Higashino K

References (8)

Title : Rivastigmine improves isolation rearing-induced prepulse inhibition deficits via muscarinic acetylcholine receptors in mice - Higashino_2016_Psychopharmacology.(Berl)_233_521
Author(s) : Higashino K , Ago Y , Umeki T , Hasebe S , Onaka Y , Hashimoto H , Takuma K , Matsuda T
Ref : Psychopharmacology (Berl) , 233 :521 , 2016
Abstract : RATIONALE: The acetylcholinesterase inhibitors donepezil, galantamine, and rivastigmine are used for the treatment of Alzheimer's disease. We previously demonstrated that donepezil and galantamine differentially affect isolation rearing-induced prepulse inhibition (PPI) deficits and that this might be due to differential effects on brain muscarinic acetylcholine (mACh) receptor function in mice. OBJECTIVES: We examined the effects of rivastigmine on isolation rearing-induced PPI deficits, brain ACh levels, and mACh receptor function in mice.
METHODS: Acoustic startle responses were measured in a startle chamber. Microdialysis was performed, and the levels of dopamine and ACh in the prefrontal cortex were measured.
RESULTS: Rivastigmine (0.3 mg/kg) improved PPI deficits, and this improvement was antagonized by the mACh receptor antagonist telenzepine but not by the nicotinic ACh receptor antagonist mecamylamine. Rivastigmine increased extracellular ACh levels by approximately 2-3-fold, less than the increase produced by galantamine. Rivastigmine enhanced the effect of the mACh receptor agonist N-desmethylclozapine on prefrontal dopamine release, a marker of mACh receptor function, and this increase was blocked by telenzepine. In contrast, galantamine did not affect N-desmethylclozapine-induced dopamine release. Furthermore, rivastigmine did not affect cortical dopamine release induced by the serotonin1A receptor agonist osemozotan, suggesting that the effect of rivastigmine has specificity for mACh receptors.
CONCLUSIONS: Taken together with our previous finding that marked increases in ACh levels are required for the PPI deficit improvement induced by galantamine, our present results suggest that rivastigmine improves isolation rearing-induced PPI deficits by increasing ACh levels and by concomitantly enhancing mACh receptor function.
ESTHER : Higashino_2016_Psychopharmacology.(Berl)_233_521
PubMedSearch : Higashino_2016_Psychopharmacology.(Berl)_233_521
PubMedID: 26518025

Title : Galantamine promotes adult hippocampal neurogenesis via M(1) muscarinic and alpha7 nicotinic receptors in mice - Kita_2014_Int.J.Neuropsychopharmacol_17_1957
Author(s) : Kita Y , Ago Y , Higashino K , Asada K , Takano E , Takuma K , Matsuda T
Ref : Int J Neuropsychopharmacol , 17 :1957 , 2014
Abstract : Galantamine, an inhibitor of acetylcholinesterase, promotes hippocampal neurogenesis, but the exact mechanism for this is not known. In the present study, we examined the mechanisms underlying the effects of acute galantamine on neurogenesis in the mouse hippocampus. Galantamine (3 mg/kg) increased the number of 5-bromo-2'-deoxyuridine (BrdU)-positive cells in the subgranular zone of the dentate gyrus. This effect was blocked by the muscarinic receptor antagonist scopolamine and the preferential M1 muscarinic receptor antagonist telenzepine, but not by the nicotinic receptor antagonists mecamylamine and methyllycaconitine. Galantamine did not alter the ratio of neuronal nuclei (NeuN)- or glial fibrillary acidic protein (GFAP)-positive cells to BrdU-labeled cells in the subgranular zone and granule cell layer. Galantamine (1, 3 mg/kg) promoted the survival of 2-wk-old newly divided cells in mice in the granule cell layer of the dentate gyrus, whereas it did not affect the survival of newly divided cells at 1 and 4 wk. Galantamine-induced increases in cell survival were blocked by the alpha7 nicotinic receptor antagonist methyllycaconitine, but not by scopolamine. Bilateral injection of recombinant IGF2 into the dentate gyrus of the hippocampus mimicked the effects of galantamine. The effects of galantamine were blocked by direct injection of the IGF1 receptor antagonist JB1. These findings suggest that galantamine promotes neurogenesis via activation of the M1 muscarinic and alpha7 nicotinic acetylcholine receptors. The present study also suggests that IGF2 is involved in the effects of galantamine on the survival of 2-wk-old immature cells in the granule cell layer.
ESTHER : Kita_2014_Int.J.Neuropsychopharmacol_17_1957
PubMedSearch : Kita_2014_Int.J.Neuropsychopharmacol_17_1957
PubMedID: 24818616

