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T Osaka

Publications and source records attributed to T Osaka.

At least 37 records · Page 2Linked to original sources
PubMed1999

Rapid increase in circulating leptin in ventromedial hypothalamus-lesioned rats: role of hyperinsulinemia and implication for upregulation mechanism.

The mechanisms of marked increase in plasma leptin soon after ventromedial hypothalamus (VMH) lesions were investigated. Although rats did not gain body weight or parametrial fat-pad mass 24 h after the operation, the acute VMH-lesioned rats exhibited substantial five- and fourfold increases in plasma leptin levels compared with sham-operated control rats in fed (22.6 +/- 3.2 vs. 5.8 +/- 1.2 ng/ml) and fasted (8.8 +/- 2.0 vs. 2.3 +/- 0.3 ng/ml) states, respectively. Plasma insulin concentration was doubled in VMH-lesioned rats compared with sham-operated controls in both fed and fasting states. Northern blot analysis revealed that mRNA of ob gene was not increased in parametrial fat pad of animals 24 h after the creation of VMH lesions. However, leptin content in the fat pad was significantly increased in VMH-lesioned rats compared with sham-operated controls (32.2 +/- 4.7 vs. 17.4 +/- 2.3 ng/g wet tissue). The leptin content in parametrial fat pad was highly correlated with plasma leptin concentrations (r = 0.898, P < 0.001). To define the effect of hyperinsulinemia on their hyperleptinemia, a small dose of streptozotocin (STZ) (25 mg/kg body wt) was intravenously administered into rats 5 days before the creation of VMH lesions. Plasma insulin levels were not increased after VMH lesions in STZ-pretreated rats. Plasma leptin levels were halved in the absence of hyperinsulinemia, but still remained twofold higher than those in their sham-operated counterparts (9.9 +/- 1.3 vs. 4.8 +/- 0.7 ng/ml). These results indicate that the destruction of VMH rapidly promotes leptin production before obesity develops through an enhanced translational process in which hyperinsulinemia occurring after VMH lesioning plays an important role. The present study also suggests that there are other mechanisms that rapidly upregulate leptin production in adipocytes in VMH-lesioned rats in which the target organ of this hormone has been destroyed.

Animals↗
PubMed1998

Increased uncoupling protein-2 and -3 gene expressions in skeletal muscle of STZ-induced diabetic rats.

Streptozotocin (STZ)-induced diabetic animals are vulnerable to cold stress. Uncoupling proteins (UCPs) play an important role in regulating thermogenesis. We investigated the gene expressions of UCPs in brown adipose tissue (BAT), white adipose tissue (WAT), liver and gastrocnemius muscle of STZ-diabetic rats using Northern blot. UCP-1, -2 and -3 mRNA expressions in BAT were all remarkably lower in STZ-diabetic rats than those in control rats. Both UCP-2 and -3 gene expressions in gastrocnemius muscle were substantially elevated in STZ-diabetic rats and insulin treatment restored UCP gene expressions to normal levels. These results suggest that in STZ-diabetic rats, the overexpression of UCP-2 and UCP-3 in skeletal muscle provides a defense against hypothermogenesis caused by decreased UCPs in BAT.

Adipose Tissue, Brown↗
PubMed1998

Temperature- and capsaicin-sensitive nerve fibers in brown adipose tissue attenuate thermogenesis in the rat.

We examined the function of putative sensory fibers that are contained in intercostal nerves and innervate interscapular brown adipose tissue (IBAT) in urethane-anesthetized rats. Warming the IBAT to 40-44 degrees C with two small heaters placed bilaterally on the skin above it attenuated the subsequent noradrenaline-induced thermogenesis (NIT) of the IBAT. In this range of warming, higher IBAT temperatures resulted in more attenuation. Denervation of IBAT blocked the effect of thermal stimulation on the NIT. Thus, activation of nerve fibers in IBAT that are sensitive to warmth or to the nociceptive effects of heat probably attenuated the NIT. Since the putative sensory fibers in the IBAT contain calcitonin gene-related peptide (CGRP) and substance P, which are thought to act in peripheral tissues, we tested the effects of injection of these neuropeptides into the IBAT. Administration of 5.2 nmol CGRP but not substance P or vehicle saline mimicked the effect of thermal stimulation of IBAT. As the neuropeptide-containing primary sensory neurons are characterized by their sensitivity to capsaicin, we also tested its effects (1 mg/kg, s.c.) and found that it also attenuated the NIT. Denervation of the IBAT or pretreatment with capsazepine, a capsaicin receptor antagonist, blocked the effect of capsaicin. We propose that temperature- and capsaicin-sensitive nerve fibers release CGRP to attenuate the NIT of brown adipocytes.

Adipose Tissue, Brown↗
PubMed1998

Capsaicin activates heat loss and heat production simultaneously and independently in rats.

