Biomedical subjects

Jiro Masuya

Publications and source records attributed to Jiro Masuya.

4 recordsLinked to original sources

PubMed2006

Caffeic acid attenuates the decrease in cortical BDNF mRNA expression induced by exposure to forced swimming stress in mice.

We previously reported that caffeic acid produces antidepressive-like effects in the forced swimming test in mice, an animal model of depression. Increased evidence suggests that brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family that has high affinity for the tyrosine kinase receptor B (TrkB), plays an important role in the pathophysiology and treatment of depression. The present study examined whether caffeic acid affects the expression levels of BDNF and TrkB mRNA in brain regions of mice subjected to a forced swimming test. Caffeic acid (4 mg/kg, i.p.) reduced the duration of immobility of mice in the forced swimming test. The levels of BDNF mRNA in the frontal cortex as well as TrkB mRNA in the amygdala were significantly decreased after the forced swimming test, and the former reduction was significantly inhibited by caffeic acid (4 mg/kg, i.p.). Caffeic acid (4 mg/kg, i.p.) did not modify the levels of BDNF and TrkB mRNA in brain regions of naive mice. These results suggest that caffeic acid can attenuate the down-regulation of BDNF transcription that results from stressful conditions.

Animals↗

PubMed2005

Effects of a 5-HT7 receptor antagonist DR4004 on the exploratory behavior in a novel environment and on brain monoamine dynamics in mice.

The present study examined whether serotonin (5-hydroxytryptamine; 5-HT)7 receptors play a role in the modulation of emotionality in mice using the selective 5-HT7 receptor antagonist 2a-[4-(4-phenyl-1,2,3,6-tetrahydropyridyl)butyl]-2a,3,4,5-tetrahydrobenzo (c,d)indol-2-(1H)-one (DR4004). The emotionality of mice was evaluated in terms of exploratory activity in the hole-board test. The mice treated with DR4004 (2.5-10 mg/kg, i.p.) displayed a dose-dependent decrease in locomotor activity by moving less distance in the hole-board, and statistically significant decreases were observed at 5 and 10 mg/kg. On the other hand, DR4004 (10 mg/kg, i.p.) did not affect spontaneous motor activity. In a neurochemical study, decreases in amygdaloid dopamine and 5-HT turnover were observed in mice in which locomotor activity in the hole-board test was attenuated following the administration of DR4004 (10 mg/kg, i.p.). Also, a simple linear regression analysis revealed that locomotor activity on the hole-board was significantly correlated with dopamine and 5-HT turnover in amygdala. Furthermore, co-injection of the selective dopamine reuptake inhibitor 1-(2-[bis(4-fluorophenyl)methoxy]ethyl)-4-(3-phenylpropyl)piperazine (GBR12909; 1.25-5 mg/kg, i.p.) or the selective 5-HT reuptake inhibitor fluvoxamine (20 mg/kg, i.p.) significantly reversed the DR4004 (10 mg/kg, i.p.)-induced decrease in locomotor activity in the hole-board test. These findings constitute the behavioral evidence that 5-HT7 receptors may play a role in the modulation of emotionality. Furthermore, it is also suggested that amygdaloid dopamine and 5-HT neuronal systems may be involved in this modulation.

Amygdala↗

PubMed2003

Caffeic acid produces antidepressive- and/or anxiolytic-like effects through indirect modulation of the alpha 1A-adrenoceptor system in mice.

We previously reported that caffeic acid produce antidepressive- and/or anxiolytic-like effects in two different types of stress models. It has recently been reported that caffeic acid affects the alpha1A-adrenoceptor system. The present study examined whether the alpha1A-adrenoceptor system is involved in the antidepressive- and/or anxiolytic-like effects of caffeic acid. Caffeic acid reduced the duration of immobility and freezing of mice produced by forced swimming and conditioned fear stress, respectively. These effects of caffeic acid were suppressed by the alpha1- and alpha1A-adrenoceptor antagonists. However, caffeic acid did not alter the binding of [3H]prazosin to alpha1A-adrenoceptor in mouse cortical membranes. These results suggest that indirect modulation of the alpha1A-adrenoceptor system may be involved in the antidepressive- and/or anxiolytic-like effects of caffeic acid.

Animals↗

PubMed2002

Preparation and characterization of anti-anti-idiotypic monoclonal antibody ("Ab1-like Ab3") in relation to carcinoembryonic antigen.

In order to analyze the epitope structure of carcinoembryonic antigen (CEA) and the idiotype network system, seven anti-idiotypic monoclonal antibodies (anti-Id MoAbs) were generated from a BALB/c mouse immunized with anti-CEA MoAb P1-356, which recognized a synthetic peptide P1 of CEA, domain I. These MoAbs were divided into four groups. The anti-Id MoAbs specifically reacted with MoAb P1-356, but not with any MoAb, and inhibited the binding of MoAb P1-356 to CEA, indicating that all of these anti-Id MoAbs recognized private idiotopes at the combining sites of MoAb P1-356. Polyclonal anti-anti-idiotypic antiserum (Ab3) generated with anti-Id MoAbs M315 (Ab2), blocked the binding of MoAb P1-356 (Ab1) to CEA and reacted with CEA(Ag) and synthetic peptide P1. The analysis of serological assays suggested that it contains "Ab1-like Ab3." Therefore, we prepared anti-anti-Id MoAbs using anti-Id MoAb M315. Among 13 candidates, anti-anti-Id MoAb 11B2 was selected, because it competed with MoAb P1-356 (Ab1) binding to CEA. A direct binding assay using MoAb11B2 showed that it reacted with purified CEA and with CEA synthetic peptide P1. In addition, MoAb 11B2 (Ab3) reacted with both CEA-producing cultured cells and colonic cancerous tissues in immunostaining. These results indicate that anti-anti-Id MoAb 11B2 is "Ab1-like Ab3." Therefore, it is suggested that anti-Id MoAb M315 bears an "internal image" of the MoAb P1-356-defined epitope on CEA.

Animals↗