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K Torii

Publications and source records attributed to K Torii.

At least 37 records · Page 2Linked to original sources
PubMed2000

Hypothalamic and amygdalar neuronal responses to various tastant solutions during ingestive behavior in rats.

The forebrain, including the amygdala (AM) and hypothalamus, may be a higher brain center that modulates the activity of a brainstem neural system that influences ingestive behavior via descending projections. In this study, to elucidate the characteristics of sensory information processing in the forebrain in relation to this putative connection, we recorded neuronal activity in the AM and hypothalamus [lateral hypothalamic area (LHA), medial hypothalamic area (MHA)] of rats during discrimination of conditioned sensory stimuli and the ingestion of various tastant solutions. Of 420 responsive AM neurons identified, 24 were taste responsive and located mainly in the central nucleus of the AM. Multivariate analyses of these taste neurons suggested that in the AM, taste quality is processed on the basis of palatability. In the hypothalamus, of 282 LHA and MHA neurons recorded, 144 responded to one or more conditioned auditory stimuli and/or licking of one or more solutions. Stress, which is known to influence feeding behavior, increased the mean spontaneous activity of LHA neurons but decreased the mean spontaneous neuronal activity of MHA neurons. This pattern of changes in spontaneous neuronal activity correlated with alterations in feeding behavior during stress. Furthermore, the activity of both AM and LHA neurons was modulated flexibly during conditioned associative learning. Together, the data suggest that the activity of the AM and hypothalamic neurons is altered when animals must modulate ingestive behavior by learning a new stimulus associated with food and by being exposed to stress, suggesting that these forebrain areas are important modulators of the activity of a basic neural system in the brainstem that influences ingestive behavior.

Acoustic Stimulation↗
PubMed2000

Mechanisms of umami taste preference and aversion in rats.

The influence of glutamate intake on growth and appetite, and the mechanisms of preference and aversion for monosodium L-glutamate (MSG) solutions were investigated in rats. Food intake, but not weight gain, was reduced significantly in rats fed a glutamate + glutamine (Glx)-deficient diet compared with those fed a control diet. Increase in the voluntary intake of Glx solutions was more rapid in rats fed the Glx-deficient diet. The preference and aversion for MSG solutions were distinctly different in 14 rat strains tested. Brown-Norway rats showed a strong preference for 60 mmol/L MSG and did not show aversive behavior toward solutions containing up to 600 mmol/L MSG. Sprague-Dawley (SD) rats showed a moderate preference for 60 mmol/L MSG and a weak aversion for MSG concentrations higher than 240 mmol/L; Long-Evans Agouti rats showed a moderate preference for 60 mmol/L MSG and a marked aversion for MSG concentrations higher than 120 mmol/L. Aversion was not due to nonspecific hyperosmotic effects. After section of gastric branches of the vagus nerve, MSG became aversive to SD rats. Aversion to 240 mmol/L MSG was reduced by 23-39% when combined with proline, alanine, glycine and glucose. These results show that the preference and aversion for MSG are determined by genetic factors, as well as vagus nerve function, and that the aversion to high MSG concentrations is reduced by the presence of other glucogenic amino acids and sugars.

Amino Acids↗
PubMed2000

Circadian release of hypothalamic norepinephrine in rats in vivo is depressed during early L-lysine deficiency.

Rats rapidly recognize an amino acid-deficient diet, presumably via central mechanisms that involve hypothalamic circuits. We evaluated the effects of a deficiency of the essential amino acid, L-lysine, on the ventromedial hypothalamus (VMH) norepinephrine (NE) circadian release in free-moving, nonstressed rats. A dialysis probe was implanted into the VMH of male Wistar rats. Continuous microdialysis measurement was done during the first 26 h of L-lysine (Lys) deficiency in rats that had free access to food and fluid. The dark phase was from 1900 to 0700 h. Rats were divided into six groups according to their food and fluid intakes. They were fed either normal (Lys sufficient) or Lys deficient powdered food and provided with distilled water, glycine (Gly, 400 mmol/L) or Lys solution (400 mmol/L). In control rats, VMH NE release showed a diurnal pattern, with the lowest levels measured at the onset of the dark phase. In Lys-deficient rats, the release was significantly depressed from the early morning (0500 h) compared with Lys-sufficient rats, without any differences in food and fluid intakes. A normal pattern of VMH NE was restored by the provision of 400 mmol/L Lys solution to deficient rats. The results suggest that the VMH NE release is involved in the early integration of signals about amino acid deficiency.