Title : [Alcohol-induced hypertriglyceridemia in subjects with decreased lipoprotein lipase--improvement after cessation of alcohol intake] - Tsutsumi_1995_Nihon.Shokakibyo.Gakkai.Zasshi_92_951
Author(s) : Tsutsumi Z , Ikeda Y , Takagi A , Tsushima M , Higashino K , Yamamoto A
Ref : Nihon Shokakibyo Gakkai Zasshi , 92 :951 , 1995
Abstract : We systematically investigated the effect of lipoprotein lipase (LPL) and alcohol intake on the development of primary type IV hyperlipoproteinemia which is manifested as a moderate increase in serum triglycerides as a consequence of an elevated very low density lipoprotein concentration and a normal level of serum cholesterol. Twenty six type IV hyperlipoproteinemic and 28 normolipidemic males underwent measurement of the immunoreactive LPL mass in postheparin plasma (30 unit of heparin/kg of body weight) and were interviewed as to their alcohol consumption. They were divided into 4 groups, with a LPL mass of 150ng/ml (20 percentile of the normal range) and an alcohol intake of 33g/day as the borderlines. All subjects with LPL mass less than 150ng/ml and alcohol intake of more than 33g/day were prone to manifest type IV hyperlipoproteinemia. One of the subjects in this group showed a recovery to normolipidemic state after cessation of alcohol intake. Subject whose LPL mass value was more than 180ng/ml (50 percentile of the normal range) were not susceptible to type IV hyperlipoproteinemia even though they drank alcohol more than 33g/day.
ESTHER : Tsutsumi_1995_Nihon.Shokakibyo.Gakkai.Zasshi_92_951
PubMedSearch : Tsutsumi_1995_Nihon.Shokakibyo.Gakkai.Zasshi_92_951
PubMedID: 7609317

Title : Enzyme-linked immunosorbent assay (ELISA) for Aleuria aurantia lectin-reactive serum cholinesterase to differentiate liver cirrhosis and chronic hepatitis - Kondo_1995_Clin.Chim.Acta_243_1
Author(s) : Kondo M , Hada T , Fukui K , Iwasaki A , Higashino K , Yasukawa K
Ref : Clinica Chimica Acta , 243 :1 , 1995
Abstract : We have established an enzyme-linked immunosorbent assay (ELISA) for total serum cholinesterase (ChE) using 2 new monoclonal antibodies (mAbs) to ChE (E.C.3.1.1.8). The ELISA results correlated very well with the results of a serum ChE activity assay, which has been widely used for differentiating patients with liver diseases, such as hepatocellular carcinoma, liver cirrhosis and chronic hepatitis, from normal individuals. We next established an ELISA for Aleuria aurantia lectin (AAL)-reactive serum ChE using one of the anti-ChE mAbs and AAL, which specifically recognizes L-fucose alpha 1-->2, L-fucose alpha 1-->3, and L-fucose alpha 1-->6 structures. The ratio of AAL-reactive ChE to total ChE in sera determined by the two ELISA procedures was increased in patients with hepatocellular carcinoma and liver cirrhosis compared with patients with chronic hepatitis and normal individuals. We then applied the ELISA for AAL-reactive ChE directly to 10-fold-diluted serum samples, and by using a cut-off value of the mean + 2S.D. for normal individuals, we could effectively differentiate liver cirrhosis from chronic hepatitis. This single ELISA for AAL-reactive ChE could be a useful aid in clinical diagnosis.
ESTHER : Kondo_1995_Clin.Chim.Acta_243_1
PubMedSearch : Kondo_1995_Clin.Chim.Acta_243_1
PubMedID: 8747509

Title : Increase of fucosylated serum cholinesterase in relation to high risk groups for hepatocellular carcinomas - Ohkura_1994_Cancer.Res_54_55
Author(s) : Ohkura T , Hada T , Higashino K , Ohue T , Kochibe N , Koide N , Yamashita K
Ref : Cancer Research , 54 :55 , 1994
Abstract : Serum cholinesterase (ChE) (E.C. 3.1.1.8) is a glycoprotein which has 36 potential sites of asparagine-N-linked sugar chains. The structures of oligosaccharides released from ChE on hydrazinolysis were studied by serial lectin affinity column chromatography, exoglycosidase digestion, and methylation analysis. Seventy-three % of the sugar chains occurred as biantennary oligosaccharides and the remainder as C-2 and C-2,4/C-2,6 branched tri- and tetraantennary oligosaccharides. Several percentages of the Lewis X antigenic determinant and fucosylated mannose core were linked to them, and their sialic acid residues were linked to nonreducing terminal galactose residues at the C-3 and C-6 positions. Aleuria aurantia lectin-reactive ChE with the Lewis X antigenic determinant increased in hepatocellular carcinomas and liver cirrhosis compared with chronic hepatitis; on the other hand, Aleuria aurantia lectin-reactive ChE did not change significantly after transcatheter arterial embolization and was not related to the serum levels of alpha-fetoprotein and carcinoembryonic antigen in patients with hepatocellular carcinomas. Accordingly, the analysis of Aleuria aurantia lectin-reactive ChE is clinically useful for differentiating liver cirrhosis from chronic hepatitis and to identify high risk groups for hepatocellular carcinomas, i.e., cirrhotic patients in Child's A grade.
ESTHER : Ohkura_1994_Cancer.Res_54_55
PubMedSearch : Ohkura_1994_Cancer.Res_54_55
PubMedID: 8261462

