Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:2.3.1.21 (CPT)
4,580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The intraperitoneal injection of d-amphetamine (5 mg/kg i.p.), preceded (10 min before) by intrastriatal injection of an adenosine A2 receptor agonist (CGS 21680, 5-10 micrograms) or followed (5 min later) by an intrastriatal adenosine A1 receptor agonist (N6-cyclopentyladenosine, CPA, 30 micrograms), induced ipsilateral rotations in rats. The opposite effect (contralateral rotations) was observed with adenosine receptor antagonists (A2 antagonist, 3,7-dimethyl-1-propargylxanthine, DMPX, 10 micrograms; A1 antagonist, 8-cyclopentyl-1,3-dimethylxanthine, CPT, 2.5 micrograms). These results confirm that both adenosine A2 and A1 receptors modulate striatal dopaminergic neurotransmission.
...
PMID:Modulation of striatal adenosine A1 and A2 receptors induces rotational behaviour in response to dopaminergic stimulation in intact rats. 808 3

The influence of adenosine receptor agonists and antagonists on amphetamine-induced stereotypy was examined in male Wistar rats. Adenosine A2 receptor agonists CGS 21680 (0.5-2 mg/kg ip) and a non-specific A2/A1 receptor agonist NECA (0.05-0.1 mg/kg ip) attenuated in a dose dependent manner amphetamine-induced stereotypy (2 mg/kg sc). CPA as specific agonist of adenosine A1 receptors counteracted this stereotypy, but only in a narrow range of doses (0.1-0.2 mg/kg ip). Adenosine A2A receptor antagonist, DMPX (3 and 6 mg/kg ip) potentiated stereotypy induced by either subthreshold dose of amphetamine 0.5 mg/kg or a high one 2 mg/kg. A non-selective adenosine receptor antagonist, caffeine (10 mg/kg ip) potentiated effect of low dose of amphetamine, but only in a dose of 20 mg/kg ip increased stereotypy induced by 2 mg/kg ip of amphetamine. A selective adenosine A1 receptor antagonist CPT (1 and 3 mg/kg ip) was ineffective in reversing amphetamine-induced stereotypy. These results confirm the existence of adenosine-dopamine interactions in the brain, and the suggestions that A2 adenosine receptor agonists may have antipsychotic properties.
...
PMID:Influence of adenosine receptor agonists and antagonists on amphetamine-induced stereotypy in rats. 1133 36

The effect of local administration of amitriptyline (AMI), desipramine (DMI) and citalopram (CIT) on veratridine-evoked glutamate (Glu) and aspartate (Asp) release in the prefrontal cortex of the conscious rat was examined using in vivo reverse microdialysis. The antidepressants (each at 100 microM) significantly reduced Glu and Asp release. The effect of AMI and CIT was attenuated by i.p. administration of the adenosine A1/A2A receptor antagonist caffeine (10 mg/kg), or by local infusion of the adenosine A1 receptor antagonist 8-cyclopentyltheophylline (CPT, 75 microM). Neither caffeine nor CPT influenced the effect of DMI (100 microM). The inhibitory action of DMI at a lower concentration (50 microM) was diminished significantly by CPT, but not caffeine. Perfusion of 5-hydroxytryptamine (5-HT; 100 microM) and the selective agonist of adenosine A1 receptors N6-cyclopentyladenosine (CPA; 50 and 100 microM) also suppressed Glu and Asp release. It is suggested that the blockade of the cellular uptake of adenosine, or indirect enhancement of its release, and subsequent activation of adenosine A1 receptors may be responsible for the inhibitory effect of antidepressants on Glu and Asp release.
...
PMID:Involvement of adenosine in the effect of antidepressants on glutamate and aspartate release in the rat prefrontal cortex. 1141 61

