Oral caffeine pretreatment produced modest increases in smoked cocaine self-administration in rhesus monkeys

Comer, Sandra D.; Carroll, Marilyn E.

doi:10.1007/bf02247378

Cited by 28 publications

(15 citation statements)

References 18 publications

(18 reference statements)

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“…The asterisks (*) and hatch symbols (#) denote significant differences (P < 0.05) between the two groups in active nose-poke responses and number of infusions self-administered, respectively Fig. 2 The percentage of rats meeting criteria for nicotine selfadministration are presented across the first 14 days of training for water-water drinking, water-caffeine and caffeine-water drinking groups in smoked cocaine self-administration in rhesus monkeys (Comer and Carroll 1996). In rats, daily intraperitoneal injections of caffeine accelerated acquisition of cocaine self-administration and acute intraperitoneal injections of caffeine or co-administration of intravenous caffeine and cocaine increased intravenous selfadministration of cocaine (Horger et al 1991;Schenk et al 1994).…”

Section: Discussionmentioning

confidence: 99%

Chronic caffeine exposure potentiates nicotine self-administration in rats

et al. 1999

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The prevalence of tobacco smoking and coffee drinking place nicotine and caffeine among the most used licit drugs in many societies and their consumption is often characterised by concurrent use. The pharmacological basis for any putative interaction between these drugs remains unclear. Epidemiological reports support anecdotal evidence, which suggests that smokers consume caffeine to enhance the euphoric effects of nicotine. The aim of the present experiment was to examine effects of chronic exposure to caffeine on responding maintained by nicotine. Sprague-Dawley rats consuming caffeine (approximately 150-180 mg/kg per day) in their drinking water for 7 days prior to the beginning and throughout behavioural testing acquired intravenous nicotine self-administration (0.03 mg/kg per infusion) more rapidly than did controls. In a cross-over design, exclusion of caffeine brought levels of nicotine self-administration back to baseline, while adding caffeine to the drinking water of control rats increased responding maintained by nicotine over 90%. These findings strongly suggest that caffeine can potentiate the reinforcing properties of nicotine, thus highlighting the importance of environmental factors in shaping and maintaining tobacco smoking.

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Section: Discussionmentioning

confidence: 99%

Chronic caffeine exposure potentiates nicotine self-administration in rats

et al. 1999

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“…At the behavioral level, by acting on the ventral striatum, A 2A receptor agonists counteract and A 2A antagonists potentiate the motor, discriminative and rewarding effects of psychostimulants (Heffner et al, 1989;Popoli et al, 1994;Rimondini et al, 1997;Shimazoe et al, 2000;Knapp et al, 2001;Poleszak and Malec, 2002;Justinova et al, 2003;Filip et al, 2006). The non-selective A 1 and A 2A antagonist caffeine also potentiates these responses to psychostimulants (Misra et al, 1986;Logan et al, 1989;Gauvin et al, 1990;Horger et al, 1991;Comer and Carroll, 1996;Gasior et al, 2000;Munzar et al, 2002). By contrast, different from the effects obtained with pharmacological blockade, A 2A receptor knockout mice show a reduction in psychostimulantinduced motor responses (Chen et al, 2000Soria et al, 2005; for discussion, see Filip et al, 2006).…”

Section: Adenosine a 2a Receptors In The Ventral Striatum And The Acumentioning

confidence: 99%

Adenosine A2A receptors in ventral striatum, hypothalamus and nociceptive circuitry

Ferré

Diamond

Goldberg

et al. 2007

Progress in Neurobiology

126

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Adenosine A 2A receptors localized in the dorsal striatum are considered as a new target for the development of antiparkinsonian drugs. Co-administration of A 2A receptor antagonists has shown a significant improvement of the effects of L-DOPA. The present review emphasizes the possible application of A 2A receptor antagonists in pathological conditions other than parkinsonism, including drug addiction, sleep disorders and pain. In addition to the dorsal striatum, the ventral striatum (nucleus accumbens) contains a high density of A 2A receptors, which presynaptically and postsynaptically regulate glutamatergic transmission in the cortical glutamatergic projections to the nucleus accumbens. It is currently believed that molecular adaptations of the cortico-accumbens glutamatergic synapses are involved in compulsive drug seeking and relapse. Here we review recent experimental evidence suggesting that A 2A antagonists could become new therapeutic agents for drug addiction. Morphological and functional studies have identified lower levels of A 2A receptors in brain areas other than the striatum, such as the ventrolateral preoptic area of the hypothalamus, where adenosine plays an important role in sleep regulation. Although initially believed to be mostly dependent on A 1 receptors, here we review recent studies that demonstrate that the somnogenic effects of adenosine are largely mediated by hypothalamic A 2A receptors. A 2A receptor antagonists could therefore be considered as a possible treatment for narcolepsy and other sleep-related disorders. Finally, nociception is another adenosine-regulated neural function previously thought to mostly involve A 1 receptors. Although there is some conflicting literature on the effects of agonists and antagonists, which may partly be due to the lack of selectivity of available drugs, the studies in A 2A receptor knockout mice suggest that A 2A receptor antagonists might have some therapeutic potential in pain states, in particular where high intensity stimuli are prevalent.

