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Choongon Jang - One of the best experts on this subject based on the ideXlab platform.
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Assessment of the rewarding effects of dimenhydrinate using the Conditioned Place Preference paradigm in mice.
Neuroscience Letters, 2010Co-Authors: Thi-lien Nguyen, In-jee You, Chae Ha Yang, Seok-yong Lee, Choongon JangAbstract:Dimenhydrinate (DIM) is an over-the-counter antihistamine consisting of diphenhydramine (DIP) and 8-chlorotheophylline (CTP). Medical use of DIM is for prevention of nausea and motion sickness. Recently, it has been reported that DIM may be used alone or in combination with other drugs for recreational purposes due to its euphoric and hallucinogenic effects. To investigate the putatively rewarding properties of DIM and its constituents DIP and CTP, we used a Conditioned Place Preference (CPP) test in mice. DIM significantly induced CPP at a dose of 30 mg/kg. Neither DIP (3, 10, and 30 mg/kg) nor CTP (3, 10, and 30 mg/kg) alone induced CPP. Because neither DIP nor CTP resulted in CPP, the rewarding property of DIM appears to be caused by the sum of the effects of its constituents. In addition, low doses of DIM (3 mg/kg), co-administered with low doses of cocaine (7.5 mg/kg), significantly induced CPP, while neither low-dose DIM (3 mg/kg) nor low-dose cocaine (7.5 mg/kg) administered separately induced CPP. This result suggests the liability of DIM use in combination with other abused drugs to create a stronger effect.
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Effects of Coptis japonica on morphine-induced Conditioned Place Preference in mice.
Archives of pharmacal research, 2003Co-Authors: Seok-yong Lee, Dong-keun Song, Choongon JangAbstract:Morphine, an analgesic with significant abuse potential, is considered addictive because of drug craving and psychological dependence. It is reported that repeated treatment of morphine can produce Conditioned Place Preference (CPP) showing a reinforcing effect in mice. CPP is a useful method for the screening of morphine-induced psychological dependence. In the present study, we investigated the effect of the methanolic extract of Coptis japonica (MCJ) on morphine-induced CPP in mice. Furthermore, we examinedc-fos expression in the parietal cortex, piriform cortex, striatum, nucleus accumbens, and hippocampus of the morphine-induced CPP mouse brain. Treatment of MCJ 100 mg/kg inhibited morphine-induced CPP. Expression ofc-fos was increased in the cortex, striatum, nucleus accumbens, and hippocampus of the morphine-induced CPP mouse brain. These increases of expression were inhibited by treatment with MCJ 100 mg/kg, compared to the morphine control group. Taken together, these results suggest that MCJ inhibits morphine-induced CPP through the regulation ofc-fos expression in the mouse brain.
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inhibition by ginsenosides rb1 and rg1 of methamphetamine induced hyperactivity Conditioned Place Preference and postsynaptic dopamine receptor supersensitivity in mice
General Pharmacology-the Vascular System, 1998Co-Authors: Hackseang Kim, Wookyu Park, Hangmook Rheu, Daehyun Cho, Yountack Hong, Younhee Seong, Choongon JangAbstract:The ginsenosides Rb1 and Rg1, the major components of ginseng saponin, inhibited not only methamphetamine-induced hyperactivity but also Conditioned Place Preference (CPP) in mice following a single or repeated administration. Dopamine (DA) receptor supersensitivity, which developed in methamphetamine-induced CPP mice, was also inhibited by both Rb1 and Rg1. Therefore, the present results suggest that Rb1 and Rg1 may be the active components of ginseng saponin in the modulation of methamphetamine-induced dopaminergic behaviors such as hyperactivity and CPP, supporting our previous conclusion that ginseng saponin might modulate methamphetamine-induced dysfunction at both the pre- and postsynaptic DA receptors.