Subcutaneous administration of capsaicin (5 mg/kg) immediately increased the temperature of the tail skin (Tsk) for 2 h in urethan-anesthetized rats, suggesting an increase in heat loss. O2 consumption, an index of heat production, also immediately increased after the capsaicin injection, and this increase lasted for >10 h. Colonic temperature (Tco) decreased within 1 h after the injection, and this decrease was followed by a long-lasting hyperthermic period. Adrenal demedullation largely attenuated the capsaicin-induced increase in O2 consumption, and sympathetic denervation of the interscapular brown adipose tissue partly attenuated the increase in O2 consumption. However, capsaicin-induced heat loss was normal in these rats. In rats with cutaneous vasodilation maximized by warming and administration of hexamethonium, capsaicin did not further increase Tsk but normally induced heat production, and Tco gradually rose without a hypothermic period. Thus capsaicin simultaneously increased heat loss and heat production, and inhibition of one response did not affect the other. These findings suggest that capsaicin simultaneously activates independent networks for heat loss and heat production.

Adipose Tissue, Brown↗
PubMed1998

Toxicity of hydrogen peroxide produced by electroplated coatings to pathogenic bacteria.

The ability of various electroplated coatings (cobalt, zinc, copper, and cobalt-containing alloys of nickel, zinc, chromium, etc.) to inhibit the growth of pathogenic bacteria (Gram-positive bacteria Enterococcus faecalis and methicillin-resistant Staphylococcus aureus and Gram-negative bacteria Escherichia coli, Pseudomonas aeruginosa, and Klebsiella pneumoniae) was determined by a drop-method antibacterial experiment. The amounts of H2O2 produced and metal ions dissolved from the surfaces of various electroplated coatings were measured and it was found that the inhibitory ability of coatings corresponded to the amounts of H2O2 produced. The more significant the inhibition of the coating to bacterial growth, the greater the amount of H2O2 production. In addition, the bacterial survival rates on the surfaces of coatings were almost zero when H2O2 was produced in amounts greater than 10(-6) mmol/cm2. However, the dominant concentrations of metal ions dissolved from coatings were outside of the bacterial lethal range.

Corrosion↗
PubMed1998

Protection by rebamipide against acetic acid-induced colitis in rats: relationship with its antioxidative activity.

The aim of this study was to examine the efficacy of rebamipide on acetic acid-induced colitis in rats. Colitis was induced in male Wistar/ST strain rats by intracolonic injection of 2 ml of 5% acetic acid. After 24 hr, lesion score, myeloperoxidase (MPO) activity, thiobarbituric acid-reactive substances (TBARS), and antioxidants were measured. Rebamipide was administered orally to the rats twice, once immediately and once 8 hr after the induction of the colitis at doses of 7.5, 15, and 30 mg/kg. To evaluate the pathogenesis of neutrophils in this colitis model, neutrophil-depleted rats were also investigated. Increases of TBARS and MPO activity and decreases of total glutathione, superoxide dismutase (SOD) activity, and alpha-tocopherol were observed in this model. Rebamipide at 30 mg/kg decreased the lesion score significantly, which was associated with the reduction of colonic TBARS. The decreases of total glutathione, SOD activity, and alpha-tocopherol were also inhibited significantly by rebamipide. The preventive effect of rebamipide in this colitis model may be attributed to its inhibition of reactive oxygen species production.

Acetic Acid↗
PubMed1997

Blockade of hippocampal long-term potentiation following soman pretreatment in the rat.

One of the most potent toxins known is the cholinesterase inhibitor, soman, which produces severe convulsions and cell loss in the central nervous system. In these experiments the effect of multiple low doses of soman on the acquisition and maintenance of long-term potentiation (LTP) was determined in rats. LTP is a form of synaptic plasticity that has been studied as a cellular substrate for learning and memory mechanisms. Under urethane anesthesia, electrodes were positioned in the dentate gyrus for recording evoked potentials before and after tetanic stimulation of the perforant path. LTP levels were greatly reduced in rats recovering from convulsion-inducing soman treatment. Rats exposed to similar amounts of soman, but not displaying convulsions, also displayed reduced levels of LTP. The responses recorded from these animals were highly variable, ranging from control levels of potentiation to no LTP. The variability could be attributed to some animals having convulsions that were not detected before surgery or to other interanimal differences in the degree of soman-induced toxicity. The long range goal of the experiments presented here is to develop a better rodent model for studying soman-induced functional changes in the CNS that can be detected prior to the gross morphological changes.

Analysis of Variance↗
PubMed1995

A novel apparatus that permits multiple routes for infusions and body-fluid collections in a freely-moving animal.