Title : [Gene analysis of human cholinesterase variants]. - Muratani_1993_Japanese.J.Clin.Med_51_495
Author(s) : Muratani K , Hada T , Higashino K
Ref : Nippon Rinsho Japanese Journal of Clinical Medicine , 51 :495 , 1993
Abstract : People with genetic variants of cholinesterase (ChE) have been reported to have prolonged apnea with the use of myorelaxant succinylcholine. For the silent type variant ChE, two cases of mutation have been reported. In one case, the exon 2 of ChE gene was disrupted by a 342 bp insertion of Alu element. In the other case, a frame shift mutation was identified at Gly-117 (GGT-->GGAG) to create a stop codon at nucleotide 384. Dibucaine resistant ChE was examined and found to have a point mutation at nucleotide 209 (A-->G) that converted Asp-70 to Gly, and consequently reduced the affinity of ChE for choline esters. In addition, another two types of a point mutation reducing ChE activity were reported on K variant (Ala-539-->Thr) and a case of (Gly-365-->Arg) in a patient with liver cirrhosis.
ESTHER : Muratani_1993_Japanese.J.Clin.Med_51_495
PubMedSearch : Muratani_1993_Japanese.J.Clin.Med_51_495
PubMedID: 8464162

Title : A variant serum cholinesterase and a confirmed point mutation at Gly-365 to Arg found in a patient with liver cirrhosis - Hada_1992_Intern.Med_31_357
Author(s) : Hada T , Muratani K , Ohue T , Imanishi H , Moriwaki Y , Itoh M , Amuro Y , Higashino K
Ref : Intern Med , 31 :357 , 1992
Abstract : A 64-year-old man was admitted to our hospital because of possible liver cirrhosis. His serum cholinesterase was anomalously low with a delta pH of 0.1 (normal range; 0.8-1.1). His enzyme was more heat-labile than the normal controls. Km value of his enzyme for benzoylcholine was 1.1 x 10(-5) mol/l, while that for normal controls was 2.3 x 10(-6) mol/l. In addition, isozymic alteration of his enzyme was observed. Sequencing of the white blood cell DNA of the patient showed a point mutation at nucleotide 1093 (GGA to CGA), which changes codon 365 from glycine to arginine.
ESTHER : Hada_1992_Intern.Med_31_357
PubMedSearch : Hada_1992_Intern.Med_31_357
PubMedID: 1611188

Title : Inactivation of the cholinesterase gene by Alu insertion: possible mechanism for human gene transposition - Muratani_1991_Proc.Natl.Acad.Sci.U.S.A_88_11315
Author(s) : Muratani K , Hada T , Yamamoto Y , Kaneko T , Shigeto Y , Ohue T , Furuyama J , Higashino K
Ref : Proc Natl Acad Sci U S A , 88 :11315 , 1991
Abstract : The human cholinesterase (ChE) gene from a patient with acholinesterasemia was cloned and analyzed. By using ChE cDNA as a probe, four independent clones were isolated from a genomic library constructed from the patient's DNA. Sequencing analysis of all of the four clones revealed that exon 2 of the ChE gene was disrupted by a 342-base-pair (bp) insertion of Alu element, including a poly(A) tract of 38 bp, which showed 93% sequence homology with a current type of human Alu consensus sequence. Southern blot analysis showed that the Alu insertion occurred in both alleles of the patient and was inherited in the patient's family. This Alu insertion was flanked by 15-bp of target site duplication in exon 2 corresponding to positions 1062-1076 of ChE cDNA, indicating that an Alu element could have been integrated by retrotransposition. Thus, this case provides an important clue to the mechanism of inactivation of a gene by integration of a retrotransposon.
ESTHER : Muratani_1991_Proc.Natl.Acad.Sci.U.S.A_88_11315
PubMedSearch : Muratani_1991_Proc.Natl.Acad.Sci.U.S.A_88_11315
PubMedID: 1662391