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T Tadano

Publications and source records attributed to T Tadano.

At least 73 records · Page 4Linked to original sources
PubMed1988

Inheritance of phosphogluconate and xanthine dehydrogenases in Aedes (Finlaya) togoi.

Phosphogluconate dehydrogenase (PGD) and xanthine dehydrogenase (XDH) were genetically studied by agar gel electrophoresis in the mosquito Aedes togoi. Adult homogenates displayed banding patterns with one zone of activity of either enzyme. Eight backcrosses were conducted to map the two loci, Pgd and Xdh, to linkage group III with the following arrangement: Pgd--(ca. 15 map units)--bl (bleached pupa)--(ca.5)--y (yellow larva)--(38.0 +/- 1.7)--pm (plum eye)--(6.1 +/- 0.9)--Xdh. All Pgd and Xdh loci thus far mapped in other mosquito species are reviewed for a comparison with those in this species.

Aedes↗
PubMed1987

Acute effects of a parkinsonism-inducing neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on mouse body temperature.

The parkinsonism-inducing neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) given in single systemic doses (i.p.) to mice produced marked hyperthermia, and subsequent long-lasting hypothermia. Administration of MPTP or its oxidized product, 1-methyl-4-phenylpyridinium ion, MPP+, via i.c.v. resulted in only hypothermia. In contrast, i.p. MPP+ administration resulted in only hyperthermia. The MPTP-induced hyperthermia (i.p.) was blocked by quaternary derivatives of anti-cholinergic agents, atropine and scopolamine, but not by the tertiary-derivative of atropine. Duration of this hyperthermic effect was potentiated by neostigmine. Pretreatment with 1-deprenyl did not prevent hypothermia, but nomifensine partially or clorgyline completely prevented the effect without preventing MPTP-induced hyperthermia. The thermic effects by MPTP, unlike its neurotoxicity for the nigrostriatal DA system, may not require metabolism to MPP+. These results indicate that peripheral cholinergic functions are responsible for the MPTP-induced hyperthermia, whereas its hypothermic effect may be centrally mediated via dysregulation of the various neuron systems.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Central hypothermic effects of some analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium ion (MPP+).

Effects of some MPTP or MPP+ analogues on mouse body temperature were studied. Of the analogues tested, 4-phenylpyridine (PPY) and 4-phenyl-1,2,3,6-tetrahydropyridine (PTP) given in single i.p. doses to mice caused marked hypothermia. Intracerebroventricular (i.c.v.) injection of PPY or PTP caused similar hypothermia. Pretreatment with clorgyline or (-)-deprenyl greatly prevented hypothermia induced by i.c.v. PPY, but hypothermia by i.c.v. PTP was prevented only by (-)-deprenyl. These results indicate that, in order to cause central hypothermia, PTP does not seem to require metabolism to PPY and both analogues per se may cause hypothermia.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Behavioral and biochemical changes following acute administration of MPTP and MPP+.

The acute effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium ion (MPP+) on mouse locomotor activity and striatal dopamine (DA) and 5-hydroxytryptamine (5-HT) levels were investigated. A single dose of either MPTP (10-30 mg/kg, i.p.) or MPP+ (5-20 ug/mouse, i.c.v.) decreased locomotor activity 10-40 min after injection: this locomotor effect was significantly suppressed by either pretreatment with nomifensine or 1-deprenyl alone, or by the combination of desmethylimipramine and 6-hydroxydopamine. Pretreatment with clorgyline did not suppress this behavior and a single dose of haloperidol enhanced the effect. The striatal levels of DA, 3-methoxytyramine and 5-HT increased in parallel with the decrease in locomotor activity caused by MPTP or MPP+. In contrast, levels of 3,4-dihydroxyphenylacetic acid, homovanillic acid and 5-hydroxyindoleacetic acid were decreased by injection of either MPTP or MPP+. Possible mechanism(s) of the behavioral and biochemical changes caused by the acute actions of MPTP and MPP+ with respect to their neurotoxic effects on the nigrostriatal DA system are discussed.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Genetic studies on hexokinase in the mosquito Aedes togoi.