A novel apparatus is described for simultaneous performance of multi-channel infusions/body-fluid collections and multichannel electrical recordings/stimulations in a freely behaving animals. This apparatus consists of a cylindrical cage and other devices described below. Electrical contacts are achieved via a slip-ring commutator. A rotation detector detects the turning of the animal in the cage, and a controller rotates the floor under the animal in the opposite direction by means of a stepping motor. Thus, excessive twisting of the fluid tubing between the animal and experimental equipment is released by rotation of the floor. Floor rotation starts when the animal turns in either direction and exceeds a present number of rotations. When the turning exceeds certain rates, the floor is rotated with higher angular velocities. This floor rotation little affected sleep-wake activities, brain temperature, food and water intake, and general behavior of the rat. Thus, multi-channel fluid routes have been realized; and by excluding the swivel apparatus from the fluid lines, advantages such as no fluid leakage at the swivel, no extra dead volume, and low torque to rotate the device have been gained.

Animals↗
PubMed1995

Noradrenaline inhibits preoptic sleep-active neurons through alpha 2-receptors in the rat.

Effects of noradrenaline (NA) on the activity of sleep-related neurons in the preoptic area (POA) and the neighboring basal forebrain were examined in the rat. Of 36 sleep-active neurons tested, 19 were inhibited and the other 17 were unaffected by NA applied through a multibarrel pipette. The alpha 2-agonist clonidine inhibited 11 of 14 sleep-active neurons and did not affect the other 3 neurons, whereas the alpha 1-agonist methoxamine (n = 13) and the beta-agonist isoproterenol (n = 11) had no effect on any of the sleep-active neurons tested. Thus, alpha 2-receptors mediated the NA-induced inhibition. Of 22 waking-active neurons tested, NA excited 10, inhibited 1, and had no effect on the remaining 11. Methoxamine excited 4 of 13 waking-active neurons tested, whereas isoproterenol (n = 9) and clonidine (n = 4) were without effect on any of the waking-active neurons tested. Accordingly, alpha 1-receptors probably mediated the NA-induced excitation. Seventy-seven state-indifferent neurons, which lacked activity related to the sleep-waking state, and 20 paradoxical sleep-active neurons were mostly (65%-70%) insensitive to NA. These results suggest that NA promotes wakefulness by inhibiting sleep-active neurons and by exciting waking-active neurons.

Animals↗
PubMed1995

Prostaglandin D2 modulates sleep-related and noradrenaline-induced activity of preoptic and basal forebrain neurons in the rat.

Prostaglandin D2 (PGD2) was applied by pressure through a multibarrel micropipette to sleep-related neurons in the preoptic and neighboring basal forebrain area in head-restrained unanesthetized rats. During wakefulness, PGD2 excited six of 13 sleep-active neurons, inhibited seven of 13 waking-active neurons, and did not affect the remaining neurons. During slow-wave sleep (SWS), however, PGD2 excited only three of 17 sleep-active neurons and inhibited two of 13 waking-active neurons. State-indifferent neurons, which lacked activity related to the sleep-waking state, were insensitive to PGD2 irrespective of wakefulness (n = 24) and SWS (n = 40). These results suggest that PGD2 promotes sleep by exciting sleep-active neurons and by inhibiting waking-active neurons. Furthermore, continuous administration of PGD2 attenuated activity changes associated with wakefulness of five sleep-active and three waking-active neurons tested. Because we had suggested the involvement of preoptic noradrenaline (NA) in arousal, we examined possible modulatory effects of PGD2 on NA-induced neuron responses. PGD2 attenuated NA-induced inhibitory responses in four of six sleep-active neurons and in one of 10 state-indifferent neurons. PGD2 also attenuated NA-induced excitation in four waking-active neurons tested. Accordingly, the modulatory action of PGD2 on sleep-related neurons is important in the mechanism of sleep.

Animals↗
PubMed1995

Activity of neurons in the lateral preoptic area during drinking behavior by the rat.

Rats were trained to drink water, sucrose solution, and saline while their heads were painlessly held in a stereotaxic apparatus with an attachment fixed to the skull. A total of 286 neurons in the lateral preoptic area (LPO) were recorded during the drinking behavior. During water intake, 40% of the neurons tested were either excited or inhibited. Sucrose elicited responses in 25% of the neurons, and saline in 34%. Of the 52 neurons recorded while rats drank all test solutions, 8 specifically responded to water, 3 were sucrose specific, 4 were saline specific, 12 responded to all solutions, and the remaining 25 did not respond to any solutions. Artificial cerebrospinal fluids (ACSFs) with physiologically hypertonic (+30 mOsm/kg, by NaCl or mannitol) and hypotonic (-30 mOsm/kg) osmotic pressure were applied to 88 neurons through a multibarrel micropipette. Of these neurons, 15 (17%) were hypotonic-sensitive; they were excited by hypotonic ACSF and/or inhibited by hypertonic ACSFs. There were 4 (5%) that were hypertonic-sensitive; they were excited by hypertonic ACSFs and/or inhibited by hypotonic ACSF. Of six hypotonic-sensitive neurons examined, three were water specific, and none were sucrose nor saline specific. Of four hypertonic-sensitive neurons, one was water specific, and another was saline specific. These results showed activity of some LPO neurons specifically related to water intake. Osmosensitive neurons in the LPO may regulate water intake.

