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Volume 83 (2000)
- Issue 4 Pages 279-
- Issue 3 Pages 167-
- Issue 2 Pages 89-
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Volume 83, Issue 2
Displaying 1-14 of 14 articles from this issue
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Reviews
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Yukihiro Noda, Toshitaka Nabeshima2000 Volume 83 Issue 2 Pages 89-94
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSCatecholaminergic and/or cyclic AMP(cAMP)systems have been demonstrated to be involved in the development of drug dependence.We investigated the involvement of both systems in psychological dependence on phencyclidine(PCP)by using tyrosine hydroxylase(TH)heterozygous(TH+/-)and cAMP response element binding protein(CREB)binding protein(CBP)heterozygous(CBP+/-)mice.PCP(8 mg/kg)induced place preference in wild−type mice pretreated with PCP(10 mg/kg once a day for 28 days).In these mice, the level of cAMP in the striatum, but not in the thalamus, was increased one day after the last injection of PCP(10 mg/kg).In TH+/- and CBP+/- mice pretreated with PCP(10 mg/kg per day for 28 days), however, no PCP(8 mg/kg)−induced place preference was observed.The level of cAMP in the striatum was increased in CBP+/- mice, but not TH+/- mice.Furthermore, we have demonstrated that the place preference induced by PCP is attenuated by 6−hydroxydopamine, a dopaminergic neurotoxin, and(+)SCH−23390, a dopamine−D1 receptor antagonist, but not by DSP−4, a noradrenergic neurotoxin, and(−)sulpiride, a dopamine−D2 receptor antagonist.These findings suggest that catecholamines and CBP are involved in the development of psychological dependence on PCP and that changes in dopaminergic and/or cAMP systems induced by repeated PCP treatment play an important role in the addiction to PCP.View full abstractDownload PDF (492K) -
Yasuko Ishikawa, Hajime Ishida2000 Volume 83 Issue 2 Pages 95-101
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSWater secretion from salivary glands, which are innervated by parasympathetic and sympathetic nerves, occurs in response to the stimulation by neurotransmitters.In general, parasympathetic or sympathetic stimulation produces a high flow of saliva as a result of the activation of M3 muscarinic or α1−adrenergic receptors, respectively.The secretory mechanisms of fluid secretion were osmotically regulated in response to a transepithelial ion gradient generated by ion transport systems that were located in the apical or basolateral membranes of the acinar cells.Recently, the identification of water−specific channels, or aquaporins(AQPs), in many mammalian tissue and cell types has provided insight into the molecular basis of water movement across biological membranes.It has been reported that several AQPs are expressed in salivary glands and especially AQP5 plays an important role in fluid secretion.This review will focus on the role of AQP5 in the movement of water across the apical plasma membrane in relation to the physiology and pathophysiology of salivary glands.View full abstractDownload PDF (591K)
Full Papers
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Muchun Wang, Shoshiro Okada, Yoshinori Murakami, Kinihiko Yokotani2000 Volume 83 Issue 2 Pages 102-106
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSWe examined the effect of nicotine on the release of endogenous noradrenaline(NA)from the isolated, vascularly perfused rat stomach.The stomach was perfused via the coeliac artery with Krebs−Ringer solution containing 10 μM pargyline at a constant flow rate of 4 ml per minute.Nicotine was once applied in the perfusion medium for 2 min.Nicotine(10-6−10-4M)evoked NA release in a concentration−dependent manner.The nicotine(3×10-5M)−evoked NA release was abolished by hexamethonium and tetrodotoxin.Diltiazem and isradipine [blockers of L−type voltage−activated calcium channel(VACC)] and ω−conotoxin GVIA(a blocker of N−type VACC)also abolished this nicotine−evoked NA release.Previously we reported that N−type, but not L−type, VACCs are located on the gastric postganglionic sympathetic nerve terminals, since the NA release evoked by electrical stimulation of periarterial nerves around the left gastric artery(postganglionic sympathetic nerves)was abolished by ω−conotoxin GVIA, but not by diltiazem(Yokotani et al., Jpn.J.Pharmacol.78, 75−77, 1998).From these results, it was suggested that nicotine activates nicotinic acetylcholine receptors located on the sympathetic ganglia, thereby evoking NA release by activation of L−type VACC located on the gastric sympathetic ganglia and N−type VACC probably located on the sympathetic nerve terminals in the rat stomach.View full abstractDownload PDF (402K) -
