Research Paper: A Neurochemical and Electrophysiological Study on the Combined Effects of Caffeine and Nicotine in the Cortex of Rats (original) (raw)
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Basic and Clinical Neuroscience, 2021
Introduction: Caffeine and nicotine are the most widely consumed psychostimulants worldwide. Although the effects of each drug alone on the central nervous system have been studied extensively, the literature on the neurochemical and electrophysiological effects of their combined treatments is scarce. The present study investigated the cortical electrophysiological and neurochemical alterations induced by acute administration of caffeine and nicotine in rats. Methods: The rats received caffeine and nicotine at a 1-hour interval between the two treatments. Results: Caffeine and nicotine administration resulted in a significant decrease in the concentrations of cortical amino acid neurotransmitters, namely glutamate, aspartate, glycine, and taurine, while γ-aminobutyric acid (GABA) significantly increased. Increased cortical lipid peroxidation and reduced glutathione and nitric oxide levels and acetylcholinesterase and Na+/K+-ATPase activities were also observed. The Electroencephalog...
Psychophysiological interactions between caffeine and nicotine
Pharmacology Biochemistry and Behavior, 1991
interactions between caffeine and nicotine PHARMACOL BIOCHEM BE-HAV 38(2) 333-337, 1991-The interactive effects of caffeine and mcotme were stud~ed m twelve subjects. Mood and phys~ologic responses to the pharmacologic components mcotme and caffeine were measured, whde controlhng for the sensory/behavioral aspects of smolong and coffee dnnkmg Two experimental sessions presented a caffeine × mcotlne design, with caffelnated or decaffemated coffee followed at thirty-minute intervals by controlled inhalations of mcotme and nonnlcotlne smoke Results showed that there was a s~gmficant interactive effect of caffeine and mcotme on subjective arousal such that mCOtlne decreased arousal only m the presence of caffeine These findings extend prewous work showing interactive effects of caffeine and self-tltrated doses of c~garette smoke m affecting subjective arousal The effects of mcotme on subjective arousal may, therefore, depend not only on mcotlne dose, but also on the presence of caffeine Heart rate was increased by mcotme and both systolic and dmstohc blood pressures were elevated by caffeine Caffeine also potentiated the increase m dmstohc blood pressure resulting from smoke mhalatlons, but th~s occurred irrespective of mCOtlne dose Nicotine Cigarette smoking Caffeme Coffee Arousal Car&ovascular
Alteration of the Behavioral Effects of Nicotine by Chronic Caffeine Exposure
Pharmacology Biochemistry and Behavior, 2000
TANDA, G. AND S. R. GOLDBERG. Alteration of the behavioral effects of nicotine by chronic caffeine exposure. PHARMACOL BIOCHEM BEHAV 66 (1)47-64, 2000.-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. Some epidemiological reports support anecdotal evidence, which suggests that smokers consume caffeine to enhance the effects of nicotine. This paper reviews various aspects of the pharmacology of caffeine and nicotine, in humans and experimental animals, important for the understanding of the interactions between these drugs. In particular, recent experiments are reviewed in which chronic exposure to caffeine in the drinking water of rats facilitated acquisition of self-adminstration behavior, enhanced nicotineinduced increases in dopamine levels in the shell of the nucleus accumbens and altered the dopaminergic component of a nicotine discrimination. These studies provide evidence that the rewarding and subjective properties of nicotine can be changed by chronic caffeine exposure and indicate that caffeine exposure may be an important environmental factor in shaping and maintaining tobacco smoking.
