PubMed Health⌕ Search

Biomedical subjects

Y Goshima

Publications and source records attributed to Y Goshima.

At least 91 records · Page 5Linked to original sources
PubMed1989

Effects of acute nicotine on catecholamine turnover in various rat brain regions.

Acute effects of in vivo nicotine application on turnover rates of noradrenaline (NA), adrenaline (AD) and dopamine (DA) in rat occipital cortex, hippocampus, striatum, hypothalamus, thalamus, midbrain, pons/medulla and cerebellum were examined by determining the amine concentrations by high performance liquid chromatography. The regional turnover rates of catecholamines were evaluated by comparing the decline in concentrations produced by blockade of synthesis. Intraperitoneally injected fusaric acid (80 mg/kg), an inhibitor of dopamine-beta-hydroxylase, significantly decreased NA concentration in all eight regions examined, and AD concentration in the hypothalamus and pons/medulla. alpha-Methyl-p-tyrosine methylester (alpha-MPT, 400 mg/kg), an inhibitor of the tyrosine hydroxylase, induced significant and uneven decreases in regional DA concentrations 1 h after the i.p. injection. alpha-MPT also significantly decreased NA concentration in all the regions except the striatum. Subcutaneously injected nicotine 0.4-1 mg/kg significantly enhanced the fusaric acid-induced decline in NA concentrations in the hippocampus and cerebellum. AD decline in the midbrain by fusaric acid was significantly accelerated by nicotine (0.4 mg/kg), but was not affected by a larger dose (1 mg/kg). In the hippocampus, nicotine (1 mg/kg) significantly enhanced the alpha-MPT-induced decrease in NA concentration, while it reduced the decrease in DA concentration. These findings suggest that nicotine can affect the turnover of brain catecholamine in a regionally specific manner.

Animals↗
PubMed1989

The optimum level of radiopacity in posterior composite resins.

Radiopacity is an indispensable property of composite resins for clinical diagnosis. The level of radiopacity that is most compatible with the radiographic diagnosis of recurrent caries was studied in a two-part experiment. In the first part, 16 composities were evaluated and divided into four groups based on their levels of radiopacity compared with an aluminum stepwedge. In the second part, caries was simulated by grooves of increasing depth in aluminum blocks of a thickness equivalent in radiopacity to enamel and the detectability assessed beneath differing thicknesses of three representative composite resins, P-30, Brilliant Lux and Occlusin. The relative radiographic density was measured and P-30 found to have the greater contrast. It is proposed that composite materials with a radiopacity similar to enamel are best for the detection of recurrent caries.

Composite Resins↗
PubMed1988

Transmitter-like release of endogenous 3,4-dihydroxyphenylalanine from rat striatal slices.

Biphasic electrical field stimulation (0.5-5 Hz, 2 ms, 25 V, 3 min) and high K+ (10-30 mM, 5 min) released endogenous 3,4-dihydroxyphenylalanine (DOPA) from superfused rat striatal slices. Characteristics of the DOPA release were compared with those of 3,4-dihydroxyphenylethylamine (dopamine, DA). Electrical stimulation at 2 Hz evoked DOPA and DA over similar time courses. alpha-Methyl-p-tyrosine (0.2 mM) markedly reduced release of DOPA but not of DA. Maximal release (0.3 pmol) of DOPA was obtained at 2 Hz and at 15 mM K+. The impulse-evoked release of DOPA and DA was completely tetrodotoxin (0.3 microM) sensitive and Ca2+ dependent and the 15 mM K+-evoked release was also Ca2+ dependent. On L-[3,5-3H]tyrosine (1 microM) superfusion, high K+ (15 and 60 mM) released DOPA and DA together with concentration-dependent decreases in tyrosine 3-monooxygenase (EC 1.14.16.2) activity as indicated by [3H]H2O formation, followed by concentration-dependent increases after DOPA and DA release ended. These findings suggest that striatal DOPA is released by a Ca2+-dependent excitation-secretion coupling process similar to that involved in transmitter release.

Animals↗
PubMed1986

Biphasic actions of L-DOPA on the release of endogenous dopamine via presynaptic receptors in rat striatal slices.

In rat striatal slices, 30 nM of L-DOPA increased the impulse (5 Hz)-evoked release of dopamine (DA), without increasing the spontaneous release and tissue content of DA. The minimum dose required to increase spontaneous DA release was 0.1 microM and the dose which led to an accumulation of DA was 100 microM. In the presence of NSD-1055, a DOPA-decarboxylase inhibitor, L-DOPA-induced increases in spontaneous DA release were prevented and L-DOPA produced dual actions on the evoked release of DA, a stereoselective propranolol-sensitive increase at 30 nM and a stereoselective sulpiride-sensitive decrease at 1 microM. L-DOPA produces dual presynaptic regulatory actions on DA release, via facilitatory beta-adrenoceptors at 30 nM and inhibitory DA receptors at 1 microM. The primary action of L-DOPA appears to be the facilitation of release of DA rather than the conversion to DA.

