Search PubMed⌕ Search

Biomedical subjects

Y Hasebe

Publications and source records attributed to Y Hasebe.

25 records · Page 2Linked to original sources
PubMed1989

Enhancement of spinal monosynaptic reflexes with phenylethylamine and related drugs through descending noradrenergic neurons.

The effects of phenylethylamine (PEA) and related drugs, such as methamphetamine, phenelzine, methylphenidate, nomifensine and mazindol on the spinal monosynaptic reflex (MSR) were investigated in rats treated with 6-hydroxydopamine (6-OHDA) or 5,6-dihydroxytryptamine (5,6-DHT). PEA (1 x 10(-5) mol/kg, i.v.) increased the amplitude of MSR in control rats, but decreased the amplitude in rats treated with 6-OHDA. Although PEA-related drugs increased the amplitude of MSR, they did not change the MSR amplitude in 6-OHDA-treated rats. In 5,6-DHT-treated rats, PEA-related drugs increased the amplitude of MSR, whereas PEA produced a decrease. These results support our previous suggestion that the enhancement of MSR by these drugs might be mediated through release of noradrenaline or inhibition of noradrenaline uptake at the noradrenergic synapses.

5,6-Dihydroxytryptamine↗
PubMed1989

Structure-activity relationships of phenylethylamine analogs in their serotonergic depressant effects on the spinal monosynaptic reflex in rats.

The effects of 2-phenylethylamine (PEA) and related compounds on the spinal monosynaptic reflex (MSR) were examined using C1-spinalized rats. At low doses, PEA, S(+)-amphetamine, S(+)-methamphetamine and phentermine increased the amplitude of the MSR, whereas high doses of these drugs reduced it. p-Substituted PEA analogs (p-C1-PEA, p-methoxy-PEA and (+/-)-p-C1-amphetamine) only reduced the MSR. Low doses of PEA-related rigid compounds, R(+)-2-aminotetralin, (+/-)-N-methyl-2-aminotetralin and (+/-)-N,N-dimethyl-2-aminotetralin only reduced the MSR. S(-)-2-Aminotetralin did not affect the MSR. Depressions of MSR produced by PEA, S(+)-methamphetamine and R(+)-2-aminotetralin were antagonized by ketanserin and haloperidol which have 5-hydroxytryptamine (5-HT) antagonistic activity, and the MSR depression caused by S(+)-methamphetamine but not PEA and R(+)-2-aminotetralin was abolished by intracisternal 5,6-dihydroxytryptamine treatment or chronic spinal transection. These results suggest that PEA-related compounds cause MSR depression by direct and indirect 5-HT agonistic mechanisms, and support the proposal that the PEA moiety which exists in R(+)-2-aminotetralin is important for the direct 5-HT agonistic activity of some hallucinogens.

Animals↗
PubMed1989

Photo-switchable ion and enzyme sensors. Photoinduced potentiometric response of glassy carbon electrode coated with polymer or polymer/enzyme dual membrane.

Photo-switchable ion and enzyme sensors were fabricated by the use of glassy carbon electrode coated with nonactindoped or enzyme modified poly(vinyl chloride) (PVC) membranes. The ion sensor with nonactin-doped PVC membrane, which contained spirobenzopyran as the photosensitive dye, exhibited a potentiometric photoresponse to NH4+ ion in the solution. The dynamic range of the NH4+ ion sensor was 10(-7)--10(-3) M. Urea, adenosine, and asparagine sensors were prepared by coating the surface of the NH4+-ion sensor with urease, adenosine deaminase, and asparaginase membranes, respectively. These enzyme sensors could be used for determining the substrates at the micro mole level. The performance characteristics of these sensors were compared with those previously prepared membrane electrode sensors.

Carbon↗
PubMed1983

Effects of valproic acid on spinal reflexes and [3H]muscimol and [3H]diazepam binding in brain membranes in rats.

It was examined whether the anticonvulsant activity of valproic acid (di-n-propylacetic acid, DPA) was exerted via the inhibitory GABA system in the central nervous systems (CNS). Dorsal root reflexes (DR-DRR) were not augmented but intensely suppressed following the administration of DPA (50 and 200 mg/kg, i.v.). DPA did not depolarize the resting dorsal root potentials. These electrophysiological findings may indicate that DPA does not potentiate GABA system in the spinal cord of rats. DPA (1 and 10 mM) neither affected the binding of 2 or 40 nM of [3H]muscimol nor the binding of [3H]diazepam in the rat brain membranes; the same concentrations of DPA did not affect the enhancement of binding of [3H]diazepam induced by the addition of GABA (100 microM). The result obtained from binding assays indicates that DPA does not interact with the GABA-benzodiazepine receptor complex. The findings in the present study do not support the proposal that the anticonvulsant action of DPA is exerted by potentiation of the GABA system in the CNS.

Animals↗