Nicotine antagonizes caffeine- but not pentylenetetrazole-induced anxiogenic effect in mice
Psychopharmacology, 2006
Rationale Nicotine and caffeine are widely consumed licit psychoactive drugs worldwide. Epidemiological studies showed that they were generally used concurrently. Although some studies in experimental animals indicate clear pharmacological interactions between them, no studies have shown a specific interaction on anxiety responses. Objectives The present study investigates the effects of nicotine on anxiety induced by caffeine and another anxiogenic drug, pentylenetetrazole, in mice. The elevated plus-maze (EPM) test was used to evaluate the effects of drugs on anxiety. Methods Adult male Swiss Webster mice (25–32 g) were given nicotine (0.05–0.25 mg/kg s.c.) or saline 10 min before caffeine (70 mg/kg i.p.) or pentylenetetrazole (15 and 30 mg/kg i.p.) injections. After 15 min, mice were evaluated for their open- and closed-arm time and entries on the EPM for a 10-min session. Locomotor activity was recorded for individual groups by using the same treatment protocol with the EPM test. Results Nicotine (0.05–0.25 mg/kg) itself did not produce any significant effect in the EPM test, whereas caffeine (70 mg/kg) and pentylenetetrazole (30 mg/kg) produced an anxiogenic effect, apparent with decreases in open-arm time and entry. Nicotine (0.25 mg/kg) pretreatment blocked the caffeine- but not pentylenetetrazole-induced anxiety. Administration of each drug and their combinations did not produce any effect on locomotor activity. Conclusions Our results suggest that the antagonistic effect of nicotine on caffeine-induced anxiety is specific to caffeine, instead of a non-specific anxiolytic effect. Thus, it may extend the current findings on the interaction between nicotine and caffeine.
Caffeine's Influence on Nicotine's Effects in Nonsmokers
American Journal of Health Behavior, 2007
Objective-To determine if nicotine's effects are influenced by caffeine in nonsmoking, moderate-caffeine consuming individuals (N=20). Methods-The first 3 sessions included one of 3 randomly ordered, double-blind caffeine doses (0, 75, or 150 mg, oral [po]) and 2 single-blind nicotine gum doses (2 and 4 mg) in ascending order. The fourth session (single blind) repeated the 0 mg caffeine condition. Results-Nicotine increased heart rate and subjective ratings indicative of aversive effects, and decreased reaction times. These effects were independent of caffeine dose and reliable across sessions. Conclusions-In nonsmokers, nicotine effects are not influenced by moderate caffeine doses.
Caffeine potentiates the discriminative-stimulus effects of nicotine in rats
Psychopharmacology, 2002
Rationale: Caffeine and nicotine are the main psychoactive ingredients of coffee and tobacco, respectively, with a high frequency of concurrent use in humans. Objectives: The aim of the present study was to examine the interaction of caffeine and nicotine in rats trained to discriminate nicotine from saline. Methods: Two groups of male Sprague-Dawley rats (n=8 per group) were trained to discriminate 0.4 mg/kg nicotine, SC, from saline under a fixed ratio schedule of food presentation. One group of rats was chronically exposed to caffeine (1.0 mg/ml) dissolved in their drinking water whereas the other group was exposed to tap water. Effects of IP injections of caffeine on nicotine-lever selection were subsequently examined. In separate groups of rats exposed to the same caffeine-drinking or waterdrinking regimen, effects of caffeine pretreatment on nicotine plasma levels were evaluated. Results: Although caffeine (1.0-30.0 mg/kg) did not generalize to nicotine when administered alone, it markedly potentiated discriminative-stimulus effects of the threshold dose of nicotine (0.05 mg/kg) in both water-and caffeine-drinking rats. Nicotine plasma levels were, however, not affected by acute or chronic caffeine exposure. Conclusions: Caffeine appears to enhance the discriminative-stimulus effects of the threshold dose of nicotine by a pharmacodynamic rather than a pharmacokinetic interaction. This suggests that caffeine consumption may be a contributing factor in the onset, maintenance of and relapse to tobacco dependence.
Neuropharmacological Analysis of Caffeic Acid in Rats
Basic <html_ent glyph="@amp;" ascii="&"/> Clinical Pharmacology <html_ent glyph="@amp;" ascii="&"/> Toxicology, 2006
The aim of the present study was to investigate the effect of intraperitoneal administration of caffeic acid (0.5, 1, 2, 4 or 8 mg/kg) on elevated plus-maze and open field tasks in rats and its possible neuroprotection/neurotoxicity using the comet assay. Caffeic acid at 1 mg/kg increased the number of entries and the time spent in the open arms on plusmaze, suggesting an anxiolytic-like effect when used in lower doses without affecting locomotion and exploration on the open field. Furthermore, a protective effect against hydrogen peroxide-induced oxidative damage on brain tissue was observed through the treatment with caffeic acid at 1 and 8 mg/kg. However, in the highest dose, caffeic acid induced DNA damage in brain tissue.