Akira Takahara, Atsushi Sugiyama, Hideki Dohmoto, Ryota Yoshimoto, Kei ...2000 Volume 83 Issue 2 Pages 107-112
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSAH−1058(4−(5H−dibenzo[a, d]cyclohepten−5−ylidene)−1−[(E)−3−(3−methoxy−2−nitro)phenyl−2−propenyl]piperidine hydrochloride)is a novel calcium channel blocker whose chemical structure is quite different from those of typical calcium channel blockers.In this study, electrophysiological and hemodynamic effects of AH−1058 were assessed in the halothane−anesthetized, closed−chest canine model.Intravenous administration of a canine antiarrhythmic dose of 100 μg/kg of AH−1058(n=6)did not affect the cardiovascular variables, except that the cardial output was decreased at 30 min after the drug administration.Additional administration of 200 μg/kg of AH−1058(n=6)suppressed the sinus nodal automaticity, AV nodal conduction and ventricular contraction and decreased the mean blood pressure, cardiac output and double product.The effects gradually appeared, while no change was detected in the intraventricular conduction, ventricular repolarization period, ventricular effective refractory period, preload to the left ventricle and total peripheral vascular resistance during the observation period of 30 min.The cardiosuppressive effects of AH−1058 can be explained by its calcium channel blocking action demonstrated in a previous in vitro experiment, while the lack of the effect on the vascular resistance would suggest that AH−1058 may become a slow−acting cardioselective calcium channel blocker.View full abstractDownload PDF (450K) -
Tomohisa Mori, Jun Baba, Yasuyuki Ichimaru, Tsutomu Suzuki2000 Volume 83 Issue 2 Pages 113-118
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSThe effects of rolipram, a selective inhibitor of phosphodiesterase 4, on the hyperlocomotion induced by several abused drugs(methamphetamine, morphine and phencyclidine)and a dopamine D1−receptor agonist(SKF81297;(±)−6−chloro−7, 8−dihydroxy−1−phenyl−2, 3, 4, 5−tetrahydro−1H−3−benzazepin hydrobromide)in mice were investigated.Methamphetamine(0.5−2.0 mg/kg), morphine(5.0−20 mg/kg), phencyclidine(1.25−5.0 mg/kg)and SKF81297(2.5−10 mg/kg)each induced dose−dependent hyperlocomotion.A low dose(1.0 mg/kg)or moderate dose(3.2 mg/kg)of rolipram suppressed methamphetamine(2.0 mg/kg)− and morphine(20 mg/kg)−induced hyperlocomotion, but not phencyclidine(5.0 mg/kg)−induced hyperlocomotion.These results suggest that cAMP in the brain is involved in methamphetamine− and morphine−induced hyperlocomotion, while the underlying mechanism(s)of phencyclidine−induced hyperlocomotion may be different from those of methamphetamine− and morphine−induced hyperlocomotion.It is well known that methamphetamine− and morphine−induced hyperlocomotion are mediated by the dopaminergic system and that interaction between postsynapic D1− and D2−receptors may play an important role in the expression of various dopamine−mediated behaviors.In the present study, SKF81297(10 mg/kg)−induced hyperlocomotion was significantly but not completely suppressed by the highest dose of rolipram(10 mg/kg).Therefore it is unlikely that postsynaptic D1−receptor−mediated functions are involved in the suppressive effects of rolipram on methamphetamine− and morphine−induced hyperlocomotion.These results suggest that rolipram may inhibit methamphetamine− and morphine−induced hyperlocomotion via increase cAMP levels at D2−receptors.View full abstractDownload PDF (463K) -
Taketoshi Ishii, Yasuko Shimpo, Yuzo Matsuoka, Kiyoshi Kinoshita2000 Volume 83 Issue 2 Pages 119-124
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSAlthough exogenously administered acetyl−l−carnitine(ALCAR, (2−acetoxy−3−carboxypropyl)−trimethylammonium)and l−carnitine(LC, (3−carboxy−2−hydroxypropyl)−trimethylammonium)prevent brain damage in several ischemic models, the protective mechanism of these compounds remains unclear.Here, we evaluated the effect of ALCAR and LC in primary cultured neurons from the cerebral cortex, striatum and thalamus of 18−day−old rat embryos.Deprivation of the serum from cultured medium for 3 days reduced the number of viable cells and mitochondrial activity and induced cell death with characteristics of apoptosis such as DNA fragmentation, nuclear condensation and histone−DNA release into the cytoplasm.ALCAR(1−100μM)and LC(1−100μM)promoted neuronal survival and mitochondrial activity in a concentration−dependent manner.Moreover, these compounds attenuated DNA fragmentation and nuclear condensation in cultured neurons and significantly decreased histone−DNA release into the cytoplasm.These results indicate that anti−apoptotic actions of ALCAR and LC contribute to their neuroprotective effect.View full abstractDownload PDF (492K) -
