean +/- SEM). PACAP38 and PACAP27 were applied to 78 and 33 of the 111 neurons, respectively. Perfusion with PACAP38 in doses between 10 nM and 1 microM increased the firing rate of 56 (71.8%) of the 78 neurons in a dose-dependent manner. The threshold dose of PACAP38 to excite the neurons seemed to lie below 10 nM. The application of PACAP27 (1 microM) also increased the firing rate of 19 (57.6%) of the 33 neurons tested. Eleven (52.4%) of 21 neurons which were excited by PACAP38 also showed excitation following perfusion with VIP (1 microM). The responses to PACAP38 in 12 of 20 neurons and those to VIP in 6 of 9 neurons tested were still observed in a low Ca2+ and high Mg2+ medium. Although there was no difference in the mean latency between the responses to PACAP38 (1 microM) and VIP (1 microM) (2.1 +/- 0.1 min and 2.4 +/- 0.4 min, respectively), the duration of the PACAP38-induced excitation (59.0 +/- 5.0 min) was much longer than that of the VIP-induced one (18.8 +/- 3.1 min). The PACAP38 (30 nM)-induced excitation was reversibly blocked by a concurrent application of PACAP5-38 (300 nM), a PACAP receptor antagonist. While a selective VIP receptor antagonist, [Lys1, Pro2,5, Arg3,4, Tyr6]-VIP (1 microM), did not affect the excitatory responses to PACAP38 (300 nM), it completely blocked the VIP (1 microM)-induced excitation. These findings suggest that PACAP may therefore modulate the secretion of the pituitary hormones at least partly by its action on the neurons in the mg.PVN through the activation of specific receptors for PACAP.

Action Potentials↗
PubMed1995

Cloning and properties of a novel natriuretic peptide receptor, NPR-D.

A novel natriuretic peptide receptor, which we have termed natriuretic peptide receptor D (NPR-D), has been cloned and characterized. cDNAs related to the natriuretic peptide receptor (NPR) were amplified by PCR from a template of poly(A)-rich RNA isolated from the eel gill. Sequencing of the PCR products revealed the presence of a new clone that showed about 70% sequence identity to the eel type-C receptor, NPR-C. The PCR fragment was used to determine the tissue distribution of the new NPR-D message by an RNase protection assay, which gave the strongest signal in brain samples, and then used to screen a brain library to obtain a full-length cDNA clone. The cDNA clone predicted a protein of 500 amino acids containing a signal sequence and a hydrophobic transmembrane segment. The predicted sequence also contained the NPR motif which is essential for the binding of natriuretic peptides. The protein NPR-D was expressed in COS cells and shown to have high affinities for eel and rat natriuretic peptides. The newly cloned NPR-D has a short cytoplasmic tail; in this respect, NPR-C and NPR-D are very similar and form a subfamily of the NPR family. Affinity labeling indicated that NPR-D exists as a disulfide-linked tetramer. This is a marked contrast to the homodimeric structure of NPR-C. HS-142-1, a non-peptide natriuretic peptide receptor antagonist of microbial origin previously shown to be selective for the guanylate-cyclase-coupled receptors NPR-A and NPR-B, competitively inhibited the binding of 125I-labeled eel natriuretic peptide to eel NPR-D, whereas it did not affect the binding activity of eel NPR-C, suggesting that HS-142-1 is an antagonist that recognizes the tetrameric structures of NPR since the guanylate-cyclase-coupled receptors have also been demonstrated to exist as tetramers.

Amino Acid Sequence↗
PubMed1995

The effect of interleukin-1 beta on the efferent activity of the vagus nerve to the thymus.

The effects of intravenous (i.v.) administration of recombinant human interleukin-1 beta (rhIL-1 beta) and human interleukin-1 beta-fraction (hfrIL-1 beta) on the activity of vagal efferent fibers innervating the thymus were observed in urethane-anesthetized rats. An i.v. injection of 10 ng rhIL-1 beta or hfrIL-1 beta caused a similar degree of increase in the efferent activity, which lasted longer than 2 h. The least effective dose was 1 ng and dose-dependent responses were observed after i.v. injection of rhIL-1 beta at doses of 1 ng, 10 ng and 100 ng. The IL-1 beta-induced activation of efferent activity of the vagal branch to the thymus implicates their involvement in the neural modulation of the thymic function.

Animals↗
PubMed1995

Cloning, properties, site-directed mutagenesis analysis of the subunit structure, tissue distribution and regulation of expression of the type-C eel natriuretic peptide receptor.