Behavioural Pharmacology, 2003
Three experiments examined the effects of chronic preexposure to caffeine on the subsequent conditioned and unconditioned locomotor activating effects of nicotine or amphetamine in rats. Rats were given daily intraperitoneal injections of caffeine anhydrous (0, 10 or 30 mg/kg base) for 30 days. Conditioning (environment-drug pairings) began after the last day of caffeine pre-exposure. Preexposure to 30 mg/kg of caffeine enhanced the acute and chronic locomotor effects of amphetamine (0.5 mg/kg). A similar enhancement of activity was not seen with the high (0.421 mg/kg base) or low dose (0.175 mg/kg) of nicotine. In a drug-free test, the distinct environment paired with amphetamine and the high dose of nicotine evoked increases in activity relative to controls. Caffeine pre-exposure did not affect expression of this conditioned hyperactivity. These effects of caffeine pre-exposure on amphetamine-induced activity could not be attributed to 1973; Clark and IZi~miu;. This locolnotor supprcssion tends to be replaced with Iiypcractivity after repcatcd daily exposure to nicotinc (0.210-0.421 mg/lcg; Clark and ICumar, 1983; Kita (.r rd., 1992; ICsir, 1994; Bcvins (V frL, 2001). Rats also show heiglitened activity rclneive to controls with repeatcd administration of amphctariiine (e.g. Schoffelmeer rt crl., 2002). In contrast to nicotinc, amlphetamine doses typically used to study hchaviornl activation do not induce an initial suppression of locomotor activity (Browman rt rrl., 1998; Fraioli lJt ul., 1999; 0.125-1.0 mg/kg in our laboratory, see later). In fact, the stimulant effccts of amphetamine can be seen on the first administration (e.g. Urowlnan rt ~d , 1998).
Nicotine's oxidative and antioxidant properties in CNS
Life Sciences, 2002
Nicotine has been reported to be therapeutic in some patients with certain neurodegenerative diseases and to have neuroprotective effects in the central nervous system. However, nicotine administration may result in oxidative stress by inducing the generation of reactive oxygen species in the periphery and central nervous system. There is also evidence suggesting that nicotine may have antioxidant properties in the central nervous system. The antioxidant properties of nicotine may be intracellular through the activation of the nicotinic receptors or extracellular by acting as a radical scavenger in that it binds to iron. The possibility that nicotine might be used to treat some symptoms of certain neurodegenerative diseases underlies the necessity to determine whether nicotine has pro-oxidant, antioxidant or properties of both. This review discusses the studies that have addressed this issue, the behavioral effects of nicotine, and the possible mechanisms of action that result from nicotine administration or nicotinic receptor activation. D
einstein (São Paulo), 2021
Objective: To describe electrocorticographic, electromyographic and electrocardiographic profiles to report the electrophysiological effects of caffeine in Wistar rats. Methods: Male adult Wistar rats weighing 230g to 250g were used. Rats were allocated to one of two groups, as follows: Group 1, Control, intraperitoneal injection of 0.9% saline solution (n=27); and Group 2, treated with intraperitoneal injection of caffeine (50mg/kg; n=27). The rats were submitted to electrocorticographic, electromyographic and electrocardiographic assessment. Results: Brain oscillations (delta, theta, alpha, beta and gamma) in the frequency range up to 40Hz varied after caffeine administration to rats. Powers in delta and theta oscillations ranges were preponderant. The contractile force of the skeletal striated and cardiac muscles increased. Electrocardiogram analysis revealed shorter RR, QRS and QT intervals under the effect of caffeine. Conclusion: In the central nervous system, there was an increase in the delta, theta and alpha amplitude spectrum, which are related to memory encoding and enhanced learning. With regard to skeletal muscle, increased contraction of the gastrocnemius muscle was demonstrated, a clear indication of how caffeine can be used to enhance performance of some physical activities. Electrocardiographic changes observed after caffeine administration are primarily related to increased heart rate and energy consumption.