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Biomedical subjects

R Tao

Publications and source records attributed to R Tao.

At least 55 records · Page 3Linked to original sources
PubMed1995

Involvement of the dorsal raphe but not median raphe nucleus in morphine-induced increases in serotonin release in the rat forebrain.

In vivo microdialysis was used to determine if morphine produces increases in extracellular serotonin in specific brain sites. With citalopram included in the dialysis solution to block reuptake, serotonin was measured in 11 brain sites of unanesthetized rats. After systemic morphine (10 mg/kg, s.c.), increases in extracellular serotonin were observed in the nucleus accumbens, amygdala, frontal cortex, striatum, thalamus, hypothalamus and ventral hippocampus. These seven areas are innervated either by dorsal raphe nucleus projections alone, or by projections from both dorsal and median raphe nucleus. In contrast, serotonin was not significantly increased in the medial septal nucleus and dorsal hippocampus. These two areas are selectively innervated by projections from the median raphe nucleus. After systemic morphine, serotonin was increased in the dorsal raphe nucleus, but not in the medial raphe nucleus. Local infusion of morphine through a microdialysis probe in the dorsal raphe nucleus induced a dose-dependent increase of serotonin in the nucleus accumbens, but not in the medial septum. In contrast, infusion of morphine into the median raphe nucleus had little effect on serotonin in either the nucleus accumbens or septum. Infusion of morphine into either the dorsal or median raphe nucleus elicited increased behavioral activity and hyperthermia. These data provide evidence that morphine acts in the area of the dorsal raphe nucleus, but not the median raphe nucleus, to enhance serotonin release in specific forebrain sites, and that the increases in serotonin in the dorsal raphe nucleus projection sites are not an indirect effect of changes in behavioral state or body temperature.

Animals↗
PubMed1995

Sorbitol synthesis in transgenic tobacco with apple cDNA encoding NADP-dependent sorbitol-6-phosphate dehydrogenase.

The apple (Malus domestica) cDNA encoding NADP-dependent sorbitol-6-phosphate dehydrogenase (S6PDH) was stably integrated and expressed in transgenic tobacco (Nicotiana tabacum cv. SR1). Expression of the cDNA in either a sense or antisense orientation was accomplished using cauliflower mosaic virus regulatory sequences (CaMV35S). Sorbitol synthesis was confirmed by gas-chromatography-mass-spectroscopy (GC-MS). Sorbitol concentration in the leaves of the transgenic plants expressing the sense orientation varied from 186 to 446 nmol (g fr wt)-1. The concentration positively correlates with S6PDH activity in leaves. Neither sorbitol nor S6PDH activity was detected in the extracts of nontransformed tobacco or transgenic tobacco expressing the antisense orientation. These results provide key genetic evidence that S6PDH expression is sufficient for the synthesis of sorbitol in tobacco, implicating it as a key enzyme in the sorbitol biosynthetic pathway in apple and perhaps other members of the woody Rosaceae.

Base Sequence↗
PubMed1995

[Thoracoscopy in persistent or recurrent spontaneous pneumothorax].

To assess the value of thoracoscopy in spontaneous pneumothorax, the procedure and results of thoracoscopy by using fiberoptic bronchoscope and rigid cold-light thoracoscope in 50 patients with persistent or recurrent pneumothorax were reported. We found subpleural blebs or bullae in 35 cases and adhesions preventing lung expansion in 10 cases. The histologic diagnosis following thoracoscopic biopsy in 13 patients showed non-specific inflammation in 12 cases and tuberculosis in one case. The overall diagnostic rate was 92% (46/50). 5 cases were cured with transendoscopical Nd-YAG laser cauterisation of the blebs or bullae not exceeding 1 cm in diameter. There were no side effects after the procedure, and no recurrence was observed in a follow-up of 24 months. 40 patients were treated with intrapleural talcum power under thoracoscopic control. The postoperative complications were transient fever and chest pain and recurrence was observed in two cases only (5%) during 2-7 years of follow-up. It is concluded that thoracoscopy enables accurate assessment of the causes of pneumothorax, talc pleurodesis is a very effective method of controlling recurrent and persistent pneumothorax, and laser therapy can play an important role in selected patients with spontaneous pneumothorax.

Adolescent↗
PubMed1994

Anesthetics block morphine-induced increases in serotonin release in rat CNS.