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blockade by naloxone of cocaine induced hyperactivity reverse tolerance and Conditioned Place Preference in mice
Behavioural Brain Research, 1997Co-Authors: Hackseang Kim, Wookyu Park, Choongon Jang, Jaeyang Kong, Hangmook Rheu, Daehyun Cho, Seogyoun KangAbstract:Cocaine-induced hyperactivity was inhibited by a single administration of naloxone (2 and 5 mg/kg, i.p.), an opioid receptor antagonist, and naloxone administered prior to and during the chronic injection of cocaine attenuated the development of both cocaine-induced reverse tolerance and Conditioned Place Preference (CPP). Dopamine (DA) receptor supersensitivity which developed in cocaine-induced reverse tolerant or CPP mice, was also inhibited by naloxone. Furthermore, naloxone reduced an apomorphine-induced striatal dopaminergic action, climbing behavior. Therefore, the present studies suggest that cocaine-induced dopaminergic behaviors, such as hyperactivity, reverse tolerance and CPP, may be commonly produced via activation of an opioid receptor. The development of DA receptor supersensitivity may be a possible common mechanism of cocaine-induced reverse tolerance and CPP, since cocaine-induced changes in sensitivity to apomorphine, as well as apomorphine-induced climbing behavior in mice, were both inhibited by naloxone.
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inhibition by mk 801 of cocaine induced sensitization Conditioned Place Preference and dopamine receptor supersensitivity in mice
Brain Research Bulletin, 1996Co-Authors: Wookyu Park, Choongon JangAbstract:Abstract Repeated administration of cocaine led to increases in ambulation-accelerating activity (sensitization) and Conditioned Place Preference (CPP). Dopamine (DA)-receptor supersensitivity was also developed in cocaine-induced sensitized and CPP mice. An N -methyl- d -aspartate (NMDA)-receptor antagonist, MK-801, blocked simultaneously developments of cocaine-induced behavioral sensitization, CPP, and DA-receptor supersensitivity. Furthermore, MK-801 inhibited a apomorphine-induced striatal dopaminergic action: climbing behavior. These results suggest that the cocaine-induced dopaminergic behaviors such as sensitization to ambulatory activity and CPP may be produced via activation of the NMDA receptor. The development of postsynaptic DA-receptor supersensitivity may be an underlying common mechanism that mediates cocaine-induced behavioral sensitization and CPP.
Raul G Paredes - One of the best experts on this subject based on the ideXlab platform.
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different doses of estradiol benzoate induce Conditioned Place Preference after paced mating
Hormones and Behavior, 2011Co-Authors: Rebeca Corona, Francisco J Camacho, Patricia Garciahorsman, Alfonso Guerrero, Annette Ogando, Raul G ParedesAbstract:Abstract The ovarian hormones estrogen and progesterone are required for the complete display of sexual behavior in female rats. Paced mating produces a reward state in intact cycling and ovariectomized (OVX), hormonally primed females as evaluated by the Conditioned Place Preference (CPP) paradigm. Most of the studies that have evaluated CPP induced by paced mating in OVX females have used relatively high doses of estradiol benzoate (EB). In the present study we determined if different doses of EB, combined with progesterone (P), could induce CPP after paced mating. For this purpose OVX female rats were divided in five groups that received one of different doses of estradiol benzoate (5, 2.5, 1.25 or 0.625 μg estradiol + 0.5 mg of progesterone) before being allowed to pace the sexual interaction and Conditioned in a CPP paradigm. We found that the lowest dose of EB used (0.625 μg) significantly reduced the lordosis quotient and the lordosis coefficient. Even though these females paced the sexual interaction, they didn't change its original Preference, suggesting that sexual interaction did not induce a positive affective, reward state. Females allowed to pace the sexual interaction with higher doses of EB developed CPP after paced mating. These results indicate that a threshold of estradiol is required for paced mating to induce CPP.