Akinori Miura, Yu Hao, Yuuichi Koike, Li-Man Wang, Yumiko Honda, Sator ...2000 Volume 83 Issue 2 Pages 125-134
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSThis study was carried out to understand the onset mechanism of adrenaline(ADR)−induced pulmonary edema(PE)and the effect of drugs related to the arachidonate cascade in a rabbit model.ADR was administered intravenously by a bolus injection to the rabbits at 50, 75 and 100μg/kg.To evaluate the severity of PE, the lung−water ratio(LWR)was calculated as a ratio of the difference between wet and dry lung weight to dry lung weight.The PE incidence and LWR exhibited a dose−dependent increase, and LWR correlated with the left atrial pressure(LAP).The involvement of the arachidonate cascade was evaluated by the co−administration of flurbiprofen, a cyclooxygenase inhibitor;ozagrel, a thromboxane synthase inhibitor;and OP−2507(15−cis−(4−n−propylcyclohexyl)−16, 17, 18, 19, 20−pentanor−9−deoxy−6, 9−α−nitriloprostaglandin F1 methyl ester), a prostaglandin I2 analogue.Co−treatment of the rabbits with ADR and flurbiprofen resulted in an increase in LAP and the incidence of PE, whereas co−administration of ozagrel did not exhibit any significant changes in the measured parameters.Conversely, OP−2507 reduced the LAP, PE incidence and LWR when co−administered with ADR.Rabbits co−treated with OP−2507 displayed an improved cardiac function.The results of these studies demonstrated the effectiveness of OP−2507 in protecting the lung and cardiac function from the ADR−induced PE.View full abstractDownload PDF (709K) -
Akira Sugimoto, Kazuhiro Goto, Atsushi Ishige, Yasuhiro Komatsu, Ken-i ...2000 Volume 83 Issue 2 Pages 135-142
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSTo clarify the mechanism of the benefical effect of Choto−san on cerebral circulation in hypertensive patients, the influence of Choto−san on cerebral blood flow(CBF)during hemorrhagic hypotension was evaluated in 10− to 11−month−old spontaneously hypertensive rats.The lower limit of CBF autoregulation, defined as the mean arterial blood pressure at which CBF decreased by 10% of the baseline value, was dosedependently lowered when Choto−san(0.5−2.0g/kg per day, p.o.)was administered for 14 consecutive days.Uncariae Ramulus et Uncus(150mg/kg per day, p.o.), one of the crude drug components of Choto−san, showed an effect equivalent to that of Choto−san.The action of Choto−san(2.0g/kg per day, p.o.)or Uncariae Ramulus et Uncus on the autoregulatory response of cerebral vessels was eliminated by treatment with NG−nitro−L−arginine methyl ester(10mg/kg, i.v.), an inhibitor of nitric oxide synthase.These results suggested that the activation of nitric oxide synthase by Uncariae Ramulus et Uncus contributed to at least part of the improvement in the cerebral circulation caused by Choto−san.View full abstractDownload PDF (625K) -
Kazumasa Shimizu, Taeko Ichikawa, Norimoto Urakawa, Shinjiro Nakajyo2000 Volume 83 Issue 2 Pages 143-149
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSIn guinea pig urinary bladder, the hyperosmotic 65 mM KCl(H−65K+)− or carbachol(CCh)−induced contraction was inhibited by an addition of papaverine in a concentration−dependent manner.The cAMP content of the muscle in the presence of H−65K+ or CCh was increased by papaverine only at the higher concentration of 100μM, but cGMP content was not affected by papaverine.Forskolin, compared with papaverine, increased cAMP content in a concentration−dependent manner, and nitroprusside did not significantly increase cGMP content.In a fura 2 loaded muscle, papaverine did not affect an increase of [Ca2+]i level by high K+ or CCh.The increase of oxidized flavoprotein(FPox)fluorescence and muscle contraction in the presence of H−65K+ or CCh was decreased by papaverine(1−100μM), and the increase of pyridine nucleotide(PNred)fluorescence was not affected by papaverine.In summary, it was concluded that papaverine induced relaxation by inhibiting mitochondrial respiration in guinea pig urinary bladder as well as ileum.Moreover, it is proposed that the mechanism of papaverine−induced relaxation in the smooth muscle, which shows predominantly a metabolic dependency on its contraction, is an inhibition of mitochondrial respiration.View full abstractDownload PDF (474K)
