TY - JOUR. T1 - Chronic caffeine exposure in rats blocks a subsequent nicotine-conditioned taste avoidance in a one-bottle, but not a two-bottle test. AU - Palmatier, Matthew I.. AU - Bevins, Rick A. PY - 2001/11/21. Y1 - 2001/11/21. N2 - Two experiments were conducted in order to investigate nicotine-conditioned taste avoidance (CTA) following chronic preexposure to caffeine. Rats were given daily intraperitoneal injections of caffeine anhydrous (0, 10, or 30 mg/kg) for 10 or 30 days. Training of the nicotine-CTA began after the last day of caffeine preexposure. On five separate occasions access to a saccharin solution was followed immediately by an injection of 1.2 mg/kg nicotine hydrogen tartrate salt or saline. Nicotine-CTA readily developed in saline-preexposed controls. That is, paired rats drank less saccharin solution than unpaired rats after repeated saccharin-nicotine pairings. A similar pattern of nicotine-CTA was found for rats preexposed to 30 mg/kg caffeine for 10 days. Following ...

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Adenosine mediates its pysiological effects through four G protein-coupled receptors (A1, A2A, A2B and A3). A large number of agonists with high affinity at A1, A2A, A3 adenosine receptors and moderate affinity at A2B receptor have been developed over the years. Many compounds originally thought to be selective for the A1 or A2A subtypes later turned to be also potent agonists at more recently discovered A3 receptor. Owing to he great interest in A1 agonists as neuroprotective, antilipolytic, antiarrhythmic, and antinociceptive agents, there is a need for novel agonists with high potency and selectivity at this receptor subtype to avoid side effects due to the stimulation of the other subtypes. We discovered that the substitution of the hydrogen in 2-position of the ribose moiety of the A1 selective agonist CCPA with a methyl group (2-Me-CCPA) reduces the affinity at human A2A and A3 receptors, thus increasing the selectivity for A1 subtype [1]. In this communication we report on the affinity ...

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TY - JOUR. T1 - Chronic exposure to adenosine receptor agonists and antagonists reciprocally regulates the A1 adenosine receptor-adenylyl cyclase system in cerebellar granule cells. AU - Hettinger-Smith, Barbara D.. AU - Leid, Mark. AU - Murray, Thomas F.. PY - 1996/11. Y1 - 1996/11. N2 - Chronic treatment with the adenosine receptor antagonist caffeine evokes an up-regulation of A1 adenosine receptors and increased coupling of the receptor to G proteins in rat brain membranes. However, chronic agonist exposure has not been explored. Primary cultures of cerebellar granule cells were exposed chronically to A1 adenosine receptor agonists and antagonists. Exposure to the A1 adenosine receptor agonist N6-cyclopentyladenosine resulted in (1) a time- and concentration-dependent reduction in the density of receptors labeled by 1,3[3H]dipropyl-8-cyclopentylxanthine, (2) an enhanced ability of guanyl nucleotides to decrease the fraction of A1 adenosine receptor sites displaying high affinity for ...

The data presented in this study demonstrate that activation of PKC-ε on stimulation of the A1R in the rat or mouse heart elicits the translocation of the kinase to a RACK2 protein of the cardiomyocyte. Previously, we reported A1R activation promotes the translocation of PKC-ε, but not PKC-δ, to the t-tubules of the cardiomyocyte (30). The present data indicate that RACK2 was the target protein for this translocation. Our present observations include the measurement of contractile activity of isolated cardiomyocytes and the visualization with imaging (rat) and coimmunoprecipitation of the kinase and RACK2 (rat and mouse). Translocation of PKC-ε to RACK2 occurred whether the PKC-ε was activated nonspecifically by a phorbol ester, or by A1R activation with PIA, or with the selective agonist CCPA. The action induced by CCPA was selective for the A1R, as indicated by the inhibition elicited by the A1R antagonist DPCPX. Furthermore, PKC-ε translocation most likely results from an A1R-induced ...

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Slusarczyk J, Trojan E, Glombik K, et al. Anti-inflammatory properties of tianeptine on lipopolysaccharide-induced changes in microglial cells involve Toll-like receptor-related pathways. J Neurochem. 2015 Dec 7. [Epub ahead of print]. PMID: 26640965.. Yoo I, Woo JM, Lee SH, et al. Influence of anxiety symptoms on improvement of neurocognitive functions in patients with major depressive disorder: A 12-week, multicenter, randomized trial of tianeptine versus escitalopram, the CAMPION study. J Affect Disord. 2015 Oct 1;185:24-30. PMID: 26142691.. Lin H, Heo BH, Kim WM, et al. Antiallodynic effect of tianeptine via modulation of the 5-HT7 receptor of GABAergic interneurons in the spinal cord of neuropathic rats. Neurosci Lett. 2015 Jun 26;598:91-5. PMID: 25982324.. Cooper CM, Whiting DA, Cowen PJ, et al. Tianeptine in an experimental medicine model of antidepressant action. J Psychopharmacol. 2015 May;29(5):582-90. PMID: 25759404. ...

TY - JOUR. T1 - Behavioral effects of nicotine, amphetamine and cocaine under a fixed- interval schedule of food reinforcement in rats chronically exposed to caffeine. AU - Jaszyna, Maria. AU - Gasior, Maciej. AU - Shoaib, Mohammed. AU - Yasar, Sevil. AU - Goldberg, Steven R.. N1 - Copyright: Copyright 2007 Elsevier B.V., All rights reserved.. PY - 1998. Y1 - 1998. N2 - Epidemiological surveys demonstrate that caffeine, the main psychoactive ingredient of coffee, is a positive correlate in drug abuse. To characterize the behavioral nature of caffeine interactions with other psychomotor stimulants, we examined the effects of chronic caffeine exposure on the behavioral responses to nicotine, amphetamine, cocaine, the selective D agonist SKF-82958 and the selective D2 receptor agonist NPA, in rats responding under a fixed interval (FI) schedule of food reinforcement. Following stabilization of rates and temporal patterns of responding (mathematically expressed as quarter-life values, QL), ...

Tianeptine is a drug used primarily in the treatment of major depressive disorder, although it may also be used to treat asthma or irritable bowel syndrome. Chemically it is a tricyclic antidepressant (TCA), but it has different pharmacological properties than typical TCAs as recent research suggests that tianeptine produces its antidepressant effects through indirect alteration of glutamate receptor activity (i.e., AMPA receptors and NMDA receptors) and release of BDNF, in turn affecting neural plasticity. Tianeptine was discovered and patented by The French Society of Medical Research in the 1960s. Currently, tianeptine is approved in France and manufactured and marketed by Laboratories Servier SA; it is also marketed in a number of other European countries under the trade name

This study is a 12-month, dose-level blinded, multicenter study of 2 inhaled dose levels of CVT-301 for the treatment of up to 5 OFF episodes per day in PD patients experiencing motor fluctuations (OFF episodes). All patients will receive active treatment, but patients will be blinded to dose level. This will serve as an extension to the CVT-301-004 study for those patients who participated in that study and remain eligible for this study. In addition, patients who previously completed the CVT-301-003, CVT-301-009 and CVT-301-005 (observational arm completers), as well as CVT-301 naïve patients may be enrolled if they meet the CVT-301-004E eligibility criteria ...

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