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infusions of naloxone into the medial preoptic area ventromedial nucleus of the hypothalamus and amygdala block Conditioned Place Preference induced by paced mating behavior
Hormones and Behavior, 2008Co-Authors: Patricia S Garciahorsman, Anders ǻgmo, Raul G ParedesAbstract:Paced mating induces positive affect as revealed by Conditioned Place Preference (CPP) in female rats. It has been suggested that endogenous opioids are involved in the generation of this positive affect since systemic administration of the opioid antagonist naloxone blocks mating-induced CPP. Several brain structures, including the medial preoptic area (mPOA), the ventromedial nucleus of the hypothalamus (VMH), the amygdala (Me), and the nucleus accumbens (Acb) have been implicated in the control of female sexual behavior. However, it is not known if these structures also participate in the positive affect produced by paced mating. To this end we determined the effects of intracranial administration of naloxone methiodide into the mPOA, VMH, Me and Acb on Conditioned Place Preference induced by paced mating in female rats. Regardless of the site of infusion 5 μg of naloxone did not affect any of the sexual behavior parameters measured during copulation. When CPP was evaluated, the groups infused with naloxone into the mPOA, the VMH, and the Me before each conditioning session did not develop Place Preference. Only the group infused with naloxone in the Acb and the control groups did so. These results demonstrate that opioid receptors within the mPOA, VMH and Me are necessary for the rewarding aspects of paced mating. We suggest that the Me and VMH are important for the transmission of sensory information produced by copulation while the mPOA is the site where the positive affect is originated.
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sexual behavior regulated paced by the female induces Conditioned Place Preference
Behavioral Neuroscience, 1997Co-Authors: Raul G Paredes, Araceli AlonsoAbstract:: The possibility that female-paced coital behavior induces a reward state of sufficient intensity and duration to induce conditioning was evaluated by the Conditioned-Place-Preference paradigm. Ovariectomized female rats, treated with estradiol benzoate and progesterone, regulated (paced) their coital interactions with a stud male through a 2-compartment chamber in which only the female could freely move from one compartment to the other. The females that paced their coital interactions showed a clear Place Preference. In contrast, no change in Preference was observed in the females that could not pace their coital contacts. The change in Preference in the females that paced their coital interactions was similar to that produced by an injection of morphine (1 mg/kg). These results suggest that coital interactions in females can induce a reward state when the females can control the pace of the sexual interaction.
Christopher L Cunningham - One of the best experts on this subject based on the ideXlab platform.
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Drug-induced Conditioned Place Preference and aversion in mice
Nature Protocols, 2006Co-Authors: Christopher L Cunningham, Christina M Gremel, Peter A GroblewskiAbstract:This protocol describes the equipment and methods used to establish Conditioned Place Preference (CPP) or aversion (CPA). Place conditioning is a form of Pavlovian conditioning routinely used to measure the rewarding or aversive motivational effects of objects or experiences (e.g., abused drugs). Here, we present a Place conditioning procedure that has been used extensively to study the motivational effects of ethanol and other abused drugs in mice. This protocol involves three phases: (i) habituation (or a pretest), (ii) conditioning of an association between the drug and a tactile or visual stimulus and (iii) a test that offers a choice between the drug-associated cue and a neutral cue. If the drug has motivational significance, mice will spend significantly more time (CPP) or less time (CPA) in proximity to the drug-associated cue. Potential problems in the design and interpretation of Place conditioning studies are discussed. A typical experiment lasts 2 weeks.
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ethanol induced Conditioned Place Preference is expressed through a ventral tegmental area dependent mechanism
Behavioral Neuroscience, 2005Co-Authors: Anita J Bechtholt, Christopher L CunninghamAbstract:The authors examined the role of the ventral tegmental area (VTA) and nucleus accumbens (NAc) in the expression of ethanol-induced Conditioned Place Preference (CPP). After cannulas were implanted, male DBA/2J mice underwent an unbiased Pavlovian-conditioning procedure for ethanol-induced CPP. Before Preference testing, the mice were injected intra-VTA (Experiments 1 and 3) or intra-NAc (Experiment 2) with the nonselective opioid antagonist methylnaloxonium (0-ng, 375-ng, or 750-ng total infusion; Experiments 1 and 2) or the gamma aminobutyric acid (GABA B ) agonist baclofen (0-ng, 25-ng, or 50-ng total infusion; Experiment 3). Intra-VTA methylnaloxonium or baclofen decreased ethanol-induced CPP, whereas intra-NAc methylnaloxonium had no effect. These findings indicate that the Conditioned rewarding effect of ethanol is expressed through a VTA-dependent mechanism that involves both opioid and GABA B receptors.