Analysis of Variance↗
PubMed2000

Effects of repeated cold stress on activity of hypothalamic neurons in rats during performance of operant licking task.

The present study investigated the effects of repeated cold stress on single neuron activity in the lateral hypothalamic area (LHA) and medial hypothalamic area (MHA) of behaving rats. The rats were trained to lick a protruding spout in response to one of several cue-tone stimuli (CTSs) to ingest water, or amino acid, NaCl or glucose solution. Following this training, the rats were raised under either stressed (repeated temperature changes between -3 and 24 degrees C) or control (24 degrees C) condition for 2 mo. During this period, neuronal activity was recorded in the LHA and MHA. For rats raised under the stressed condition, mean spontaneous firing rate of LHA neurons was significantly greater than for rats under the control condition. More LHA neurons in the stressed rats responded, with an accompanying decrease in activity (inhibitory response), to CTSs than in the control rats. During extinction learning, some LHA neurons enhanced or reversed the responses to CTSs in the stressed rats, whereas no LHA neurons showed such response changes in the control rats. In contrast to the effects of the stressed condition on LHA neuron activity, mean spontaneous firing rate of MHA neurons in the stressed rats was significantly smaller than in the control rats. Fewer MHA neurons in the stressed rats responded to CTSs and/or ingestion of sapid solutions. The preceding results suggested that repeated cold stress produces a specific pattern of changes in spontaneous activity and responses to sensory stimuli in LHA and MHA neurons; this could underlie the behavioral changes induced by repeated cold stress such as hyperphagia and hyper-reactivity to sensory stimuli.

Acoustic Stimulation↗
PubMed2000

[Sarcoidosis with primary acute cavitation exacerbated by bronchial asthma].

A 22-year-old woman complaining of blurred vision visited our hospital in March 1995 and was given a diagnosis of uveitis. Chest X-ray and computed tomographic (CT) films demonstrated bilateral hilar lymphadenopathy (BHL), diffuse granular shadows in both lung fields, and a cavity with a thin, smooth wall in the right upper lung field. Because histopathologic findings from transbronchial lung biopsy specimens of the lung and cavity tissues disclosed sarcoid granuloma, the diagnosis was sarcoidosis with primary cavitation, which is very rare for this disease. Although BHL disappeared without medication, in November the patient experienced dyspnea due to attacks of bronchial asthma that had been in remission for a long period. Treatment with inhalation of becromethazone propionate markedly alleviated her symptoms. In May 1998, follow-up chest CT films demonstrated that the cavity had disappeared. This case suggested that sarcoidosis leads to a deterioration of asthma control, a conclusion supported by previous reports.

Adult↗
PubMed1999

Purification and characterization of dibenzothiophene (DBT) sulfone monooxygenase, an enzyme involved in DBT desulfurization, from Rhodococcus erythropolis D-1.

Dibenzothiophene (DBT), a model of organic sulfur compound in petroleum, is microbially desulfurized to 2-hydroxybiphenyl by Rhodococcus erythropolis D-1. Three desulfurization (Dsz) enzymes--DszC, A, and B--and flavin reductase are involved in sulfur-specific DBT desulfurization. In this study, DszA was purified, characterized, and crystallized from R. erythropolis D-1. DszA, DBT sulfone monooxygenase, is the second enzyme in microbial DBT desulfurization metabolism and catalyzes the conversion of DBT sulfone to 2'-hydroxybiphenyl 2-sulfinic acid in the presence of flavin reductase with cleavage of the carbon-sulfur bond in the DBT skeleton. Using anion-exchange column chromatography, the four enzyme fractions responsible for DBT desulfurization were separated, and DszA was then purified to homogeneity. Polygonal crystals of DszA were observed within a week. DszA was found to have a molecular mass of 97 kDa and to consist of two subunits with identical masses of 50 kDa. The N-terminal amino acid sequence of the purified DszA completely coincided with the deduced amino acid sequence for dszA of R. erythropolis IGTS8 except for a methionine residue at the latter N-terminal. The optimal temperature and pH for DszA activity were 35 degrees C and about 7.5. The activity of the enzyme was inhibited by Mn2+, Ni2+, 2,2'-bipyridine, and 8-quinolinol, suggesting that a metal might be involved in its activity. DszA acted on not only DBT sulfone but also on dibenz[c,e][1,2]oxathiin 6-oxide and dibenz[c,e][1,2]oxathiin 6,6-dioxide. Dihydroxybiphenyl was formed from the latter two substrates.

