|1.||Etherington, Lori-An V: 1 article (05/2004)|
|2.||Frenguelli, Bruno G: 1 article (05/2004)|
|3.||Borowicz, Kinga K: 1 article (04/2002)|
|4.||Łuszczki, Jarogniew: 1 article (04/2002)|
|5.||Czuczwar, Stanisław J: 1 article (04/2002)|
|6.||Kuroda, Yoichiro: 1 article (03/2002)|
|7.||Fujii, Satoshi: 1 article (03/2002)|
|8.||Kato, Hiroshi: 1 article (03/2002)|
|9.||Yamazaki, Y: 1 article (06/2000)|
|10.||Sasaki, H: 1 article (06/2000)|
05/01/2004 - "In the presence of 8-cyclopentyl-1,3-dimethylxanthine (CPT), an adenosine A(1) receptor antagonist, the occurrence of spontaneous seizure activity was greatly increased as was the duration and intensity of evoked seizures, whilst the postictal depression of basal synaptic transmission was greatly attenuated. "
10/05/1993 - "Paradoxically, the selective adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT) antagonized DMCM- and pentylenetetrazole-induced seizures. "
02/01/1989 - "Antagonists of adenosine receptors, theophylline and 8-cyclopentyltheophylline, increased the cycle period due to marked prolongation of duration of ictal discharge, often to more than 30 min. Dipyridamole, an inhibitor of adenosine reuptake, lengthened the interictal phase of the seizure with no effect on ictal duration. "
04/01/2002 - "2-Chloroadenosine (1 mg/kg) showed also anticonvulsive efficacy against pentylenetetrazol-evoked seizures, raising the CD(50) value for pentylenetetrazol from 77.2 to 93.7 mg/kg. The drug (at 0.5 mg/kg) significantly enhanced the protective action of clonazepam in this test, decreasing its ED(50) value from 0.033 to 0.011 mg/kg. Moreover, aminophylline, a non-selective adenosine receptor antagonist (5 mg/kg), and 8-cyclopentyl-1,3-dimethylxanthine (8-CPX), a selective A(1) adenosine receptor antagonist (5 mg/kg) reversed the 2-chloroadenosine (0.125 mg/kg)-induced enhancement of the protective activity of carbamazepine and clonazepam. "
06/01/1992 - "In this study, rats were exposed to moderate hypoxic conditions (5% O2- 95% N2, 40 min x three days) in the presence or absence of 8-cyclopentyltheophylline, and the effects of reducing adenosinergic inhibition during hypoxia were assessed histologically and behaviorally. "
04/17/1995 - "Hypoxia-induced depression of the synaptic components of evoked field potentials was blocked in a concentration dependent manner by the selective A1 receptor antagonist 8-cyclopentyltheophylline (8-CPT), demonstrating extracellular accumulation of adenosine during hypoxia. "
08/01/1992 - "3. In slices from young Sprague-Dawley rats, the hypoxia-induced synaptic depression was reduced in a concentration-dependent manner by the adenosine antagonist 8-cyclopentyltheophylline (8-CPT; 100 nM-2.0 microM). "
06/01/1992 - "Endogenous adenosine depresses synaptic transmission in rat hippocampal slices during periods of hypoxia, a potentially neuroprotective cellular response that is attenuated by the adenosine antagonist 8-cyclopentyltheophylline. "
04/02/1990 - "The specific A1 adenosine receptor antagonist 8-cyclopentyltheophylline (8-CPT) significantly reduced hypoxia-induced synaptic depression in a concentration-dependent manner. "
|3.||Status Epilepticus (Complex Partial Status Epilepticus)
06/01/1995 - "In the present study we compared neuronal death following status epilepticus (SE) induced in the presence of 8-cyclopentyl-1,3-dimethylxanthine (8-CPT), an A1-adenosine receptor antagonist, with that following SE induced by continuous hippocampal stimulation. "
01/01/1994 - "In a recurrent electrical stimulation model, whereas no vehicle-treated animals developed status epilepticus after 20 recurrent electrical stimulations, rats injected with 10 mg/kg of the specific A1-adenosine antagonist 8-cyclopentyl-1,3-dimethylxanthine intraperitoneally developed status epilepticus after stimulation. "
04/01/2000 - "However, this effect of APNEA was not affected by the presence of 8-cyclopentyl-1,3-dimethylxanthine (CPT), a selective A1 antagonist; but instead completely abolished by 8-(3-chlorostyryl)caffeine (CSC), a selective A2a antagonist, or omega-conotoxin GVIA. "
05/30/1997 - "Aminophylline (5 mg/kg) and 8-cyclopentyl-1,3-dimethylxanthine (8-CPX, 5 mg/kg), reversed the APNEA (1 mg/kg)-induced enhancement of the anticonvulsive action of phenobarbital, diphenylhydantoin and valproate, but not that of carbamazepine produced by APNEA at 0.0039 mg/kg. The adenosine agonist did not alter the plasma levels of antiepileptic drugs studied, so a pharmacokinetic interaction is not probable. "
|1.||Purinergic P1 Receptors (Adenosine Receptor)
|5.||2-Chloroadenosine (2 Chloroadenosine)
|8.||Adenosine A1 Receptor
|10.||Valproic Acid (Valproate, Semisodium)