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“…Presession acute injection with caffeine increased responding maintained by nicotine in squirrel monkeys responding under a fixed-ratio 30 (FR30) schedule of IV nicotine injection . Similarly, caffeine potentiated the effects of cocaine and amphetamine in behavioral assays such as locomotor activity (Anden and Jackson 1975;White and Keller 1984;Misra et al 1986;Schenk et al 1989), schedule-controlled responding (Logan et al 1989;Evans and Wenher 1990), drug self-administration (Schechter 1977;Horger et al 1991;Schenk et al 1994Schenk et al , 1996Worley et al 1994;Comer and Carroll 1996), drug discrimination (Holloway et al 1985;Harland et al 1989;Gauvin et al 1990), conditioned place preference (Tuazon et al 1992), and memory consolidation (Cestari and Castellano 1996) in experimental animals. In the above-mentioned studies, drug interactions were examined only after acute treatment with caffeine before experimental sessions, which does not take into consideration the development of tolerance to the behavioral effects of caffeine which occurs with repeated exposure (e.g., Holtzman 1983).…”

Section: Introductionmentioning

confidence: 95%

Behavioral effects of nicotine, amphetamine and cocaine under a fixed-interval schedule of food reinforcement in rats chronically exposed to caffeine

Jaszyna

Gąsior

Shoaib³

et al. 1998

Psychopharmacology

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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 D1 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), twenty-one Sprague-Dawley rats responding under a 5-min FI schedule of food reinforcement were divided into two groups; one (twelve rats) maintained on tap water (control) and the other (nine rats) on caffeine (3 mg/ml added to the drinking water). Following the substitution of caffeine solution for tap water, behavior was temporarily disrupted as evidenced by decreases in responding and QL values which reached a maximum after 72 h (rate 60% and QL 30% below baseline levels). Rats developed complete tolerance to these effects of caffeine over 5 days of caffeine exposure. After response rate and QL values stabilized, effects of drugs were evaluated. Nicotine (0.01-1.0 mg/kg; SC), amphetamine (0.1-5.6; IP), and cocaine (1.0-17; IP) each produced biphasic dose-dependent changes in response rate with maximum increases in response rate following intermediate doses and decreases in response rates following higher doses. The increase in rates of responding produced by amphetamine or cocaine (but not nicotine) were greater (P<0.05) in caffeine-drinking than in water-drinking rats. Both SKF-82958 (0.001-0.3 mg/kg; IP) and NPA (0.0001-0.1; IP) produced only dose-dependent decreases in rates of responding. Caffeine-drinking rats were less sensitive to the rate-depressant effects of SKF-82958 (P<0.05) than water-drinking rats. However, similar changes (P>0.05) were produced by NPA in both groups. Except for amphetamine, the remaining drugs produced similar (P>0.05) dose-dependent decreases in QL values in water- and caffeine-drinking rats. Amphetamine produced smaller decreases in QL values in caffeine-drinking rats than in water-drinking rats (P<0.05). Chronic exposure to caffeine produced complete insurmountable tolerance to the response-rate increasing (stimulant) effects of acute caffeine (3.0-17 mg/kg; IP) in caffeine-drinking rats. In conclusion, our study revealed that chronic caffeine exposure potentiates the behavioral response to amphetamine and cocaine but not to that of nicotine in rats responding under a FI schedule of food reinforcement. Thus, it is likely that these effects are mediated through different pharmacological mechanisms.

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Oral caffeine pretreatment produced modest increases in smoked cocaine self-administration in rhesus monkeys

Cited by 28 publications

References 18 publications

Chronic caffeine exposure potentiates nicotine self-administration in rats

Chronic caffeine exposure potentiates nicotine self-administration in rats

Adenosine A2A receptors in ventral striatum, hypothalamus and nociceptive circuitry

Behavioral effects of nicotine, amphetamine and cocaine under a fixed-interval schedule of food reinforcement in rats chronically exposed to caffeine

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