Biomedical subjects

C H Jeng

Publications and source records attributed to C H Jeng.

10 recordsLinked to original sources

PubMed2000

Chronic methamphetamine exposure decreases high affinity uptake function in norepinephrine afferents in the cerebellar cortex: an electrophysiological and electrochemical study.

It has been reported that chronic methamphetamine (MA) treatment decreases monoamine release in different brain regions. However, the clearance of norepinephrine (NE) after chronic MA intake is not clear. In the present study, we administered MA to Sprague-Dawley rats for 1 month. The animals were later anesthetized with urethane for electrophysiological recording. Previous studies have indicated that gamma-aminobutyric acid (GABA)-induced electrophysiological responses are enhanced by norepinephrine (NE) acting via postsynaptic beta-adrenergic receptors. We found that local application of the NE high affinity uptake inhibitor desmethylimipramine (DMI) significantly potentiated GABA-induced electrophysiological depressions in cerebellar Purkinje neurons in control rats. In contrast, DMI did not augment GABA responses in rats chronically treated with MA for 1 month, or in rats withdrawn from MA for 7-14 days after a 1-month MA treatment. To further examine if DMI-induced GABA modulation is altered by post- or pre-synaptic mechanisms in chronic MA-treated rats, we examined the electrophysiological interaction of GABA and isoproterenol (ISO), a postsynaptic beta-adrenergic receptor agonist, in Purkinje neurons. We found that GABA-induced inhibition is potentiated by local application of ISO in both control and chronic MA rats, suggesting that the reduction in DMI/GABA interactions is probably not mediated through post-synaptic noradrenergic mechanisms. Presynaptic NE clearance was further examined using in vivo chronoamperometric methods. Extracellular NE levels in the cerebellar cortex were measured using Nafion-coated carbon fiber sensors. We found that local application of DMI inhibited NE clearance in control rats, but not in chronic MA animals, suggesting that presynaptic NE clearance is reduced after chronic MA treatment. In addition, NE levels in cerebellar tissue were measured using HPLC-ECD. The NE concentration was significantly decreased in chronic MA rats. Taken together, our data suggest that regulation of uptake by DMI at central noradrenergic nerve terminals is abnormal after chronic MA exposure.

Action Potentials↗

PubMed2000

Ethanol potentiates dopamine release during acute hypoxia in rat striatum.

We, and others, have previously demonstrated that N-methyl-D-aspartate (NMDA) receptor is involved in hypoxia or ischemia-mediated responses. We found that the NMDA antagonist ketamine attenuates cortical nitric oxide release during cerebroischemia. It has been reported that ethanol (EtOH) antagonizes NMDA-induced responses in various systems. In the present study, the interaction of EtOH and KCl-evoked striatal dopamine release in vivo during acute hypoxia was examined. High-speed chronoamperometric recording techniques, using Nafion-coated carbon fiber electrodes, were used to evaluate extracellular dopamine (DA) concentration in the striatum of urethane-anesthetized Sprague-Dawley rats. KCl was directly applied to the striatum to evoke release of DA. These anesthetized animals were paralyzed with d-tubocurarine and connected to a respirator to allow controlled respiration. Systemic concentrations of oxygen were altered by changing the rate of the respirator. We previously reported that lowering the respiratory rates from 90 to 20 times/min for 5 min decreased arterial PO(2) and facilitated KCl-induced DA release in the striatum. In this study, we found that application of NMDA antagonist MK801 attenuates hypoxic DA release, suggesting that NMDA receptor is involved in this hypoxic reaction. In contrast, EtOH dose dependently enhanced KCl-evoked DA release during hypoxia. To further examine the interactions of excitatory amino acid and EtOH on DA release, glutamate was locally applied to the striatum. Glutamate-induced DA release was not affected by the systemic application of EtOH. Taken together, these data suggest that EtOH enhances DA release in vivo during short-term hypoxia, possibly through mechanisms other than excitatory amino acid pathways.

Animals↗

PubMed2000

Serotonergic modulation of ethanol-induced electrophysiological depression in young and aged rats.