Action Potentials↗
PubMed1995

Osmosensitive hypothalamic neurons and their responses to cardiovascular receptor activation.

Neurons in the rostral hypothalamic areas were examined with physiologically hypertonic (+30 mOsm/kg, by NaCl or mannitol) and hypotonic (-30 mOsm/kg) artificial cerebrospinal fluids (ACSFs) applied by pressure through a multibarrel micropipette in urethane-anesthetized rats. Of 304 neurons tested, 39 were excited by the hypertonic ACSFs and/or inhibited by the hypotonic ACSF, and 35 were inhibited by the hypertonic ACSFs and/or excited by the hypotonic ACSF. The former cells were designated hypertonic-sensitive and the latter hypotonic-sensitive. Both types of osmosensitive neurons were diffusely scattered in the examined areas, but neurons in the lateral preoptic area and the bed nucleus of the stria terminalis responded more frequently (30-40%) to the osmotic stimuli. Osmosensitive and insensitive neurons were recorded during activation of the baro- and volume receptors of the cardiovascular system. Of seven neurons that were excited during temporal hypotension induced by intravenous administration of nitroprusside, five were hypertonic-sensitive and two were osmotically insensitive. Hypertonic-sensitive neurons may be activated during dehydration, which increases the osmotic pressure and decreases the volume of body fluids. Of six neurons that were excited during temporal hypertension induced by intravenous administration of phenylephrine, four were hypotonic-sensitive and two were osmotically insensitive. Hypotonic-sensitive neurons may be activated during rehydration or overhydration. Osmosensitive neurons probably integrate cardiovascular and osmotic information that is important for the central regulation of body fluids.

Action Potentials↗
PubMed1995

Adjuvant-induced persistent photosensitivity models in guinea pigs. II. Characterization of immunological mechanisms.

The immunological characteristics of our adjuvant-induced persistent photosensitivity (AIPP) guinea pig model were examined. The sensitivity to long-wavelength ultraviolet light (UVA) was transferred with peritoneal exudate cells. Proliferative response was observed in peritoneal exudate cells and lymph node cells concomitantly cultured in the presence of sera that had previously been irradiated with UVA. Cervical lymph nodes of AIPP animals were found to be hypertrophic, and the ratio of major histocompatibility complex (MHC) class II positive cells was increased as compared to that of intact guinea pigs. These results suggest that persistent photosensitivity elicited with UVA is based on cellular autoimmunity. Thus, the AIPP guinea pig model should be useful to study the mechanism of persistent photosensitivity disease in humans.

Adjuvants, Immunologic↗
PubMed1994

Prostaglandin D2-sensitive, sleep-promoting zone defined in the ventral surface of the rostral basal forebrain.

The site of action for the sleep-promoting effect of prostaglandin (PG) D2 was extensively examined in the brain of adult male rats (n = 231). PGD2 was administered at 100 pmol/0.2 microliter per min for 6 hr (2300-0500 hr) through chronically implanted microdialysis probes or infusion cannulae. Among the administrations of PDG2 by dialysis probes (n = 176), only those (n = 8) to a ventro-rostral part of the basal forebrain by the probes implanted on the midline consistently increased slow-wave sleep (SWS), by 51 +/- 6 min (mean +/- SEM) above the baseline value (111 +/- 11 min). Since this area is separated by a cleft into right and left regions, the results were interpreted to mean that, through this cleft, PGD2 diffused in the subarachnoid space over the adjacent ventral surface, where it had the effect of promoting sleep. When PGD2 was directly infused into the subarachnoid space (n = 55), extraordinary increases exceeding 90 min were consistently attained for the SWS at sites located between 0.5 and 2 mm rostral to the bregma and between 0 and 1.2 mm lateral to the midline defined according to the stereotaxic coordinates adopted from the brain atlas of Paxinos and Watson [Paxinos, G. & Watson, C. (1986) The Rat Brain in Stereotaxic Coordinates (Academic, San Diego)]. Thus, we demarcated a "PGD2-sensitive, sleep-promoting zone" within this region in the ventral surface of the rostral basal forebrain. During the bilateral infusion of PGD2 into the subarachnoid space of this zone, the hourly mean SWS level of the nocturnal animals (n = 6) in the night reached the maximum at the second hour of the infusion period; this maximum hourly SWS level, corresponding to the daytime level of the same animals, lasted until the end of PGD2 infusion.

Animals↗