Journal Article↗
PubMed1999

Immunological localization and ontogenetic development of inhibin alpha subunit in rat brain.

This study examined the immunolocalization and ontogeny of the inhibin-specific alpha subunit in the brain of male rats. Immunohistochemistry using antiserum directed against the mature region of porcine inhibin alpha (1-19, Tyr20) revealed positive reactions in process-bearing cells resembling astroglia in several regions, especially in the dorsal region of the third ventricle, medial and ventral arcuate nucleus, hippocampal dentate gyrus, and layers 1-3 of the cerebral cortex. Generally, inhibin alpha-positive cells in the limbic cortex had larger cell bodies and longer processes than those in the hypothalamus. These inhibin alpha-positive cells were verified to be positive for glial fibrillary acidic protein (GFAP), a differentiated astroglial marker, by double immunolabelling. The expression of inhibin alpha mRNA was higher in the brains of neonatal rats than in those of adult rats, as revealed by reverse transcription-competitive polymerase chain reaction, although the similar changes of immunoreactive inhibin alpha subunit in the brain was not observed. Orchiectomy did not affect expression of inhibin alpha mRNA in the hypothalamic area. This study suggests that inhibin-related peptide is produced by differentiated astrocytes, especially in the hypothalamic arcuate nucleus, the hippocampal dentate gyrus, and the cerebral cortex, and that the expression of inhibin alpha is regulated during brain development.

Animals↗
PubMed1999

Potassium-current oscillation of rat megakaryocytes: As a model system for drug evaluation (Review).

Megakaryocytes respond to externally applied agonists showing a periodic K+ current that reflects oscillation in cytoplasmic calcium concentration ([Ca2+]i). We have revealed several signal transducing factors that are involved in the K+ current oscillation of megakaryocytes. In this megakaryocyte system, it is relatively easy to determine what point of the signal transduction pathway a drug affects. In addition, as a progenitor cell, megakaryocytes resemble platelets which have important roles in many diseases. Therefore, this experimental system can be used for evaluation of new drugs.

Animals↗
PubMed1998

Effects of D2 dopamine receptor agonist and antagonist on brain activity in the rat assessed by functional magnetic resonance imaging.

The effects of D2 dopamine receptor agonist, bromocriptine (BROMO), and antagonist, haloperidol (HPD), on brain activity were investigated in rats by functional magnetic resonance imaging. T2*-weighted signal intensity was increased in the hypothalamus at 120 min after acute administration of BROMO, and in the ventral posterior and dorsomedial nuclei of the thalamus from 30 to 120 min. In contrast, the signal intensity was decreased in the caudate-putamen at 30 min after acute administration of HPD, in the hypothalamus from 30 to 60 min, and in the perirhinal cortex at 30 min. After chronic (2 weeks) HPD treatment, acute administration of HPD decreased signal intensity in the caudate-putamen at 60 min, in the hypothalamus at 30 min, the perirhinal cortex from 2 to 120 min, the dorsomedial and ventral posterior nuclei of the thalamus from 2 to 120 min, and the medial nucleus of the amygdala from 60 to 120 min. These results suggest that (1) the D2 receptor agonist increased the activity of the thalamic nuclei and the hypothalamus, while the D2 receptor antagonist suppressed brain activity in the regions where D2 receptors were present, (2) the suppression of brain activity in the thalamic nuclei and the perirhinal cortex by acute HPD administration was enhanced by chronic HPD treatment, and (3) the effects of antipsychotic drugs on the thalamus, amygdala, and perirhinal cortex may be related to their therapeutic efficacy, since clinical improvement in schizophrenic patients appears several days after the start of HPD treatment.