Animals↗
PubMed1986

Diminished alpha 2-adrenoceptor-mediated modulation of noradrenergic neurotransmission in the posterior hypothalamus of spontaneously hypertensive rats.

An azepine derivative, 6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo-[4,5-d]-azepine (B-HT 920; 100 nM), inhibited the evoked noradrenaline release from slices of rat posterior hypothalamus, and yohimbine (100 nM) potentiated the release from slices of rat anterior and posterior hypothalamus. In the posterior hypothalamus of 4- and 15-16-week-old spontaneously hypertensive rats (SHRs), as compared with age-matched Wistar-Kyoto rats (WKYs), the inhibitory effect of B-HT 920 and the facilitatory effect of yohimbine were decreased. In the anterior hypothalamus there was no significant difference in the yohimbine effect between WKYs and SHRs, at either age. It is concluded that alpha 2-adrenoceptor-mediated autoinhibition of noradrenergic neurotransmission is diminished in the posterior hypothalamus of SHRs.

Animals↗
PubMed1986

Biphasic actions of L-DOPA on the release of endogenous noradrenaline and dopamine from rat hypothalamic slices.

Effects of L-DOPA on the release of endogenous noradrenaline and dopamine from rat hypothalamic slices evoked by electrical field stimulation at 5 Hz were investigated in the absence and presence of p-bromobenzyloxyamine (NSD-1055), a DOPA-decarboxylase inhibitor. In the absence of NSD-1055, L-DOPA produced a facilitation of impulse-evoked release of noradrenaline at 0.1 microM but not at 1 and 10 microM, and had no effect on the spontaneous release. On the other hand, L-DOPA 0.1 to 10 microM dose-dependently increased the spontaneous release of dopamine and the highest concentration only increased the evoked release and tissue content of dopamine. In the presence of NSD-1055 10 microM, the increase in the spontaneous release of dopamine was prevented and L-DOPA produced biphasic regulatory effects on the evoked release of noradrenaline and dopamine, a facilitation at 0.1 microM and an inhibition at 1 microM. The facilitation was antagonized by (-)-propranolol 0.1 microM, but not by the (+)-isomer, whereas the inhibition was antagonized by S-sulpiride 1 nM, but not by the R-isomer. In conclusion, L-DOPA appears to produce biphasic actions on the release of endogenous noradrenaline and dopamine from rat hypothalamic slices, not through its conversion to dopamine but through presynaptic regulatory mechanisms, an inhibition via dopamine receptors at a micromolar concentration and a facilitation via beta-adrenoceptors at the lower concentration.

Animals↗
PubMed1986

Evidence for the existence of stereoselective presynaptic beta 1-adrenoceptors on noradrenergic and dopaminergic neurons in the rat hypothalamus.

Using high performance liquid chromatography with an electrochemical detector, we examined antagonistic effects of l- and d-acebutolol and atenolol against isoproterenol-induced facilitation of impulse-evoked release of endogenous norepinephrine and dopamine in rat hypothalamic slices. Isoproterenol (10 nM) increased the release of the both catecholamines, and this facilitation was similarly antagonized by 100 nM l-acebutolol and 100 nM atenolol, but was not antagonized by 100 nM d-acebutolol. In conclusion, there exist stereoselective presynaptic beta 1-adrenoceptors on noradrenergic and dopaminergic neurons in the rat hypothalamus.

Animals↗
PubMed1985

Autoregulation of endogenous epinephrine release via presynaptic adrenoceptors in the rat hypothalamic slice.

High-K+ (30 mM)-evoked release of endogenous epinephrine in hypothalamic slices from three rats in the presence of tetrodotoxin, 3 X 10(-7) M, was measured by high-performance liquid chromatography with an electrochemical detector. Spontaneous and evoked release of epinephrine was markedly reduced, when rats were pretreated with 2,3-dichloro-alpha-methylbenzylamine, an inhibitor of phenylethanolamine N-methyltransferase, the enzyme catalyzing the formation of epinephrine from norepinephrine, 80 mg/kg i.p., before decapitation. The amount of epinephrine released during the resting state was lower by a factor of approximately 2 orders than that of norepinephrine and dopamine but was consistently higher than the limit of the sensitivity of this assay system, 0.1 to 0.3 pmol. The evoked release of epinephrine was Ca++ dependent. Isoproterenol, 10(-8) M to 10(-7) M, dose dependently increased this parameter. I-Propranolol, 3 X 10(-8) M, shifted the dose-effect curve of isoproterenol to the right. Atenolol, 10(-6) M, and butoxamine, 3 X 10(-8) M, beta-1 and beta-2 antagonists, respectively, antagonized the action of isoproterenol, 3 X 10(-8) M. Tazolol, 3 X 10(-7) and 10(-6) M, a beta-1 agonist, and salbutamol, 10(-8) and 3 X 10(-8) M, a beta-2 agonist, dose dependently increased the evoked release of epinephrine. I-Propranolol, 3 X 10(-7) M and 3 X 10(-6) M alone, dose dependently decreased this parameter, but the d-isomer produced no effect. Clonidine, 10(-8) and 10(-7) M, an alpha-2 agonist, dose dependently decreased the parameter, and this decrease was antagonized by yohimbine, 10(-6) M, an alpha-2 antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1985