The effect of morphine on serotonin (5-HT) was examined by microdialysis in unanesthetized and anesthetized rats. In unanesthetized rats, morphine (10 mg/kg, s.c.) produced increases in extracellular 5-HT in nucleus accumbens (n. accumbens) and dorsal raphe nucleus (DRN), but not in the dorsal hippocampus. Similarly, extracellular 5-HT in the n. accumbens, but not the dorsal hippocampus, was increased after morphine (1 mM) was infused for 60 min by reverse dialysis into the DRN. Chloral hydrate, pentobarbital, and ketamine anesthesia had different effects on 5-HT in the n. accumbens. Chloral hydrate induced a transient increase and ketamine a sustained increase in extracellular 5-HT. Pentobarbital caused a sustained decrease. The effects of systemic and intraraphe administration of morphine were abolished by all three anesthetics. Infusion of muscimol, a GABAA receptor agonist, into the DRN also induced a decrease in 5-HT and abolished the effects of morphine on 5-HT in the DRN and n. accumbens. These results are consistent with other evidence suggesting that morphine-induced increases in monoamine neurotransmission are a disinhibitory effect resulting from opioid-mediated inhibition of GABA release. More conclusively, it is apparent that anesthetized animals are inappropriate for testing the effect of morphine on 5-HT neurotransmission.

Anesthetics↗
PubMed1994

Increased extracellular serotonin in rat brain after systemic or intraraphe administration of morphine.

The effect of morphine on serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in the CNS of unanesthetized rats was investigated by microdialysis. Morphine was administered either subcutaneously, by local perfusion into the diencephalon, or by intraraphe microinjection. Systemic administration of morphine resulted in a significant increase in both extracellular 5-HT and 5-HIAA in the diencephalon. The effect of morphine on 5-HT was dose dependent during local perfusion of the diencephalon with inhibitors of uptake or monoamine oxidase. Systemic morphine also produced significant increases in extracellular 5-HT in the striatum and hippocampus during uptake inhibition. The site of opioid effects on 5-HT was tested by locally perfusing morphine into the diencephalon. This had no effect on 5-HT or 5-HIAA. In contrast, intraraphe injection of morphine caused a dose-dependent increase in extracellular 5-HT and 5-HIAA in the diencephalon. These results suggest that systemic morphine induces an increase in 5-HT release in widespread areas of the forebrain. This appears to be due to an effect on 5-HT cell bodies and not on 5-HT nerve endings in projection sites.

Animals↗
PubMed1993

[Effects of methylflavonolamine on TXA2 and PGI2 plasma levels in rabbits with myocardial infarction].

Effects of methylflavonolamine (MFA) on TXA2 and PGI2 plasma levels in rabbits of myocardial infarction were investigated. It was found that TXB2 levels were inhibited by MFA 2.5 or 5.0 mg.kg-1 i.v. while 6-keto-PGF1 alpha levels were only slightly inhibited after repeated doses of 5.0 mg.kg-1 i.v. within 6 h. This result indicates that MFA exhibit stronger inhibition on cyclo-oxygenase in platelets than in endothelial cells. In addition, the myocardial injury and the size of myocardial infarction were much less in the MFA treated groups than in the control.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Morphine induces an increase in extracellular serotonin in the rat diencephalon.

The effect of systemic morphine on extracellular serotonin (5-HT) in the diencephalon of unanesthetized, unrestrained rats was investigated by in vivo microdialysis coupled to high performance liquid chromatography with electrochemical detection. Administration of morphine resulted in a dose dependent increase in extracellular 5-HT. Significant increases were first seen at a dose of 5 mg/kg, and a maximal increase occurred at 10 mg/kg. This increase was blocked by pretreatment with naltrexone, indicating that the effect of morphine on 5-HT was mediated by opiate receptors. Morphine also had a significant effect on extracellular 5-hydroxyindoleacetic acid (5-HIAA), leading to a gradual increase across a range of doses. The effect of morphine on 5-HT was compared to effects of morphine on nociception and catalepsy. Increases in 5-HT and 5-HIAA were first detected at doses that were analgesic but too low to elicit catalepsy. Consistent with many reports that opioids cause an increase in synthesis and turnover of 5-HT in the rat forebrain, the present results provide more direct evidence that 5-HT release is increased after morphine administration.

Animals↗