Eel natriuretic peptide receptor C (NPR-C) was cloned, characterized and found to have a unique interchain disulfide linkage when compared to that of mammalian NPR-C. The NPR-C cDNA was obtained from an eel gill cDNA library; the open reading frame codes for a polypeptide of 502 amino acids exhibiting the known features of NPR-C, including a weak ligand specificity and a disulfide-linked homodimeric structure. The deduced amino acid sequence shares approximately 60% similarity with the mammalian NPR-C but it lacks the Gly-rich prosequence present in the mammalian counterparts. Site-directed mutagenesis revealed that eel and mammalian NPR-C are quite different in their interchain disulfide-bonding pattern; eel uses the second Cys residue and mammals the fifth Cys residue for the covalent dimerization. The ligand-binding activity of the extracellular domain is not independent of the short cytoplasmic tail. RNase protection analysis revealed that the eel receptor is highly expressed in the gill and heart and, to a much lesser extent, in other tissues including the brain and intestine. The NPR-C mRNA levels were found to be down-regulated in most tissues when eels were transferred from fresh water to seawater; however, in the anterior intestine, the levels were up-regulated, suggesting that NPR-C plays a role in the adaptation to salinity changes in the euryhaline eel.

Amino Acid Sequence↗
PubMed1995

Interferon-alpha acts at the preoptic hypothalamus to reduce natural killer cytotoxicity in rats.

We previously demonstrated that an intracerebroventricular injection of recombinant human interferon-alpha (rhIFN-alpha) reduced the cytotoxicity of splenic natural killer (NK) cells in rats and mice. In the present study, we investigated the brain sites at which rhIFN-alpha acts to suppress splenic NK activity in unanesthetized rats implanted unilaterally with a chronic hypothalamic cannula. A microinjection of 200 U of rhIFN-alpha into the medial part of the preoptic hypothalamus reduced NK activity to approximately 60% of control 30 min after the injection. Administration of 50 U of rhIFN-alpha also decreased NK activity to approximately 80%. The injection of 200 U of rhIFN-alpha into other hypothalamic areas (lateral preoptic hypothalamus, ventromedial hypothalamus, lateral hypothalamus, and paraventricular nucleus) had no effect. The medial preoptic hypothalamus-rhIFN-alpha-induced immunosuppression was completely blocked by splenic denervation, but not by adrenalectomy. These results suggest that IFN-alpha suppresses splenic NK activity predominantly through the medial preoptic hypothalamus-sympathetic pathway.

Animals↗
PubMed1995

Intracerebroventricular injection of prostaglandin E2 increases splenic sympathetic nerve activity in rats.

The effects of central administration of prostaglandin E2 (PGE2) and its selective agonists on splenic sympathetic nerve activity (SNA) were investigated in urethan- and alpha-chloralose-anesthetized rats. An intra-third-cerebroventricular (13V) injection of PGE2 (0.1-10 nmol/kg) increased splenic SNA in a dose-dependent manner. An I3V injection of an EP1 agonist, 17-phenyl-omega-trinor PGE2 (1-30 nmol/kg), also resulted in a dose-dependent increase in splenic SNA, with a time course similar to that of PGE2-induced responses. In contrast, EP2 agonists, butaprost (10-100 nmol/kg I3V) and 11-deoxy-PGE1 (10-100 nmol/kg I3V), had no effect on splenic SNA. An I3V injection of M & B-28767 (an EP3/EP1 agonist, EP3 >> EP1) increased splenic SNA only at high doses (10-100 nmol/kg). Pretreatment with an EP1 antagonist, SC-19220 (200 and 500 nmol/kg), completely blocked the responses of splenic SNA to PGE2 (0.1 nmol/kg) and M & B-28767 (10 nmol/kg), respectively. These findings indicate that brain PGE2 increases splenic SNA through its action on EP1 receptors.

Animals↗
PubMed1995

Cerebellar afferents to neuroendocrine cells: implications for adaptive responses to simulated weightlessness.

The hypothalamo-neurohypophyseal system as well as the autonomic nervous system is involved in homeostatic responses associated with changes in head position and orthostatic reflex. The responses induced by body tilt on earth are thought to be attributed to changes in inputs from baroreceptors, vestibular organs and proprioreceptors that are normally required for postural control. The information from these organs is sent to the hypothalamus which thereby influences both neuroendocrine and autonomic systems as well as various kinds of emotional behavior. Our findings showing the fastigial input to the hypothalamus suggested that the FN plays a significant role in these homeostatic responses through its connections with the brain stem and the hypothalamus. Figure 4 shows the input-output organization among the hypothalamus, cerebellum and brain stem, described in detail in sections III to V. This hypothesis may help to account for the autonomic and endocrine disorders often observed in weightlessness.

Adaptation, Physiological↗
PubMed1995

The hypothalamo-sympathetic nervous system modulates peripheral cellular immunity.

Our findings reviewed in this article have revealed that the stimulation of opioid receptors of the hypothalamic neurons by interferon alpha and beta-endorphin synthesized in the brain or by stress causing the opioid-dependent analgesia suppresses the natural killer cytotoxicity, an important component of immunosurveillance, through an activation of the hypothalamic CRF-sympathetic nervous system.

Animals↗