The Experts below are selected from a list of 192 Experts worldwide ranked by ideXlab platform
Pao-luh Tao - One of the best experts on this subject based on the ideXlab platform.
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Chronic intrathecal morphine treatment does not cause down-regulation of spinal adenosine A1 receptors in rats.
Naunyn-Schmiedeberg's archives of pharmacology, 1996Co-Authors: Pao-luh Tao, Chih-shung Wong, Mei-chuan LinAbstract:We have shown previously that systemic chronic morphine treatment causes down-regulation of spinal adenosine A1 receptors in rats. Recently, we have found that chronic supraspinal morphine treatment also causes this effect. In the present study, we investigated whether chronic spinal morphine treatment has the same effect of down-regulation of spinal adenosine A1 receptors. Adult male Sprague-Dawley rats were rendered tolerant to morphine either by multiple intrathecal (i.t.) injections or continuous Lt. infusion by osmotic pump administration for 2 or 4 days. Spinal A1-adenosine receptor binding activity was measured by using the selective A1 adenosine agonist [3H]Cyclohexyladenosine. No significant decrease in [3H]Cyclohexyladenosine binding was found in the spinal cord after 2 or 4 days of multiple Lt. injections of morphine. There was also no significant change in the amount of spinal [3H]Cyclohexyladenosine bound after 4 days of continuous Lt. infusion of morphine by osmotic pump. From these and our previous results, it is concluded that only supraspinal chronic morphine treatment down regulates the spinal A1 adenosine receptor and this may play a role in the mechanism of supraspinal morphine tolerance but not spinal morphine tolerance.
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Chronic intracerebroventricular administration of morphine down-regulates spinal adenosine A1 receptors in rats.
European journal of pharmacology, 1995Co-Authors: Pao-luh Tao, Chi-feng Liu, Hui-chen TsaiAbstract:Previous studies from our laboratory have shown that systemic chronic morphine treatment causes down-regulation of spinal adenosine A1 receptors in rats. In this study, we further investigated whether supraspinal morphine treatment causes this effect. Adult male Sprague-Dawley rats were rendered tolerant to morphine by multiple intracerebroventricular (i.c.v.) injections for 2 or 4 days. Adenosine A1 receptor binding activities were measured with [3H]Cyclohexyladenosine in the spinal cord and midbrain. A significant decrease in [3H]Cyclohexyladenosine binding was found in the spinal cord but not in the midbrain region after 2 or 4 days of chronic i.c.v. morphine treatment. A decrease in the number of binding sites (Bmax) with no change in the affinity (Kd) of the ligand for the adenosine A1 receptor was observed. These results suggest that supraspinal morphine administration could cause the down-regulation of spinal adenosine A1 receptors and this may play a role in the mechanism of morphine tolerance.
Zarrindast Mr - One of the best experts on this subject based on the ideXlab platform.
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Effects of adenosine receptor agonists and antagonists on physostigmine-induced yawning.
European Journal of Pharmacology, 1995Co-Authors: Zarrindast Mr, Reza Adeli, Sedigheh Hosseini-semnaniAbstract:The effect of adenosine receptor agonists and antagonists on physostigmine-induced yawning was investigated in intact or cannulated rats. Intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) administration of physostigmine to rats induced yawning dose dependently. I.p. or i.c.v. treatment of the animals with atropine, theophylline, 5-N-ethylcarboxamidoadenosine (NECA) or N6-Cyclohexyladenosine reduced the yawning induced by i.p. injection of physostigmine. I.p. administration of theophylline decreased the yawning induced by i.c.v injection of physostigmine. The inhibitory action of N6-Cyclohexyladenosine (i.p.) also was decreased by 8-phenyltheophylline (i.p.) pretreatment. It is concluded that yawning induced by a central cholinergic mechanism and a central adenosine mechanism interacts with the cholinergic-induced behaviour.
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Effects of adenosine receptor agonists and antagonists on physostigmine-induced yawning.