Hexokinases (EC 2.7.1.1) were genetically analyzed in the mosquito Aedes togoi by agar gel electrophoresis. Enzyme activity was observed anodally in one major banding region (HK-1) on the gel and in another faintly stained region (HK-2). A total of six bands was detected in the HK-1 region. All six bands could be detected in three body parts, head, thorax, and abdomen, of adults with different banding intensities. The third and fourth bands, numbered from the more anodal side, showed the broadest substrate specificity and the greatest enzyme activity throughout development. Genetic analysis of the six HK-1 bands was undertaken on the hypothesis of a single gene locus (or three extremely tightly linked loci). The analysis gave the following gene order: HK-1--4.2 +/- 1.8 (recombination units +/- SE)--To-2--Odh-2--29.5 +/- 2.5--sex (M/m)--s. A comparison is made of gene loci for hexokinases among the mosquito species Culex pipiens, Aedes aegypti, and this species, along with a comment on linkage relationships between Hk and Odh (octanol dehydrogenase) loci in three Aedes species.

Aedes↗
PubMed1987

Involvement of alpha-adrenoceptors in para-hydroxyamphetamine-induced head-twitch response.

The effect of some drugs with a higher selectivity for either the alpha 1- or alpha 2-adrenoceptors on the head-twitches induced by intracerebroventricular administration of p-hydroxyamphetamine (p-OHA) in mice, have been studied. Pretreatment with yohimbine increased the number of head-twitches induced by p-OHA, whereas pretreatment with clonidine or prazosin reduced the number of responses. The decrease in head-twitches produced by clonidine was completely antagonized by pretreatment with yohimbine. Pretreatment with 6-hydroxydopamine prior to the combined treatment with clonidine and p-OHA, resulted in recovery of the reduced level head-twitches to the level induced by p-OHA alone. Pretreatment with 6-hydroxydopamine alone resulted in a marked increase in the number of p-OHA-induced head-twitches. These results clearly indicate that a noradrenaline system in the brain may, at least in part, be involved in the p-OHA-induced head-twitches in mouse, most probably by modulating a serotonergic system which is responsible for the head-twitch response.

Amphetamines↗
PubMed1987

Suppressive effects of intraventricular injected dopamine and nomifensine on muricide induced by thiamine deficiency.

The effects of dopamine (DA) and nomifensine (NF) on muricide activity induced by thiamine deficiency were examined. The chronic administration of L-dopa and nomifensine during feeding of thiamine deficient diet attenuated the muricide activity. Moreover, acute administration of L-dopa or nomifensine (IP) and dopamine or nomifensine (ICV) suppressed the thiamine deficiency-induced muricide activity dose-dependently. Small doses of apomorphine inhibited the muricide response significantly. The suppressive effects of dopamine and nomifensine were antagonized by pretreatment with 6-hydroxydopamine, but were not changed by pretreatment with p-chlorophenylalanine. These results suggest that the dopaminergic system has an important role in the regulation to the thiamine deficiency-induced muricide response.

Aggression↗
PubMed1987

Genetic studies on two carboxylesterase loci in Aedes albopictus.

Two esterase loci, Est-4 and Est-5, in Aedes albopictus encode carboxylesterases in 4th-instar larvae, pupae and adults. The electrophoretic bands migrate on agar gels toward the most anodal side, those of Est-5 followed by those of Est-4. Linkage studies on the two loci revealed that they were arranged on linkage group 2 in the following order: Est-4-(0.9 +/- 0.7 to 4.3 +/- 1.4 map units)-p(pigmented pupa)-(2 map units, as previously determined)-Wb(White-body)-(18.2 +/- 2.6 to 21.0 +/- 1.8 map units)-Idh-2(isocitrate dehydrogenase-2)-(13 map units, as previously determined)-alpha-Gpdh(alpha-glycerophosphate dehydrogenase)-(9.0 +/- 1.8 to 19.9 +/- 3.1 map units)-Est-5. The esterase loci were compared with those reported in other Aedes species with respect to their linkage homology.

Aedes↗
PubMed1986

The ex vivo effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on rat intra- and extraneuronal monoamine oxidase activity.