BACKGROUND: Ethanol (EtOH)-induced electrophysiological depressions in cerebellar Purkinje neurons have been shown to be potentiated by exogenously applied serotonin (5HT). In this study, we determined whether this modulatory action can be activated by endogenous release from presynaptic serotonergic terminals, and whether such a response is altered by age or rat strain. METHODS: Extracellular 5HT levels in cerebellar cortex were measured in real time by in vivo chronoamperometry, by using Nafion-coated carbon fiber electrodes, in anesthetized young (3-5 months old) or aged (18-24 months old) Sprague Dawley and Fischer 344 rats. Some animals were prelesioned with 5,7 dihydroxytryptamine (5,7 DHT). Single unit electrophysiological activity was recorded from cerebellar Purkinje neurons. Serotonin or its presynaptic antagonist methiothepin was applied directly to cerebellar neurons through multibarrel pipettes. RESULTS: Local application of methiothepin dose-dependently induced 5HT overflow in young Sprague Dawley and Fisher 344 rats. Methiothepin-induced 5HT release was decreased significantly in aged or 5,7 DHT-lesioned rats. Local application of methiothepin or 5HT potentiated EtOH-induced electrophysiological depression of Purkinje neurons in young animals of both strains. Methiothepin-potentiated, EtOH-elicited neuronal inhibition was reduced greatly in aged or 5,7 DHT-lesioned rats. Serotonin-facilitated EtOH responses were reduced in the aged Sprague Dawley rats. CONCLUSIONS: EtOH-induced electrophysiological responses in cerebellum can be facilitated by endogenous 5HT release by using a 5HT autoreceptor antagonist. Such actions are attenuated in aged rats perhaps through a presynaptic serotonergic mechanism.

5,7-Dihydroxytryptamine↗

PubMed1998

Methamphetamine modulates GABA-induced electrophysiological depression by alternating noradrenergic actions in cerebellar Purkinje neurons.

Previous studies have indicated that gamma-aminobutyric acid (GABA)-induced electrophysiological responses can be enhanced by noradrenaline (NE) acting via beta-adrenergic receptors. Methamphetamine (MA) has been reported to be a noradrenergic releasing agent. In the present study, we examined the interaction of MA and GABA in cerebellar Purkinje neurons of urethane-anesthetized rats. We found that local application of MA did not potentiate GABA-induced electrophysiological depressions in Purkinje neurons. Since MA may act indirectly or directly on alpha or beta noradrenergic receptors, we further examined the interactions of MA with selective noradrenergic antagonists. We found that after blocking alpha-adrenergic receptors with prazocin, MA significantly facilitated GABA responses. On the other hand, co-administration of timolol with MA did not attenuate GABA-induced neuronal depressions. To examine further the interactions between alpha and beta receptors in modulating GABA response, we found that stimulation of alpha-adrenergic receptors in the absence of beta receptor activation, such as by application of the alpha-agonist phenylephrine alone, did not decrease GABA-induced inhibition. However, stimulation of alpha-adrenergic receptors in the presence of beta-receptor activation, such as by co-application of phenylephrine and the beta-agonist isoproterenol (ISO), attenuated ISO-facilitated GABA inhibition. Taken together, these data suggest that MA may activate two noradrenergic modulatory mechanisms: beta-adrenergic receptor-induced GABA potentiation and alpha-adrenergic inhibition, which attenuates beta-mediated modulation. In conclusion, our data suggest that MA may regulate GABA-induced electrophysiological response by altering both the alpha- and beta-noradrenergic inputs in cerebellar Purkinje neurons.

Action Potentials↗

PubMed1996

Electrophysiological and electrochemical responses of NMDA in the cerebellum: interactions with nonadrenergic pathway.