European Journal of Pharmacology, 1995Co-Authors: Zarrindast Mr, Reza Adeli, Sedigheh Hosseini-semnani, Mohammad SharifzadehAbstract:The effect of adenosine receptor agonists and antagonists on physostigmine-induced yawning was investigated in intact or cannulated rats. Intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) administration of physostigmine to rats induced yawning dose dependently. I.p. or i.c.v. treatment of the animals with atropine, theophylline, 5-N-ethylcarboxamidoadenosine (NECA) or N6-Cyclohexyladenosine reduced the yawning induced by i.p. injection of physostigmine. I.p. administration of theophylline decreased the yawning induced by i.c.v injection of physostigmine. The inhibitory action of N6-Cyclohexyladenosine (i.p.) also was decreased by 8-phenyltheophylline (i.p.) pretreatment. It is concluded that yawning induced by a central cholinergic mechanism and a central adenosine mechanism interacts with the cholinergic-induced behaviour.
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Influences of different adenosine receptor subtypes on catalepsy in mice
Psychopharmacology, 1993Co-Authors: Zarrindast Mr, Maryam Modabber, M. SabetkasaiAbstract:The effects of adenosine A1 and A2 receptors on catalepsy were studied in mice. The adenosine agonists 5-N′-ethylcarboxamide-adenosine (NECA), N6-phenylisopropyladenosine (PIA) and N6-Cyclohexyladenosine (CHA) induced dose dependent catalepsy. The A1 adenosine antagonist 8-phenyltheophylline (8-PT) potentiated catalepsy induced by NECA, R-PIA and CHA. However, theophylline did not potentiate but inhibited the responses induced by NECA, R-PIA and CHA. Neither 8-PT nor theophylline alone has any effect on catalepsy in mice. It is concluded that catalepsy induced by the adenosine agonists may be due to A2 receptor stimulation and that the A1 antagonism may potentiate the response.
Samuel G Speciale - One of the best experts on this subject based on the ideXlab platform.
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adenosine a1 receptors mediate inhibition of camp formation in vitro in the pontine rem sleep induction zone
Brain Research, 2005Co-Authors: Gerald A. Marks, C G Birabil, Samuel G SpecialeAbstract:Abstract Microinjection of adenosine A1 receptor agonist or an inhibitor of adenylyl cyclase into the caudal, oral pontine reticular formation (PnOc) of the rat induces a long-lasting increase in REM sleep. Here, we report significant inhibition of forskolin-stimulated cAMP in dissected pontine tissue slices containing the PnOc incubated with the A1 receptor agonist, cyclohexaladenosine (10 −8 M). These data are consistent with adenosine A1 receptor agonist actions on REM sleep mediated through inhibition of cAMP.
F Nicolas - One of the best experts on this subject based on the ideXlab platform.
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Opposite effects of Cyclohexyladenosine and theophylline on hypoxic damage in cultured neurons.
Neuroscience letters, 1994Co-Authors: J L Daval, F NicolasAbstract:To study the central effects of adenosine on hypoxia, the influence of treatment by the A1 receptor agonist Cyclohexyladenosine (1 microM) or by the antagonist theophylline (10 microM) was tested on cell damage in a model of neuronal culture. Whereas theophylline enhanced cell injury induced by 8 h hypoxia, Cyclohexyladenosine decreased lactate dehydrogenase leakage, abolished the transient increase in 2-D-deoxyglucose transport and improved cell morphology. Such actions might involve regulation of excitatory amino acid release and maintenance of calcium homeostasis.
Hui-chen Tsai - One of the best experts on this subject based on the ideXlab platform.
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Chronic intracerebroventricular administration of morphine down-regulates spinal adenosine A1 receptors in rats.
European journal of pharmacology, 1995Co-Authors: Pao-luh Tao, Chi-feng Liu, Hui-chen TsaiAbstract:Previous studies from our laboratory have shown that systemic chronic morphine treatment causes down-regulation of spinal adenosine A1 receptors in rats. In this study, we further investigated whether supraspinal morphine treatment causes this effect. Adult male Sprague-Dawley rats were rendered tolerant to morphine by multiple intracerebroventricular (i.c.v.) injections for 2 or 4 days. Adenosine A1 receptor binding activities were measured with [3H]Cyclohexyladenosine in the spinal cord and midbrain. A significant decrease in [3H]Cyclohexyladenosine binding was found in the spinal cord but not in the midbrain region after 2 or 4 days of chronic i.c.v. morphine treatment. A decrease in the number of binding sites (Bmax) with no change in the affinity (Kd) of the ligand for the adenosine A1 receptor was observed. These results suggest that supraspinal morphine administration could cause the down-regulation of spinal adenosine A1 receptors and this may play a role in the mechanism of morphine tolerance.