Short Communications
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Toyoshi Umezu2000 Volume 83 Issue 2 Pages 150-153
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSThe present study was conducted to further explore plant−derived essential oils that possess an anticonflict effect using the Geller type conflict test in ICR mice.The benzodiazepine anxiolytic diazepam increased the response(lever pressing)rate during the alarm period(i.e., an anticonflict effect), but the 5−HT1A partial agonist buspirone did not.Oils of juniper, cypress, geranium and jasmine did not produce any effect in this test.Frankincense oil decreased the response rate during the safe period at 1600 mg/kg, but did not exhibit any effect on the response rate during the alarm period.In contrast, lavender oil increased the response rate during the alarm period in a dose−dependent manner in the same manner as diazepam.These results indicate that not only rose oil but also lavender oil possess an anticonflict effect in mice.View full abstractDownload PDF (244K) -
Ana Baamonde, Álvarez-Vega Marco, Hidalgo Agustín, Men&e ...2000 Volume 83 Issue 2 Pages 154-156
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSWe studied the effects of intraplantar morphine in the formalin test in mice.Intraplantarly administered morphine(30−300μg)induced analgesic effects at lower doses than intraperitoneally administered morphine.Following the administration of [3H]morphine, the % of radioactivity present in brain was the same by either route.In contrast, higher radioactivity values appeared in the injected paw in those mice intraplantarly injected.Since local morphine induces analgesia at doses lower than the intraperitoneally administered drug, especially in the second phase of the test, and the access to brain is undistinguishable, we propose that local morphine enhances central opiate analgesia in the formalin test in mice.View full abstractDownload PDF (208K) -
Noriaki Makimoto, Akira Yamazaki, Hiroyuku Kobayashi, Nobuyuki Kishiba ...2000 Volume 83 Issue 2 Pages 157-160
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSEffect of KW−5092({1−[2−[[[5−(piperidinomethyl)−2−furanyl]methyl]amino]ethyl]−2−imidazolidinylidene}propanedinitrile fumarate)on intestinal motility and release of endogenous acetylcholine(ACh)were measured simultaneously in the small intestine of anesthetized dog using the in vivo microdialysis method.Intraarterial and intravenous administrations of KW−5092 accelerated the intestinal motility and increased dialysate ACh concentrations.These KW−5092−induced responses paralleled the increase in blood concentration of KW−5092.Thus, the acceleration of intestinal motility by KW−5092 was found in vivo to be associated with an increase in ACh release from the intestinal cholinergic neurons.View full abstractDownload PDF (243K)
Rapid Communication
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Xun Ye, Makoto Inoue, Hiroshi Ueda2000 Volume 83 Issue 2 Pages 161-163
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSMice with partial ligation of the sciatic nerve exhibited marked increase in the second phase nociceptive biting and licking behavior following intraplantar injection of formalin.The intrathecal pretreatment with botulinum toxin C3 dose−dependently attenuated the hyperalgesia in the second phase.These results suggest that a small G protein, Rho, and its downstream mechanisms are involved in the hyperalgesia following partial nerve injury.View full abstractDownload PDF (201K) -
Hiroyasu Kinemuchi, Masato Jinbo, Atsushi Tabata, Yoshie Toyoshima, Yu ...2000 Volume 83 Issue 2 Pages 164-166
Published: 2000
Released on J-STAGE: January 31, 2001
JOURNAL FREE ACCESSVarious mammalian tissues contain plasma membrane−bound amine oxidase, termed semicarbazide−sensitive amine oxidase(SSAO).In the present study, 2−bromoethylamine has been studied with regard to inhibitory properties towards tissue−bound SSAO in rat lung.Without preincubation, 2−bromoethylamine was a competitive and reversible SSAO inhibitor with a Ki value of 2.5 μM.After preincubation, it time−dependently and non−competitively inhibited SSAO activity, probably by forming the covalently−bound enzyme−inhibitor adduct.The data presented suggest that 2−bromoethylamine may act as a suicide inhibitor of SSAO.View full abstractDownload PDF (205K)
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