In the present experiments, we measured N-methyl-D-aspartate (NMDA)-induced norepinephrine (NE) release and extracellular action potentials in the cerebellar cortex of urethane-anesthetized rats. The overflow of NE was measured using a Nafion coated-carbon fiber electrode and in vivo chronoamperometry. We found that both NMDA and quisqualate evoked NE release. Our previous work demonstrated that the electrophysiological activity of cerebellar Purkinje neurons could be either excited or inhibited by local NMDA application. It was reported that bicuculline antagonized NMDA-induced inhibition in Purkinje neurons, suggesting that a GABAergic mechanism was activated during NMDA application. We and others previously found that GABA-mediated electrophysiological depressions were enhanced by NE acting via beta-adrenergic receptors while these responses were decreased by activation of alpha-adrenergic receptors. Since NMDA evokes overflow of endogenous NE, the electrophysiological depression induced by NMDA may contain an NE-mediated modulatory component. In this study, we first examined the interaction of NMDA with beta-adrenergic agonist. We found that local application of isoproterenol facilitated NMDA- or GABA-mediated electrophysiological depressions of the Purkinje neurons. Applications of phenoxybenzamine, which antagonized the alpha-adrenergic response of synaptically released NE, also facilitated NMDA-elicited depression. In contrast, the depression induced by GABA, which did not induce NE overflow, was not potentiated by phenoxybenzamine. The facilitation of NMDA-induced depression by phenoxybenzamine was antagonized by the beta-adrenergic antagonist timolol. Taken together, these data suggested that the nonadrenergic pathway is involved in NMDA-induced electrophysiological responses in the cerebellum. NMDA may induce neuronal depression through modulation of GABAergic inhibition via NMDA-evoked NE release onto cerebellar Purkinje neurons.

Adrenergic Fibers↗

PubMed1996

Serotonin modulates ethanol-induced depression in cerebellar Purkinje neurons.

In the present study, we found that local application of serotonin (5-HT) potentiated ethanol-induced depressions of the spontaneous activity of Purkinje neurons in urethane-anesthetized rats. 5-HT also potentiated depressions induced by gamma-aminobutyric acid; however, this modulatory response was quantitatively smaller than 5-HT-induced potentiation of ethanol depression. Previous reports suggested that the release of 5-HT can be regulated by presynaptic 5-HT autoreceptors. We found that local application of methiothepin, which may induce 5-HT overflow through the inhibition of presynaptic autoreceptors, facilitated ethanol-mediated responses. This methiothepin effect was greatly diminished in neonatally 5,7-dihydroxytryptamine-lesioned animals, suggesting a presynaptic mechanism was involved. We also found that the 5-HT1A antagonist UH301 did not attenuate 5-HT-facilitated ethanol reactions. On the other hand, local application of 5-HT1B agonist CGS12066B potentiated ethanol-induced depression. Taken together, our data suggest that 5-HT can modulate ethanol-mediated electrophysiological depression, possibly mediated through 5-HT1B receptors in the cerebellum.

Animals↗

PubMed1995

Methamphetamine facilitates ethanol-induced depressions in cerebellar Purkinje neurons of prazocin- or DSP4-treated rats.

Methamphetamine (MA) and ethanol (EtOH) are two commonly abused drugs. Previous behavioral studies indicated that MA may synergistically alter EtOH responses. In the present study, we found that local application of MA did not potentiate ethanol-induced depressions of the spontaneous activity of Purkinje neurons in urethane-anesthetized rats. We and others previously found that, in cerebellar Purkinje neurons, EtOH and gamma-amino-butyric acid (GABA)-mediated depressions can be enhanced by norepinephrine (NE) acting via beta-adrenergic receptors while these responses are decreased by activation of alpha-adrenergic receptors. In the present experiment, after blocking alpha-adrenergic receptors with prazocin, MA significantly enhanced EtOH responses in most of neurons studied. It has been reported that MA may directly and indirectly enhance alpha-adrenergic and beta-adrenergic receptor-mediated responses. The present study may suggest that MA can negatively modulate (antagonize) the depressant effects of ethanol via the alpha-adrenergic receptor, which oppose the positive modulatory mechanism (potentiation of EtOH depression) via actions of the beta-adrenergic receptors. We found that lesioning NE neurons with N-chloroethyl-N-ethyl-2-bromobenzylamine hydrochloride (DSP4), a selective noradrenergic neurotoxin, enhance the MA-facilitated ethanol responses, suggesting that this action of MA may not require NE. Since it has been reported that MA increases serotonin (5-HT) and catecholamine release from their nerve terminals, MA may potentiate EtOH depressions by facilitating the release of NE and 5-HT. Taken together, our data suggested that MA may modulate EtOH responses via catecholaminergic and serotonergic mechanisms in cerebellar Purkinje neurons.