After i.p. injection of 30 mg/kg 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) daily for 4 days and sacrificing the rats 4 h after the last injection, striatal monoamine oxidase (MAO)-A and -B activities, assayed by conventional method with 5-hydroxytryptamine (5-HT) and benzylamine, were not changed. By an uptake technique, with dopamine as the substrate for both uptake and MAO, intrasynaptosomal MAO-A and -B activities were found to be greatly reduced with a greater MAO-A reduction. Intrasynaptosomal 5-HT oxidation by MAO-A was not changed in other forebrain regions treated with these MPTP doses. Similar results were also found with two brain preparations treated with single MPTP doses (30 mg/kg). This reduction in intrasynaptosomal MAO activity was completely absent after treatment with lower MPTP doses (15 mg/kg, daily for 5 days) and 5 days of a withdrawal period. The decrease in MAO activity might have been due to the decrease in DA transport into striatal synaptosomes during the enzyme assay and/or to reversible inhibition of intrasynaptosomal MAO by MPP+.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

Inhibition of rat brain monoamine oxidase by some analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and 1-methyl-4-phenylpyridinium ion.

To clarify the essential chemical structures of the neurotoxins, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its oxidized product, 1-methyl-4-phenylpyridinium ion (MPP+), that govern nigrostriatal dopamine neuron toxicity, interactions of several structurally related compounds of MPTP or MPP+ with monoamine oxidase (MAO) in rat forebrain homogenates were studied. Of the compounds tested, 4-phenyl-1,2,3,6-tetrahydropyridine (PTP), 4-phenylpyridine and 4-phenylpiperidine strongly and dose-dependently inhibited MAO-A and -B activity. Inhibition of PTP and 4-phenylpiperidine was MAO-A-selective, while that by 4-phenylpyridine was MAO-B-selective. Of these 3 compounds, only PTP time-dependently inhibited MAO-B, but not -A. Without preincubation, the modes of inhibition of MAO-A and -B by PTP were competitive. After 1 h preincubation, the mode of MAO-B inhibition changed to non-competitive, while inhibition of -A remained unchanged. PTP was oxidized by MAO-B, but not by -A, under these conditions. In contrast, 4-phenylpyridine and 4-phenylpiperidine were not substrates for either form of MAO in rat forebrain homogenates. These results, along with the other observations, indicate that PTP may essentially cause a neurotoxic effect on the nigrostriatal dopamine pathway.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1986

Evidence for central alpha2-adrenergic mechanism of clonidine-induced ejaculatory disturbance in dogs.

In order to clarify the central mechanism of clonidine (CL)-induced sexual dysfunction such as erectile and ejaculatory disturbances, we examined the effects of intracerebroventricularly (i.c.v.) administered CL on erection and ejaculation in male dogs. CL (0.5-5 micrograms/kg) produced a dose-related inhibition of ejaculation but not significant inhibition of erection by the manual stimulation of the penis. Sperm was not found in the urine drawn from the urinary bladder, suggesting that the inhibitory effect of CL on ejaculation was not due to retrograde ejaculation. The ejaculatory disturbance elicited by CL (5 micrograms/kg) was antagonized by an alpha 2-adrenoceptor antagonist, yohimbine (1-10 micrograms/kg, i.c.v.) in a dose-related manner. In contrast to the effect of yohimbine, it was unaffected by an alpha 1-adrenoceptor antagonist, prazosin (3 and 10 micrograms/kg, i.c.v.). These results indicate that i.c.v. administered CL may selectively inhibit the ejaculatory response, which is presumably mediated through the stimulation of alpha 2-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1986

Head-twitches induced by p-hydroxyamphetamine in mice.

Head-twitches have been regarded as an experimental model of hallucination, and we have recently observed that p-hydroxyamphetamine (p-OHA) markedly induced head-twitches in mice. The present work was undertaken to study possible participation of a serotonergic system in the mechanism of head-twitches induced by p-OHA. Head-twitches induced by p-OHA continued for 20-80 min, and the peak time of this effect was approximately 30-40 min after the administration. The i.c.v. administration of p-OHA (20, 40, 80 and 160 micrograms/mouse) produced characteristic head-twitches in a dose-dependent manner. Simultaneous injection of serotonin (10 micrograms/mouse, i.c.v.) and p-OHA caused a 2-2.5-fold increase in the number of head-twitches compared with non-serotonin controls. Pretreatment with p-chlorophenylalanine (200 mg/kg, i.p. and 500 micrograms/mouse, i.c.v.), in contrast, reduced head-twitches as did the pretreatment with cyproheptadine or dimethothiazine. These results suggest that p-OHA-induced head-twitches may involve the central serotonergic system which may exert an excitatory effect on head-twitches.