The involvement of adenosine A(1) and A(2A) receptors in the motor effects of caffeine is still a matter of debate. In the present study, counteraction of the motor-depressant effects of the selective A(1) receptor agonist CPA and the A(2A) receptor agonist CGS 21680 by caffeine, the selective A(1) receptor antagonist CPT, and the A(2A) receptor antagonist MSX-3 was compared. CPT and MSX-3 produced motor activation at the same doses that selectively counteracted motor depression induced by CPA and CGS 21680, respectively. Caffeine also counteracted motor depression induced by CPA and CGS 21680 at doses that produced motor activation. However, caffeine was less effective than CPT at counteracting CPA and even less effective than MSX-3 at counteracting CGS 21680. On the other hand, when administered alone in habituated animals, caffeine produced stronger motor activation than CPT or MSX-3. An additive effect on motor activation was obtained when CPT and MSX-3 were coadministered. Altogether, these results suggest that the motor-activating effects of acutely administered caffeine in rats involve the central blockade of both A(1) and A(2A) receptors. Chronic exposure to caffeine in the drinking water (1.0 mg/ml) resulted in tolerance to the motor effects of an acute administration of caffeine, lack of tolerance to amphetamine, apparent tolerance to MSX-3 (shift to the left of its 'bell-shaped' dose-response curve), and true cross-tolerance to CPT. The present results suggest that development of tolerance to the effects of A(1) receptor blockade might be mostly responsible for the tolerance to the motor-activating effects of caffeine and that the residual motor-activating effects of caffeine in tolerant individuals might be mostly because of A(2A) receptor blockade.
...
PMID:Involvement of adenosine A1 and A2A receptors in the motor effects of caffeine after its acute and chronic administration. 1270 Jun 82

The influence of adenosine receptor agonists and antagonists on amphetamine-induced conditioned place preference (CPP) was examined in male Wistar rats. Selective adenosine A1 receptor agonist, CPA, significantly reduced the acquisition of CPP induced by amphetamine. NECA (A2/A1 adenosine receptor agonist) produced similar effect, but selective A2 adenosine receptor agonist CGS 21680, attenuated acquisition of amphetamine-induced CPP only at the lower dose used. The blockade of adenosine receptors by CPT, DMPX and caffeine, did not influence the expression and acquisition of amphetamine-induced CPP. With regard to the expression of amphetamine-induced CPP, only A2A adenosine agonist (CGS 21680) slightly decreased the action of amphetamine. Other adenosine agonists were without effect. Our results indicate that activation of A1 receptor decreases the acquisition of CPP induced by amphetamine. It suggests that adenosine A1 receptor is involved in rewarding effects of amphetamine. Therefore, it seems that selective adenosine A1 receptor agonists may have some attenuating influence on the development of amphetamine dependence.
...
PMID:Effects of adenosine receptor agonists and antagonists in amphetamine-induced conditioned place preference test in rats. 1450 10

Adenosine, by acting on adenosine A1 and A2A receptors, is known to antagonistically modulate dopaminergic neurotransmission. We have recently reported that nonselective adenosine receptor antagonists (caffeine and 3,7-dimethyl-1-propargylxanthine) can partially substitute for the discriminative-stimulus effects of methamphetamine. In the present study, by using more selective compounds, we investigated the involvement of A1 and A2A receptors in the adenosinergic modulation of the discriminative-stimulus effects of both cocaine and methamphetamine. The effects of the A1 receptor agonist N6-cyclopentyladenosine (CPA; 0.01-0.1 mg/kg) and antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT; 1.3-23.7 mg/kg) and the A2A receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine hydrochloride (CGS 21680; 0.03-0.18 mg/kg) and antagonist 3-(3-hydroxypropyl)-8-(3-methoxystyryl)-7-methyl-1-propargylxanthin phosphate disodium salt (MSX-3; 1-56 mg/kg) were evaluated in rats trained to discriminate either 1 mg/kg methamphetamine or 10 mg/kg cocaine from saline under a fixed-ratio 10 schedule of food presentation. The A1 and A2A receptor antagonists (CPT and MSX-3) both produced high levels of drug-lever selection when substituted for either methamphetamine or cocaine and significantly shifted dose-response curves of both psychostimulants to the left. Unexpectedly, the A2A receptor agonist CGS 21680 also produced drug-appropriate responding (although at lower levels) when substituted for the cocaine-training stimulus, and both CGS 21680 and the A1 receptor agonist CPA significantly shifted the cocaine dose-response curve to the left. In contrast, both agonists did not produce significant levels of drug-lever selection when substituted for the methamphetamine-training stimulus and failed to shift the methamphetamine dose-response curve. Therefore, adenosine A1 and A2A receptors appear to play important but differential roles in the modulation of the discriminative-stimulus effects of methamphetamine and cocaine.
...
PMID:Involvement of adenosine A1 and A2A receptors in the adenosinergic modulation of the discriminative-stimulus effects of cocaine and methamphetamine in rats. 1455 81