Amygdala↗
PubMed1998

Hypothalamic control of amino acid appetite.

Preference for umami taste materials, such as monosodium L-glutamate (MSG) and the 5'-ribonucleotides, inosine 5'-monophosphate (IMP) and guanosine 5'-monophosphate (GMP), varies as a consequence of protein nutrition. Rats fed diets deficient in dietary protein or an essential L-amino acid (AA), L-lysine (Lys), avidly consumed Lys, glycine and NaCl but not umami substances. However, when the rats' protein nutrition was normal or when they were recovering from deficiency, a preference for umami substances was evident. These data suggest that the central mechanism for recognition of protein malnutrition may be coupled with umami taste preference. To test this, Lys-deficient and normal rats were employed as a model for taste preference changes. AA levels in plasma and brain remain essentially unchanged throughout the day while the rat is on standard chow but are altered during Lys deficiency. The recognition site for the deficit in the rats' brains was localized to the ventromedial (VMH) and lateral (LHA) hypothalamus as determined by functional magnetic resonance imaging (fMRI, 4.7 Telsa). Studies of single neuron activity in the LHA of Lys-deficient rats suggested that neuronal plasticity occurred. Following Lys deficiency, cells responded specifically to Lys, both iontophoretically applied and during ingestion of AA. Other LHA neurons of nondeficient rats differentially responded to MSG. The present results suggest that the LHA and probably the VMH play important roles in recognition of deficient nutrients. Neural plasticity of hypothalamic cells helps maintain AA homeostasis. Furthermore, a preference for umami substances may be an indicator that the organism (rat or human) is free of protein malnutrition.

Amino Acids↗
PubMed1998

Activin antiserum infused into the lateral hypothalamic area affects operant behavior of rats fed lysine-deficient diet.

Rats were trained to maintain a high rate of bar pressing to receive 50-mg pellets of a complete diet when given a lysine-deficient (Lys-def) diet ad libitum. This bar-pressing behavior was significantly inhibited when rats were also allowed ad libitum access to 0.4 M Lys to drink. A brain activin system may modulate motivation to engage in bar-pressing behavior, since previous work has established that antagonism of activin by infusion of inhibin or follistatin, but not activin, into the lateral hypothalamic area (LHA) also inhibits bar-pressing behavior. The present study sought to clarify whether the effect of inhibin or follistatin might be mediated by antagonism of endogenous activin or by a separate direct effect of inhibin or follistatin. Thus, we infused an antiserum, which specifically inhibits activin A activity, into the LHA. Infusion of antiserum greatly inhibited bar-pressing behavior of rats fed a Lys-def diet and was additive with Lys consumption further to decrease bar pressing. Ad libitum Lys consumption was unchanged from control levels, indicating that it is likely that an endogenous activin system in the LHA mediates behavioral responsiveness when rats are fed a Lys-def diet but does not appear specifically to affect appetite for Lys.

Activins↗
PubMed1997

Activin exerts a neurotrophic effect on cultured hippocampal neurons.

Activin is a member of the transforming growth factor (TGF)-beta superfamily, which comprises a growing list of multifunctional proteins that serve as regulators of cell proliferation and differentiation. Recently, activin was shown to regulate the neurotransmitter phenotype in peripheral neurons. It is also a potent survival factor for neurogenic clonal cell lines, retinal neurons and midbrain dopaminergic neurons. We have studied the effect of activin on hippocampal cells which show abundant expression of activin receptors or binding sites. Exposure of primary cultures of rat hippocampal neurons to activin supported neuronal survival. This neurotrophic action of activin was blocked by treatment with the tyrosine kinase inhibitor genistein or the protein kinase C inhibitor calphostin C. However, the Ca2+/calmodulin kinase inhibitor KN-62 had no effect. Nicardipine, a blocker of the L-type Ca2+ channel, also inhibited the neurotrophic effect of activin. Furthermore, activin potentiated the depolarization-induced elevation in intracellular Ca2+ concentration ([Ca2+]i). The neurotrophic effect and the potentiation of depolarization-induced increase of [Ca2+]i caused by activin were completely abolished by the protein synthesis inhibitor cycloheximide. These results suggest that activin supports neuronal survival by increasing the expression of voltage-dependent Ca2+ channel through the action of a tyrosine kinase and of protein kinase C, but not of Ca2+/calmodulin kinase.