Involvement of epinephrine in the presynaptic beta adrenoceptor mechanism of norepinephrine release from rat hypothalamic slices.

Using high-performance liquid chromatography with electro-chemical detector, we measured field impulse (5 or 2 Hz)- and high K+ (20 mM)-evoked release of endogenous norepinephrine from rat hypothalamic slices. Release by impulses at 5 Hz was tetrodotoxin-sensitive and both types of release were Ca++-dependent. Isoproterenol (10(-10) to 10(-8) M) dose-dependently facilitated impulse-evoked release and l-propranolol (10(-8) M) shifted dose-effect curve of isoproterenol to the right. Atenolol (10(-8) to 10(-6) M) or butoxamine (10(-9) to 10(-8) M), beta-1 and beta-2-antagonist, respectively, dose-dependently antagonized the facilitatory effect of isoproterenol (10(-8) M). Tazolol (10(-8) to 10(-7) M), beta-1-agonist, and salbutamol (10(-10) to 10(-8) M), beta-2-agonist, dose-dependently increased impulse-evoked release. Epinephrine (10(-9) M) also facilitated impulse-evoked release and the action was antagonized by l-propranolol (10(-8) M). Isoproterenol (10(-8) M) also facilitated high K+-evoked release in the presence of tetrodotoxin (3 X 10(-7) M) to exclude possible involvement of axonal conduction or neuronal loops. This facilitatory effect was antagonized by l-propranolol (10(-8) M). l-Propranolol (3 X 10(-7) M) alone decreased release by impulses at 2 Hz, but the d-isomer produced no effect. When rats were pretreated with 2,3-dichloro-alpha-methylbenzylamine, an inhibitor of phenylethanolamine N-methyltransferase, the enzyme catalyzing the formation of epinephrine from norepinephrine, 80 mg/kg i.p. before decapitation, the l-propranolol-induced decrease was abolished completely.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Presynaptic inhibitory dopamine receptors on noradrenergic nerve terminals: analysis of biphasic actions of dopamine and apomorphine on the release of endogenous norepinephrine in rat hypothalamic slices.

Electrical field stimulation (5 Hz)- or high K+ (20 mM)-evoked release of endogenous norepinephrine from superfused rat hypothalamic slices in the presence of cocaine (20 microM) was measured by high-performance liquid chromatography with an electrochemical detector. Apomorphine (10-1000 nM) dose-dependently facilitated the electrically evoked release. Apomorphine (1 microM)-induced facilitation was abolished by pretreatment with yohimbine (100 nM), was converted to inhibition by yohimbine (1 microM), but was not antagonized by propranolol (300 nM). Epinephrine (100 nM) decreased the electrically evoked release and the decrease was antagonized by yohimbine (100 nM) and by apomorphine (100 nM), but not by S-sulpiride (100 nM). In the presence of yohimbine (1 microM), apomorphine (10-1000 nM) dose-dependently inhibited the electrically evoked release. Furthermore, in the presence of tetrodotoxin (300 nM), apomorphine (100 nM) also decreased the high K+-evoked release and this decrease was antagonized by S-sulpiride (100 nM). Dopamine produced biphasic actions on the electrically evoked release, a dose-dependent decrease at 30 and 100 nM and an increase at 300 and 1000 nM. Dopamine (300 nM)-induced increase was antagonized by propranolol (300 nM) but not by yohimbine (100 nM). The dopamine (100 nM)-induced decrease was antagonized by S-sulpiride (1 nM), but not by the R-isomer. S-sulpiride (10 to 100 nM) alone dose-dependently increased the electrically evoked release, whereas the R-isomer had no effect. Haloperidol (100 nM) also increased the electrically evoked release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Adrenaline involvement in the presynaptic beta-adrenoceptor-mediated mechanism of dopamine release from slices of the rat hypothalamus.