Using a splanchnic nerve-spinal cord preparation in vitro, we have previously demonstrated that tonic sympathetic activity is generated from the thoracic spinal cord. Here, we sought to determine if adenosine receptors play a role in modulating this spinally generated sympathetic activity. Various adenosine analogs were applied. N6-Cyclopentyladenosine (CPA, adenosine A1 receptor agonist) and 5'-N-ethylcarboxamidoadenosine (NECA, adenosine A1/A2 receptor agonist) reduced, while N6-[2-(4-aminophenyl)ethyl]adenosine (APNEA, non-selective adenosine A3 receptor agonist) did not alter sympathetic activity. The inhibitory effect of CPA or NECA on sympathetic activity was reversed by 8-cyclopentyltheophylline (CPT, adenosine A1 receptor antagonist) or abolished by CPT pretreatment. In the presence of 3,7-dimethyl-1-propargylxanthine (DMPX, adenosine A2 receptor antagonist), sympathetic activity was still reduced by CPA or NECA. Sympathetic activities were not changed by applications of the more selective adenosine A2 or A3 receptor agonists or antagonists, including 4-[2-[[6-amino-9-(N-ethyl-beta-D-ribofuranuronamidosyl)-9H-purin-2-yl]amino]ethyl]benzenepropanoic acid (CGS21680), 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM241385), 2-chloro-N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (Chloro-IB-MECA), and 3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1,4-(+/-)-dihydropyridine-3,5-dicarboxylate (MRS1191). These findings exclude a possible involvement of A2 or A3 receptors in sympathetic regulation at the spinal levels. Interestingly, CPT alone did not affect sympathetic activity, suggesting that adenosine A1 receptors are endogenously quiescent under our experimental conditions. We conclude that intraspinal adenosine A1 receptors may down-regulate sympathetic outflow and serve as a part of the scheme for neuroprotection.
...
PMID:The role of intraspinal adenosine A1 receptors in sympathetic regulation. 1514 5

The effect of adenosine receptor ligands on dizocilpine-induced locomotion was studied in mice. Dizocilpine-induced hyperactivity (0.1 mg/kg i.p.) in mice was antagonized by all adenosine receptor agonists: CPA--A1 receptor agonist, CGS 21680--A2 receptor agonist, and NECA--A1/A2 receptor agonist, but the effect of NECA was the most apparent. Locomotion induced by the threshold dose of dizocilpine (0.05 mg/kg i.p.) was enhanced by DPMX (A2A adenosine receptor antagonist) and by the theophylline (A1 and A2 receptor antagonist), but not by A1 receptor antagonist--CPT. These data suggest that adenosinergic system is involved in the mechanism of dizocilpine-induced hyperactivity, and it seems that A2A adenosine receptor plays a more important role.
...
PMID:Involvement of adenosine receptors in dizocilpine-induced motor activity in mice. 1653 36

The interplay between interference and absorption leads to interesting phenomena like coherent perfect absorption and coherent perfect transparency (CPA and CPT), which can be exploited for fully optical modulation. While it is known that it is possible to harness CPA and CPT for switching a strong signal beam with a weak control beam, it is not immediate that this process suffers from a fundamental compromise between the device efficiency (quantified by device loss and modulation depth) and the asymmetry between signal and control intensity desired for operation. This article quantifies this compromise and outlines a possible way to overcome it by means of a combination of optical gain and loss in the same photonic component. A general formulation and a specific device realization are both discussed.
...
PMID:Understanding and overcoming fundamental limits of asymmetric light-light switches. 2940 89

We study the optical response of a double optomechanical cavity system assisted by two Rydberg atoms. The target atom is only coupled with one side cavity by a single cavity mode, and gate one is outside the cavities. It has been realized that a long-range manipulation of optical properties of a hybrid system, by controlling the Rydberg atom decoupled with the optomechanical cavity. Switching on the coupling between atoms and cavity mode, the original spatial inversion symmetry of the double cavity structure has been broken. Combining the controllable optical non-reciprocity with the coherent perfect absorption/transmission/synthesis effect (CPA/CPT/CPS reported by [ X.-B.Yan Opt. Express 22, 4886 (2014)], we put forward the theoretical schemes of an all-optical transistor which contains functions such as a controllable diode, rectifier, and amplifier by controlling a single gate photon.
...
PMID:All-optical transistor based on Rydberg atom-assisted optomechanical system. 2971 44


1

---