Action Potentials↗

PubMed1988

Establishment of a human ovarian clear cell carcinoma cell line (RMG-I) and its single cell cloning--with special reference to the stem cell of the tumor.

A cell line, designated RMG-I, has been established from ascites of a patient with ovarian clear cell carcinoma. RMG-I cells have grown well for more than 6 years with mirror ball formation. Chromosome analysis revealed aneuploidy with a modal number of 47 and 3 marker chromosomes. The histological characteristics of the transplanted tumor were similar to those observed in the original tumor which was composed of dark cells, clear cells, and hobnail cells. Thus, the RMG-I cell line was identified to be an ovarian clear cell carcinoma. Immunohistochemically, basic fetoprotein (BFP) and ferritin were demonstrated in the original tumor, the cultured cells, and the transplanted tumor. Furthermore, in order to clarify whether these 3 kinds of cells originate from one stem cell or not, monoclonal cell population were transplanted into nude mice, and its histological investigation revealed that 3 types of cells existed in the transplanted tumor, proving that they originate from one stem cell.

Adenocarcinoma↗

PubMed1986

[Penetration of cefoperazone into the exudate of the retroperitoneal space after (semi-)radical hysterectomy].

The purpose of the study was to examine the penetration of cefoperazone (CPZ) into the exudate of retroperitoneal space after (semi-)radical hysterectomy in patients with uterine carcinoma and to evaluate the suitability of its prophylactic use. Two grams of CPZ was administered by intravenous infusion over 1 hour just after the operation and the same dose was repeated every 12 hours for 3 consecutive days. The exudate was collected from the abdominal drainage for every 3 hours for measurements of hemoglobin, total protein and CPZ levels. Concentrations of CPZ in exudate samples were found to remain above the MICs for major causative organisms of the inflammation in both groups of patients of radical (14 cases) and semiradical (5 cases) hysterectomy. On the operative and 1st days, exudate CPZ level in the group of semiradical hysterectomy patients showed higher than that in the group of radical hysterectomy patients. But on the 2nd day, there was no significant difference in exudate CPZ level between these 2 groups. The above results indicated that the presence of blood in the retroperitoneal space might affect the concentration of the antibiotic in the exudate. From these findings, it is concluded that the present dosage regimen is efficient to prevent the postoperative infection after (semi-)radical hysterectomy.

Bacterial Infections↗

PubMed1984

[Modulation of alkaline phosphatase by butyrate and prednisolone in uterine cervical cancer cell line (SKG-III)].

The production of late placental alkaline phosphatase (ALP) isoenzyme and the co-presence of a small amount of tissue-unspecific ALP isoenzyme was confirmed in the newly established uterine cervical epidermoid cancer cell line SKG-III. Sodium butyrate (3mM), which has been shown to modulate oncodevelopmental gene expression, was examined after introduction of the agents into confluent cultures. 72 hours after the first sodium butyrate treatment, the amount (per mg cell protein) of total ALP activity increased to 5 times that of control cells and tissue-unspecific insoenzyme occupied about two thirds of the concentration of the modulated ALP. Treatment of SKG-III cells with prednisolone (5 micrograms/ml) for 48 hours caused a 3.5 times increase in total ALP activity, and most of the modulated ALP was occupied by late placental isoenzyme. From these data, it was concluded that sodium butyrate mainly induced tissue-unspecific isoenzyme, while prednisolone induced late placental isoenzyme. The results suggested that SKG-III cells had at least two ALP isoenzyme genes and chemical agents such as sodium butyrate or prednisolone could modulate the ALP isoenzyme profile of these cultured cells in vitro.

Alkaline Phosphatase↗