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localization of genes influencing ethanol induced Conditioned Place Preference and locomotor activity in bxd recombinant inbred mice
Psychopharmacology, 1995Co-Authors: Christopher L CunninghamAbstract:Genetic differences in ethanol's ability to induce Conditioned Place Preference were studied in 20 BXD Recombinant Inbred (RI) mouse strains and in the C57BL/6J and DBA/2J progenitor strains. Male mice from each strain were exposed to a Pavlovian conditioning procedure in which a distinctive floor stimulus (CS+) was paired four times with ethanol (2 g/kg). A different floor stimulus (CS-) was paired with saline. Control mice were injected only with saline. Floor Preference testing without ethanol revealed significant genetic differences in Conditioned Place Preference, with some strains spending nearly 80% time on the ethanolpaired floor while others spent only 50% (i.e., no Preference). Control mice showed genetic differences in unConditioned Preference for the floor cues, but unConditioned Preference was not genetically correlated with Conditioned Preference. There were also substantial genetic differences in ethanol-stimulated activity, but contrary to psychomotor stimulant theory, ethanol-induced activity on conditioning trials was not positively correlated with strength of Conditioned Place Preference. However, there was a significant negative genetic correlation (r=−0.42) between test session activity and Preference. Quantitative trait loci (QTL) analyses showed strong associations (P<0.01) between Conditioned Place Preference and marker loci on chromosomes 4, 8, 9, 18 and 19. Weaker associations (0.01
Marina R Picciotto - One of the best experts on this subject based on the ideXlab platform.
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variability in nicotine Conditioned Place Preference and stress induced reinstatement in mice effects of sex initial chamber Preference and guanfacine
Genes Brain and Behavior, 2020Co-Authors: Angela M Lee, Cali A Calarco, Sherry A Mckee, Yann S Mineur, Marina R PicciottoAbstract:Relapse to smoking occurs at higher rates in women compared with men, especially when triggered by stress. Studies suggest that sex-specific interactions between nicotine reward and stress contribute to these sex differences. Accordingly, novel treatment options targeting stress pathways, such as guanfacine, an α2-adrenergic receptor agonist, may provide sex-sensitive therapeutic effects. Preclinical studies are critical for elucidating neurobiological mechanisms of stress-induced relapse and potential therapies, but rodent models of nicotine addiction are often hindered by large behavioral variability. In this study, we used nicotine Conditioned Place Preference to investigate stress-induced reinstatement of nicotine Preference in male and female mice, and the effects of guanfacine on this behavior. Our results showed that overall, nicotine induced significant Place Preference acquisition and swim stress-induced reinstatement in both male and female mice, but with different nicotine dose-response patterns. In addition, we explored the variability in nicotine-dependent behaviors with median split analyses and found that initial chamber Preference in each sex differentially accounted for variability in stress-induced reinstatement. In groups that showed significant stress-induced reinstatement, pretreatment with guanfacine attenuated this behavior. Finally, we evaluated neuronal activation by Arc immunoreactivity in the infralimbic cortex, prelimbic cortex, anterior insula, basolateral amygdala, lateral central amygdala and nucleus accumbens core and shell. Guanfacine induced sex-dependent changes in Arc immunoreactivity in the infralimbic cortex and anterior insula. This study demonstrates sex-dependent relationships between initial chamber Preference and stress-induced reinstatement of nicotine Conditioned Place Preference, and the effects of guanfacine on both behavior and neurobiological mechanisms.
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nucleus accumbens creb activity is necessary for nicotine Conditioned Place Preference
Neuropsychopharmacology, 2009Co-Authors: Darlene H Brunzell, Yann S Mineur, Rachael L Neve, Marina R PicciottoAbstract:The ability of nicotine to alter firing of dopamine neurons is the first step leading to nicotine reward, but activation of intracellular signaling pathways downstream of nicotinic acetylcholine receptors is likely to be critical for longer-term consequences of nicotine exposure, including Conditioned reward. The transcription factor cyclic AMP-response element binding protein (CREB) is important for new gene transcription and in its phosphorylated form (pCREB) promotes long-term changes in synaptic strength. Previous studies have implicated nucleus accumbens (NAc) CREB activity in the modulation of cocaine and morphine reward, and have shown that nicotine Conditioned Place Preference (CPP) is associated with NAc CREB activation. It is not clear whether CPP elicits phosphorylation of CREB or if elevations in pCREB support nicotine CPP. In the current study, we investigated levels of CREB and pCREB during Pavlovian conditioning with nicotine in a novel context in the absence of chamber choice. Nicotine context conditioning resulted in elevated pCREB levels in the NAc shell but not the NAc core of mice following Placement in the nicotine-paired chamber in the absence of nicotine. To test if CREB activity in the NAc shell contributes to cue-induced responses that may precipitate nicotine-seeking, we used viral-mediated gene transfer of a dominant-negative CREB construct in the NAc shell of C57BL/6J mice and found that disruption of CREB activation before training blocked nicotine Place Preference across a range of doses. Taken together, these studies identify the NAc shell as a brain region where CREB activity is essential for nicotine CPP.