Amphetamines↗
PubMed1986

Genetic mapping of a phosphoglucomutase locus in Aedes togoi.

An electrophoretic survey of the phosphoglucomutase (PGM) enzyme was performed using agar gels in 6 strains (3 Japanese strains and 3 strains from Taiwan, Thailand and Canada) of Aedes togoi. The survey revealed at least 3 alleles involved at the Pgm locus among the 6 strains examined. Backcross experiments showed that the Pgm locus was located on the sex chromosome in the following order: Odh (octanol dehydrogenase)--M(sex)--(13.8 map units)--Pgm--(17.0 map units)--h(hooked leg)--s(straw-colored larva).

Aedes↗
PubMed1986

Inheritance of glucosephosphate isomerase in Aedes togoi.

Two isozymes of glucosephosphate isomerase (GPI:E.C. 5.3.1.9.) were observed in the mosquito Aedes togoi by means of agar gel electrophoresis. The locus (Gpi-1) controlling the more anodally migrated isozyme (GPI-1) was located on linkage group 1 (sex chromosome) of this species; the gene arrangement being Gpi-1--(18.2 map units)--To-2 (tetrazolium oxidase-2)--(27.3 map units)--M/m(sex)--(about 40 map units, as estimated by previous studies)--s (straw-colored larva). Linkage homologies concerning Gpi and Odh (octanol dehydrogenase) are compared among three species: Ae. aegypti, the Ae. scutellaris group, and the Ae. triseriatus group in terms of chromosomal evolution.

Aedes↗
PubMed1984

Linkage studies on alpha-glycerophosphate and isocitrate dehydrogenases in Aedes albopictus (Diptera: Culicidae).

Linkage studies were carried out on alpha-glycerophosphate dehydrogenase (alpha-GPDH) and isocitrate dehydrogenase (IDH) in the mosquito Aedes (Stegomyia) albopictus. Only one locus coding for alpha-GPDH was revealed on agar gels by applying adult homogenates. Two loci for IDH were observed using either fourth-instar larvae, pupae, or adults. This study was restricted to the more anodal Idh-2 of the two loci, and alpha-Gpdh. Both alpha-Gpdh and Idh-2 encode dimeric enzymes. Thirteen backcrosses indicated that the alpha-Gpdh and Idh-2 loci are arranged in linkage group 2 in the following order: p (pigmented pupa)--(ca. 2 map units)--Wb (white-body)--(7.5-17.8)--Idh-2--(13.1)--alpha-Gpdh. Females exhibited more recombination than males.

Aedes↗
PubMed1983

Genetics of octanol and alpha-glycerophosphate dehydrogenases in the mosquito Aedes (Finlaya) togoi.

Genetic studies were performed on octanol dehydrogenase (EC 1.1.1.73) and alpha-glycerophosphate dehydrogenase (EC 1.1.1.8) in the mosquito Aedes (Finlaya) togoi by agar gel electrophoresis. The electrophoretic survey revealed two octanol dehydrogenase loci (Odh-1, Odh-2) and one alpha-glycerophosphate dehydrogenase locus (alpha-Gpdh) in this species. Five alleles were observed at the Odh-2 locus in seven laboratory strains, whereas the alpha-Gpdh locus was completely monomorphic in six of seven strains examined and the second allele at this locus was detected in only one strain at a frequency of 0.14. Both loci code for dimeric enzymes. Linkage studies on Odh-2 and alpha-Gpdh suggested that the gene arrangement and recombination units were Odh-2--(25.8)--M (sex locus)--(30.5)--s (strawcolored larva) and M--(25.6)--alpha-Gpdh--(15.4)--s. These results, together with linkage data previously reported, give the following gene linkage on the sex chromosome: Odh-2--Est-3 (carboxylesterase)--Acph (acid phosphatase)--M--alpha-Gpdh--s--Est-2 (carboxylesterase). The total map length of this arrangement is approximately 75 map units.

Aedes↗