Activins↗
PubMed1997

Increased cartilage and bone formation in spontaneously hypercholesterolemic rats.

Spontaneously hypercholesterolemic (SHC) rats are known to exhibit accelerated bone resorption. We compared endochondral bone formation induced by implantation of demineralized bone matrix (DBM) to 4-week-old SHC rats with that of age-matched Sprague-Dawley (SD) rats. When DBM prepared from adult SD rats was implanted, the cartilageous area enlarged, and C-propeptide of type II procollagen content on day 7 was higher in SHC rats. Alkaline phosphatase activity and calcium content on day 12 and tartrate-resistant acid phosphatase activity on day 19 were higher in SHC rats. These results suggest active chondrogenesis, with a subsequent increase in osteogenesis, and stimulated osteoclastic bone resorption in SHC rats. When DBM from 10-week-old SHC rats was implanted into SD or SHC rats, the levels of bone forming parameters on day 12 were reduced to one-third, suggesting inhibiting factor(s) for bone induction in bone matrix of SHC rats. In contrast, when DBM from 6-month-old SHC rats was implanted, although bone forming parameters in SD rats were comparable to the case of implantation of DBM from SD rats, the accelerated bone formation detected in SHC rats was blocked, indicating resistance to systemic bone inducing factor(s) of SHC rats in aged bone matrix. These results suggest that age-related decrease in responses to some systemic bone inducing factor may lead to the bone loss with advancing age.

Acid Phosphatase↗
PubMed1997

Suppressed bone induction by follistatin in spontaneously hypercholesterolemic rat bone.

Bone inducing activity in demineralized bone matrix (DBM) of young spontaneously hypercholesterolemic (SHC) rats has been shown to be lower than that of aged SHC rats. This study examined the involvement of bone follistatin, an activin-binding protein, in bone induction. Immunoreactive follistatin was higher in DBM from 10-week-old SHC rats (DBM-10wk) than in DBM from 6-month-old SHC rats (DBM-6mo). When DBM without follistatin supplement was implanted, the C-propeptide of type II procollagen and calcium contents on day 12 in implants of DBM-6mo were 68% and 40% higher than those of DBM-10wk, respectively. In contrast, follistatin supplement to DBM decreased C-propeptide of type II procollagen and calcium contents in implants of both DBM-10wk and DBM-6mo, and the levels of these parameters were comparable between DBM-10wk and DBM-6mo, indicating reduced formation of cartilage and bone. These findings suggest that 1) follistatin content in bone matrix decreases with advancing age in SHC rats, and 2) the follistatin interferes with endochondral bone formation. We demonstrate that the lower bone induction of DBM from young SHC rats was partly due to the abundance of follistatin in bone matrix.

Aging↗
PubMed1997

Effects of lentinan on abnormal ingestive behaviors induced by tumor necrosis factor.

Lentinan (LNT), a beta-glucan derived from Lentinus edodes (Berk.) Sign., is known to work positively against cachexia in patients with malignant tumors. Because the cachectin/tumor necrosis factor (TNF) is supposed to be one of the factors that mediate cancer cachexia, we tested the effects of LNT on TNF-induced cachexia in rats. First, we analyzed in detail the cachectic actions of TNF (0.2 mg/kg/day, 5 days, IV) on food and water intake, body weight, and locomotor activity. The day after the first administration of TNF (acute phase), food and water intake, as well as body weight, of all rats decreased. However, over the next few days of treatment (chronic phase), the rats gradually developed a tolerance to the cachectic actions of TNF. Specifically, after the third administration, the rats treated with TNF had a higher amount of water intake than the control rats. This was mainly due to an increase in daytime water intake. We also analyzed the effects of LNT (0.1 or 1.0 mg/kg, twice/wk. IV) on TNF-induced cachexia, and compared the data with those from the rats treated with TNF alone. The higher dosage of LNT significantly suppressed TNF-induced daytime polydipsia and increased the amount of nighttime water intake, as well as the meal size of nighttime food intake. These results suggest that LNT partially normalizes TNF-induced cachexia in rats.