Barbara A. Sorg - One of the best experts on this subject based on the ideXlab platform.
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inactivation of the paraventricular thalamus abolishes the expression of cocaine Conditioned Place Preference in rats
Drug and Alcohol Dependence, 2014Co-Authors: Heiko T Jansen, Jenny R Browning, Barbara A. SorgAbstract:Abstract Background The paraventricular thalamus (PVT) is rapidly becoming recognized as part of the addiction circuitry. In addition to its strong anatomical connection to most of the brain regions underlying addiction, such as the nucleus accumbens, prefrontal cortex, amygdala, and hippocampus, the PVT has recently been shown to contribute to cocaine sensitization and reinstatement. In the present study, we examined the role of the PVT in the expression of cocaine Conditioned Place Preference (CPP). Methods We tested the impact of PVT inactivation by baclofen/muscimol (bac-mus) microinjection on the expression of cocaine-induced CPP in rats. Rats were implanted with guide cannulae into the PVT. Bac-mus (GABA B –GABA A agonists) or saline was injected into the PVT prior to CPP testing. Results Inactivation of the PVT by bac-mus prevented the expression of CPP, while Placements outside the PVT did not affect CPP. Intra-PVT injections of bac-mus did not affect locomotor activity during the session. Conclusions In the present study, we contribute to the growing body of research supporting a role for the PVT in addiction by demonstrating that the PVT is necessary for the expression of cocaine CPP.
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manipulation of dopamine d1 like receptor activation in the rat medial prefrontal cortex alters stress and cocaine induced reinstatement of Conditioned Place Preference behavior
Neuroscience, 2003Co-Authors: C J Sanchez, T M Bailie, Weiran Wu, Na Li, Barbara A. SorgAbstract:Abstract These studies examined the ability of the dopamine D1-like agonist SKF 81297 and D1-like antagonist SCH 23390 in the medial prefrontal cortex to alter the reinstatement of cocaine-induced Conditioned Place Preference behavior. Male Sprague–Dawley rats were fitted with bilateral cannulae over the medial prefrontal cortex and subsequently trained in a Conditioned Place Preference task. Animals were trained in this task using four pairings of cocaine (12 mg/kg, i.p.). Conditioned Place Preference was demonstrated in all animals, and this behavior was then extinguished over a 5–10-day period before testing for reinstatement. Just prior to reinstatement by immobilization stress or a cocaine priming injection (5 mg/kg, i.p.), a microinjection of the D1-like receptor antagonist SCH 23390 (0.01, 0.1 or 1.0 μg/side), or the D1-like receptor agonist SKF 81297 (0.1, 0.3 or 1.0 μg/side) was given into the medial prefrontal cortex. SCH 23390 blocked both stress- and cocaine-induced reinstatement of Conditioned Place Preference after the two higher doses were administered into the medial prefrontal cortex. The highest dose of SKF 81297 (1.0 μg/side) prevented immobilization stress- but not cocaine-induced reinstatement. The highest dose of these drugs given in the absence of stress or cocaine did not produce reinstatement. The results indicate that immobilization stress given within the Place-Preference chamber is capable of producing reinstatement of cocaine-seeking behavior. The microinjection studies suggest that D1-like receptor antagonism within the prefrontal cortex is sufficient to block reinstatement by stress and cocaine. Furthermore, the results from D1-like receptor activation in the medial prefrontal cortex point to utilization of different neural pathways for stress- and cocaine-induced reinstatement.