Slices of rat hypothalamus were superfused and endogenous release of dopamine (DA) was measured by high performance liquid chromatography combined with electrochemical detection. The K+ (20 mM)-evoked release in the presence of tetrodotoxin was Ca2+-dependent. The evoked release was facilitated by a beta-agonist, isoproterenol and this effect was completely abolished by a beta-antagonist, 1-propranolol. Isoproterenol also concentration-dependently facilitated the electrically (at 5Hz) evoked release of DA. The pretreatment with 1-propranolol, beta 1-antagonist, atenolol and beta 2-antagonist, butoxamine shifted the concentration-effect curve of isoproterenol to the right. On the other hand, beta 1-agonist, tazolol, beta 2-agonist, salbutamol and low concentration (10(-9) M) of adrenaline also facilitated the release. 1-Propranolol alone reduced the electrically (at 2 Hz) evoked release, and this effect was completely abolished when the adrenaline content in the brain was drastically reduced by use of a potent PNMT inhibitor, DCMB. These findings suggest that in the rat hypothalamus adrenaline released from adrenaline-containing nerve terminals probably modulates DA release via presynaptic beta 1- and beta 2-adrenoceptors on DA nerve terminals.

Action Potentials↗
PubMed1983

Presynaptic alpha 2- and dopamine-receptor-mediated inhibitory mechanisms and dopamine nerve terminals in the rat hypothalamus.

Slices of rat hypothalamus were superfused and endogenous release of dopamine was measured. The potassium (20 mM)-evoked release in the presence of tetrodotoxin was Ca2+-dependent. The evoked release was reduced by adrenaline 10(-7) M, with a potent alpha 2-agonist action, and was reduced by a dopamine receptor agonist, apomorphine 10(-7) M, in the presence of yohimbine 10(-6) M. These inhibitory effects were antagonized by an alpha 2-antagonist, yohimbine 10(-6) M, and a dopamine receptor antagonist, (-)-sulpiride 10(-7) M, respectively. The electrically evoked release of DA was enhanced by (-)-sulpiride but not by the (+)-isomer. Taking into consideration that yohimbine at a relatively high concentration (10(-6) M) increases the electrically evoked DA release, it is suggested that DA release in the rat hypothalamus may be mediated not only via autoreceptors but also in part via presynaptic alpha 2-receptors on the DA nerve terminals.

Animals↗
PubMed1983

Presynaptic mediation by alpha 2-, beta 1- and beta 2-adrenoceptors of endogenous noradrenaline and dopamine release from slices of rat hypothalamus.

Using high performance liquid chromatography with an electro-chemical detector, we studied effects of different compounds on the impulse-evoked release of endogenous noradrenaline (NA) and dopamine (DA) release from slices of the rat hypothalamus. Adrenaline (10(-7) M), with a potent alpha-agonistic action decreased both NA and DA release, and these effects were blocked by pretreatment with yohimbine (10(-7 M). The alpha 2-antagonist, yohimbine alone (10(-8) - 10(-6) M) concentration-dependently increased these releases, while alpha 1-antagonist, prazosin showed weak increase on NA but not DA release at 10(-6) M. Isoproterenol (10(-10) - 10(-8) M) concentration-dependently increased these releases and the effects were antagonized by pretreatment with a non-selective beta-antagonist, 1-propranolol, a beta 1-antagonist, atenolol or a beta 2-antagonist, butoxamine. 1-Propranolol (3 X 10(-7) M) alone, but not the d-isomer inhibited the releases. Thus, in the rat hypothalamus, the release of NA and DA may be mediated via presynaptic alpha 2-, beta 1- and beta 2-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Coexistence of presynaptic beta 1- and beta 2-adrenoceptors in splenic strips from young rats and betaxolol-induced beta 1-stereoselective antagonism.

The pharmacological properties of facilitatory presynaptic beta-adrenoceptors were characterized using three kinds of beta-agonists and antagonists in superfused strips from young Sprague-Dawley rats, loaded with [3H]noradrenaline. Isoproterenol (10(-9) M to 10(-7) M) concentration-dependently facilitated [3H] release evoked by transmural field stimulation at 5 Hz. Salbutamol (10(-8) M and 10(-7) M) and prenalterol (10(-8) M to 10(-6) M) also facilitated the stimulation-evoked [3H] release. Pretreatment with ICI 118,551 (10(-6) M) completely antagonized the concentration-facilitation curve for isoproterenol (10(-9) M to 10(-7) M). Atenolol (10(-6) M) antagonized only the isoproterenol (10(-9) M)-induced facilitation. dl-Betaxolol (10(-6) M) antagonized the isoproterenol (10(-9) M and 10(-8) M)-induced facilitation and the antagonistic action for isoproterenol (10(-8) M) was more marked than that of atenolol, whereas the same concentration of d-betaxolol produced no antagonism. Thus, presynaptic beta 1- and beta 2-adrenoceptors coexist on noradrenergic neurons innervating splenic strips of young rats. Betaxolol is a useful tool to characterize presynaptic beta 1-adrenoceptors.

Adrenergic beta-Agonists↗