Biomedical subjects

S L Duh

Publications and source records attributed to S L Duh.

3 recordsLinked to original sources

PubMed1999

Nicotine-induced hyperlocomotion is not modified by the estrous cycle, ovariectomy and estradiol replacement at physiological level.

The present study was designed to investigate whether nicotine's effect on locomotion might be modulated by the ovarian hormone at physiological level. Rats at normal cycling of estrus and diestrus were selected for the comparison of nicotine-induced hyperlocomotion based on the document that the release of striatal dopamine was greatest at the estrous phase. Ovariectomized rats primed with or without estrogen at physiological level were also selected for comparison. Increase in spontaneous locomotion by nicotine was statistically significant at the doses of 0.15 and 0.3 mg/kg (p < 0.001). The stimulating effect of nicotine led the locomotor response to almost the same magnitude in all hormonal groups studied. Nicotine-induced hyperlocomotion appeared to be mediated by central nicotinic receptor because it was blocked by mecamylamine (0.5 and 1.0 mg/kg, i.p.). Also it was blocked by haloperidol (0.04 and 0.08 mg/kg, i.p.) indicating the involvement of dopaminergic neurotransmission. These effects were similar in all groups regardless of the estrous cycle or ovariectomy. The observed data provided behavioral evidence to suggest that the effect of nicotine on locomotion-related dopaminergic neurons might not be modified by the physiological action of estrogen.

Animals↗

PubMed1997

Nucleus accumbens dopaminergic mediation of protection against gastric mucosal ulcerations by cold-restraint stress in the male hyperprolactinemic rats.

An investigation was undertaken to study the relationship between change in gastric lesion induced by cold-restraint stress and brain dopamine (DA) activity in male rat with chronic hyperprolactinemia. Male rats of Wistar strain were divided into two groups: one received extra two pieces of anterior pituitary (AP) from its littermates, the other grafted with several pieces of muscle served as control. Experiment I: From the 5th day to 40th day after transplantation, the levels of serum prolactin (PRL) in the AP-grafted group were higher than those of control (p < 0.05 or p < 0.01). Experiment II: On the 40th day after transplantation, AP-grafted and control rats were restrained and placed supine in a ventilated refrigerator with an ambient temperature of 5 degrees C for 3 hrs. Although gastric mucosal ulceration was observed in both groups, the ulcer index (including total number and length of gastric mucosal ulceration) was lower in AP-grafted group than that in control group (p < 0.05 or p < 0.01). Experiment III: On the 40th day after transplantation, all rats were divided into AP-grafted and muscle-grafted rats. Subsequently, they were allowed to expose to cold-plus-restraint stress and unstress (room temperature: 24 +/- 1 degrees C) respectively. After stress and unstress, all animals were immediately sacrificed by decapitation, the brains were dissected with Palkovits' micropunch technique. DA and its metabolites, DOPAC content in Nucleus accumbens (NAc) area of brain were assayed by HPLC with electrochemical detection. These results showed that concentrations of DA, DOPAC and their ratios (DOPAC/DA) in the NAc area of brain, were not statistically different under room temperature condition between muscle-grafted and AP-grafted rats. The DOPAC/DA ratio in both groups showed significant increase in the brain's NAc area under cold-restraint stress condition as compared with unstress condition. But AP-grafted rats exhibited significantly higher DOPAC content in the brain's NAc area when compared with muscle-grafted rats under cold-restraint stress condition (171.7 +/- 22.1 versus 101.5 +/- 14.2 ng/mg protein, p < 0.05). According to these findings, we suggest that reduced effect of chronic high serum PRL level from extra pituitary grafts on gastric mucosal ulceration produced by cold-restraint stress is probably mediated via Nucleus accumbens dopaminergic neuronal mechanism.

Animals↗

PubMedDate not supplied

Evidence for the involvement of dopamine D(1) and D(2) receptors in mediating the decrease of food intake during repeated treatment with amphetamine.

Repeated treatment with amphetamine (AMPH), a well-known anorectic agent, into animals could induce anorexia on day 1 and produce a gradual reversion of food intake (tolerant anorexia) on the following days. It is unknown whether these feeding changes are related to dopamine (DA) and/or noradrenergic neurotransmission. Thus, the present study investigated the subtype of receptor mediating AMPH-induced anorexia. Daily food intake was measured after various drugs were given. Pretreatment with haloperidol, an antagonist of DA receptors, may lead to inhibition of AMPH-induced anorexia. However, pretreatment with the alpha-adrenoceptor antagonist phentolamine, and the beta-adrenoceptor antagonist propranolol, failed to modify the action of AMPH, suggesting the involvement of DA receptors but not adrenoceptors in the action of AMPH-induced anorexia. Furthermore, pretreatment with SCH 23390 at a dose sufficient to block D(1) receptors or pimozide at a dose sufficient to inhibit D(2) receptors blocked AMPH-induced anorexia, indicating the involvement of D(1) and D(2) receptors. In a study of tolerant anorexia, repeated treatment with the D(1)/D(2) agonist apomorphine, but not the D(1) agonist SKF 38393 or D(2) agonist quinpirole, induced an AMPH-like tolerant feeding response, providing evidence for conjoint action of D(1) and D(2) receptors in the effect. The present results suggest that both D(1) and D(2) receptors are involved in anorexia and tolerant anorexia induced by chronic intermittent administration of AMPH.

Amphetamine↗