Animals↗
PubMed1997

Development of degenerative muscle weakness by chronic administration of beta,beta'-iminodipropionitrile in the drinking water to rats: a model for motorneuropathy.

Progressive muscle weakness accompanied by progressive muscle atrophy was investigated in rats administered beta,beta'-iminodipropionitrile (IDPN) chronically in the drinking water. Spontaneous running wheel activity declined slowly and reached a constant low level before postural muscle weakness was apparent. The rats being offered IDPN in the drinking water showed definite postural muscle weakness about 25 weeks after first being given IDPN, and muscle strength declined gradually throughout the remainder of the experiment (to 66 weeks). Flaccid paralysis became apparent in the hind limbs in the later stages of the experiment. Neurogenic muscle atrophy, measured by group atrophy of the muscle fibers, also progressed slowly, almost in parallel with the loss of muscle strength. At the end of the experiment, muscle weight of the gastrocnemius had decreased to about 20% that of control [F(2, 12) = 40.4, p < 0.05]. Plasma creatinine in the rats given IDPN in the drinking water for 66 weeks was significantly elevated over that of controls [F(2, 12) = 20.1, p < 0.05]. On the other hand, in rats given IDPN intraperitoneally, postural muscle weakness and muscle atrophy were less apparent, and plasma creatinine was normal. However, in these animals, abnormal behaviors, such as hyperexcitement, circling, and choreic movement (ECC syndrome), were apparent. These results suggest that the present model, which administers IDPN chronically in the drinking water ad lib and does not show involuntary movements and ECC syndrome, is of potential importance for investigation of chronic diseases of progressive muscle weakness with progressive muscle atrophy, and for assessing the efficacy of drugs and therapies for treating chronic neuromuscular diseases.

Animals↗
PubMed1997

Effect of dietary supplementation with branched-chain amino acids on spontaneous motor activity and muscle function in beta,beta'-iminodipropionitrile-treated rats: a model for motorneuropathy.

Beta,beta'-iminodipropionitrile (IDPN)-induced muscle weakness in rats is a model for motorneuropathy diseases. The effects of oral administration of branched-chain amino acids on the progression of muscle weakness and muscle atrophy induced by the administration of IDPN in the drinking water, were investigated in this study. The spontaneous motor activity of the animals, as measured with a running wheel, slowly declined after IDPN administration, reaching a steady and low level at approximately week 15. Progressive muscle weakness and muscle atrophy were observed beginning at approximately 15 weeks after the initiation of administration of IDPN. Administration of branched-chain amino acids (BCAA) as a dietary supplement did not improve the lowered spontaneous motor activity seen in IDPN animals, but it did significantly improve measures of postural weakness and muscle strength [range of F values (2, 24) = 4.1-9.5, p < 0.05]. Plasma creatinine of the IDPN-treated rats was markedly elevated, and BCAA administration also significantly suppressed this elevation [F(2, 24) = 41.2, p < 0.05]. Moreover, although BCAA in plasma were elevated in the rats administered BCAA [range of F values (2, 21) = 25.7-29.7, p < 0.05], skeletal muscle showed no differences (at the p < 0.05 level) in the amounts of BCAA, whether or not BCAA were administered. These data suggest that the BCAA taken up in the skeletal muscle were utilized in the muscle of motorneuropathic rats and improved muscle function, such as energy metabolism, and that the BCAA treatment is one important therapeutic approach for retarding the progression of muscle weakness seen in certain neuromuscular disorders.

Amino Acids, Branched-Chain↗