Disease relevance of Cyclopentyltheophylline

• 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 [1].
• 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 [2].
• This effect was reversed by either the selective adenosine A1 receptor antagonist, 8-cyclopentyltheophylline (IC50 = 50.3 +/- 19.9 nM) or overnight incubation with Pertussis toxin (100 ng/ml) [3].
• 8-Cyclopentyl 1,3-dimethylxanthine prolongs epileptic seizures in rats [4].
• 3. When the tetanus or LFS was applied to CA1 inputs in the presence of an adenosine A1 receptor antagonist, 8-cyclopentyltheophylline (1 microM), the field EPSP was enhances in LTP and attenuated in DP, while the E-S relationship was not significantly affected in either LTP or DP [5].

Psychiatry related information on Cyclopentyltheophylline

• The dose-response effects of administration of 8-cyclopentyltheophylline (CPT) (10, 20, and 40 mg/kg intraperitoneally [IP]) and alloxazine (ALX) (12.5, 25, and 50 mg/kg, IP) on sleep and wakefulness in rats were examined and compared to those of caffeine (12.5 mg/kg IP) [6].

High impact information on Cyclopentyltheophylline

• METHODS: Intracellular microelectrodes were used to study actions of ADO, the agonists 2-chloro-N6-cyclopentyl ADO, its 1-deaza derivative, 5'-N-ethylcarboxamido ADO, and CGS 21680 or the antagonists 8-cyclopentyl-1,3-dimethylxanthine, its 1,3-dipropyl analog, and 1,3-dipropyl-8-p-sulfophenylxanthine on synaptic behavior in myenteric neurons [7].
• In guinea pig isolated hearts, m-DITC-ADAC (5 microM) prolonged the stimulus to His bundle (SH) interval by 2.1-fold; this response could be prevented by the antagonist 8-cyclopentyltheophylline (5 microM) [8].
• Pretreatment with ZM241385 (A(2A)-Ado receptor antagonist) alone or in combination with MRS1706 (A(2B)-Ado receptor antagonist) resulted in a pure constriction upon Ado, whereas 8-cyclopentyltheophylline (CPT) (A(1)-Ado receptor antagonist) inhibited the constrictor response [9].
• This CHA-induced secretion of MMP-2 was inhibited by the adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT) and by the ERK1/2 pathway inhibitor U0126 [10].
• At 1.5% formalin, caffeine still produced only a partial reversal of effect; this appeared to be due to a block of adenosine A1 receptors, as it was also seen with the selective adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dimethylxanthine [11].

Chemical compound and disease context of Cyclopentyltheophylline

• 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 [12].

Biological context of Cyclopentyltheophylline

• 2. The A1 adenosine receptor antagonist 8-cyclopentyltheophylline (8-CPT) produced a concentration-dependent increase in synaptic potentials in slices from both young and aged rats [13].
• Vasodilation induced by adenosine was markedly suppressed by ZM 241385 (1 micromol/l, A2A antagonist) and alloxazine (1 micromol/l, A2B antagonist), but not by 8-cyclopentyltheophylline (CPT, 1 micromol/l, A1 antagonist) [14].

Anatomical context of Cyclopentyltheophylline

• A comparison of the effects of caffeine, 8-cyclopentyltheophylline, and alloxazine on sleep in rats. Possible roles of central nervous system adenosine receptors [6].
• The inhibitory effect of CHA on the Phase I contractile response in the vas deferens could be antagonized by the selective A1-receptor antagonist 8-cyclopentyltheophylline, while the selective alpha 2-receptor antagonist idazoxan preferentially antagonized the inhibitory effect of clonidine on the Phase I response [15].
• Paeoniflorin increased the uptake of a radiolabeled, non-metabolizable glucose derivative into isolated white adipocytes of Wistar rat in a concentration-dependent manner and this action was abolished by the antagonist, 8-cyclopentyltheophylline, at concentrations sufficient to block the adenosine A 1 receptor [16].
• Forskolin and 8-cyclopentyltheophylline synergistically facilitate the neuronal activity in the CA2 area of rat hippocampus via cAMP and non-cAMP cascades [17].

Associations of Cyclopentyltheophylline with other chemical compounds

• Neither the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (100 microM) nor the A1 adenosine receptor agonist R(-)-N6-(2-phenylisopropyl)adenosine (100 microM) affected release [18].
• The adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dimethylxanthine (CPT: 50 microM) potentiated the rising phase (167%) and abolished the subsequent ATP-evoked reduction phase [19].
• The adenosine A1 receptor agonist, N6-cyclopentyladenosine (CPA) and the antagonist, 8-cyclopentyltheophylline (CPT) were used as model drugs [20].
• The penetration of the adenosine antagonists 8-cyclopentyl-1,3-dimethylxanthine (CPT), 8-cyclopentyl-1,3-dipropylxanthine (CPX), 8-(p-sulfophenyltheophylline (8-PST), and 8-[4-[[[[(2-amino-ethyl)amino]carbonyl]methyl]oxy]phenyl]- 1,3-dipropylxanthine (XAC) into mouse brain was determined using ex vivo binding and locomotor studies [21].
• The SP-induced IPSC depression was prevented by SCH23390, a dopamine D1-like receptor antagonist and by 8-cyclopentyltheophylline, an adenosine A1 receptor blocker [22].

Gene context of Cyclopentyltheophylline

• The adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine blocked the increase, and partially blocked the decrease in firing rate in response to adenosine [23].
• Systemic administration of the selective A1R antagonist 8-cyclopentyltheophylline (8-CPT) inhibited sleep for 30 min in WT, whereas saline and 8-CPT both inhibited sleep in KO [24].
• This CHA-induced ERK activation was blocked by pretreatment with the A(1) receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine or pertussis toxin [25].
• 3. The adenosine A1 receptor antagonist, 8 cyclopentyltheophylline (CPT) was a less potent stimulator of mucin secretion than was the A2 receptor antagonist dimethylpropargylxanthine (DMPX) [26].
• 6. The results suggest that AMP mediates the inhibitory effects of ATP on epileptiform activity, a conclusion which can explain the earlier finding that cyclopentyltheophylline but not adenosine deaminase inhibited the effect of ATP [27].

Analytical, diagnostic and therapeutic context of Cyclopentyltheophylline

• 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 [28].
• 2. Three groups of normotensive conscious rats received an short intravenous infusion of 1.4 mg kg-1 CADO during constant infusions of the A1-selective antagonist, 8-cyclopentyltheophylline (CPT; 20 micrograms min-1 kg-1), the A2a-selective antagonist, 8-(3-chlorostyryl) caffeine (CSC; 32 micrograms min-1 kg-1) or the vehicle [29].
• Microdialysis application (retrodialysis) of the A1 receptor antagonist, 8-cyclopentyl-1,3-dimethylxanthine (CPT) increased phasic vasopressin cell intraburst firing rates progressively over the first 5 s by 4.5 +/- 1.6 Hz (P < 0.05), and increased burst duration by 293 +/- 64% (P < 0.05) [30].
• This increase is due, at least in part, to a decrease in Gi mediated inhibition of cAMP production and can be prevented by co-culture with the adenosine A1 receptor antagonist, cyclopentyltheophylline [31].

References