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Christopher L. Cunningham - One of the best experts on this subject based on the ideXlab platform.
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ethanol induced Conditioned Taste Aversion in 15 inbred mouse strains
Behavioral Neuroscience, 2002Co-Authors: Julie Broadbent, Kathryn J Muccino, Christopher L. CunninghamAbstract:This study used a genetic correlational strategy to characterize the neurobiological basis of ethanol's (0, 2, or 4 g/kg) aversive effects as indexed by Conditioned Taste Aversion. Substantial strain differences in Taste Aversion and hypothermia were observed, but the genetic correlation between these phenotypes was not significant. However, significant genetic correlations were observed between Taste Aversion and ethanol-related behaviors measured in previous studies, including home-cage ethanol preference (r = .68) and ethanol withdrawal severity (r = -.69). Strains showing stronger Taste Aversion tended to show lower ethanol preference and higher withdrawal severity. This pattern of findings is consistent with previous studies suggesting a commonality in neurobiological mechanisms underlying these phenotypes. These results do not support the hypothesis that ethanol-induced Taste Aversion is mediated by the drug's rewarding properties.
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ethanol induced Conditioned Taste Aversion in bxd recombinant inbred mice
Alcoholism: Clinical and Experimental Research, 1998Co-Authors: Fred O. Risinger, Christopher L. CunninghamAbstract:Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced Conditioned Taste Aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during Taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced Conditioned Taste Aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between Taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, Conditioned place preference). However, there were significant genetic correlations between Taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that Taste Aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter Taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced Conditioned Taste Aversion. Some of these genes appear to influence Taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.
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Genetic differences in naloxone enhancement of ethanol-induced Conditioned Taste Aversion.
Psychopharmacology, 1996Co-Authors: Julie Broadbent, Hanna V. Linder, Christopher L. CunninghamAbstract:The influence of the opioid system on acquisition of an ethanol-induced Conditioned Taste Aversion was examined in alcohol-preferring and avoiding inbred strains of mice (C57BL/6J and DBA/2J). Fluid-deprived mice from each strain received either ethanol alone, naloxone alone, or both ethanol and naloxone immediately after access to a novel tasting fluid. Naloxone alone (1 or 3 mg/kg) did not induce a Conditioned Taste Aversion in either strain of mice. Administration of ethanol (1.5 g/kg) to DBA/2J mice produced a moderate Taste Aversion that was not affected by co-administration of naloxone. Although ethanol administered alone (3 g/kg) did not cause a Taste Aversion in C57BL/6J mice, the combination of ethanol and the higher dose of naloxone produced a significant Taste Aversion that increased across trials. A second experiment addressed the possibility that naloxone failed to enhance the ethanol-induced condition Taste Aversion in DBA/2J mice due to a “floor” effect on consumption. A lower ethanol dose (1 g/kg) was given alone or in combination with naloxone (1 or 3 mg/kg). Again, ethanol produced a moderate Conditioned Taste Aversion that was not potentiated by naloxone. Subsequent conditioning with a high ethanol dose produced further suppression of intake, confirming that naloxone's failure to enhance Aversion on earlier trials was not due to a “floor” effect. These data demonstrate a strain specific interaction between the aversive effect of ethanol and naloxone. More specifically, the results indicate that blockade of opioid receptors enhances the aversive effect of ethanol in C57BL/6J but not DBA/2J mice, suggesting that genetically determined differences in the endogenous opioid system of alcohol-preferring mice may mitigate ethanol's aversive effect.
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Genetic differences in ethanol-induced hyperglycemia and Conditioned Taste Aversion.
Life sciences, 1992Co-Authors: Fred O. Risinger, Christopher L. CunninghamAbstract:Genetic differences in the hyperglycemic response to acute ethanol exposure and ethanol-induced Conditioned Taste Aversion were examined using inbred mice. Adult male C57BL/6J and DBA/2J mice were injected with ethanol (0-6 g/kg, I.P.) and blood glucose levels determined over 4 h. C57 mice demonstrated greater dose-dependent elevations in blood glucose compared to DBA mice. In a Conditioned Taste Aversion procedure, water deprived mice received ethanol injections (1-4 g/kg, I.P.) immediately after access to a NaCl flavored solution. DBA mice developed Aversion to the ethanol-paired flavor at a lower dose (2 g/kg) than C57 mice. These results provide further support for a possible inverse genetic relationship between sensitivity to ethanol-induced hyperglycemia and sensitivity to Conditioned Taste Aversion.
Steve Reilly - One of the best experts on this subject based on the ideXlab platform.
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Conditioned Taste Aversion, drugs of abuse and palatability.
Neuroscience and biobehavioral reviews, 2014Co-Authors: Jian-you Lin, Joe Arthurs, Steve ReillyAbstract:We consider Conditioned Taste Aversion to involve a learned reduction in the palatability of a Taste (and hence in amount consumed) based on the association that develops when a Taste experience is followed by gastrointestinal malaise. The present article evaluates the well-established finding that drugs of abuse, at doses that are otherwise considered rewarding and self-administered, cause intake suppression. Our recent work using lick pattern analysis shows that drugs of abuse also cause a palatability downshift and, therefore, support Conditioned Taste Aversion learning.
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Conditioned Taste Aversion : behavioral and neural processes
2009Co-Authors: Steve Reilly, Todd R. SchachtmanAbstract:Forward Michael Domjan Section 1: Introduction and Historical Significance 1. Introduction Steve Reilly and Todd R. Schachtman 2. The Origins of Conditioned Taste Aversion Learning: An Historical Analysis Kevin B. Freeman and Anthony L. Riley Section II: Behavioral Processes 3. Conditioned Taste Aversion and Latent Inhibition: A Review Robert E. Lubow 4. Preexposure to the US in Nausea-Based Aversion Learning Geoffrey Hall 5. Drug-induced Suppression of CS intake: Reward, Aversion, and Addiction Patricia Sue Grigson, Robert C. Twining, Christopher S. Freet, Robert A. Wheeler, and Rastafa I. Geddes 6. Conditioned Disgust, but Not Conditioned Taste Avoidance, May Reflect Conditioned Nausea in Rats Linda A. Parker, Cheryl L. Limebeer, and Shadna A. Rana 7. Memory Phenomena and CTA Susanne M. Meehan and David C. Riccio 8. Postconditioning Event Manipulations on Processing of the Target CS in CTA Todd R. Schachtman, Ashley Ramsey, and Oskar Pineno 9. Conditioned Taste Aversion Based on Running or Swimming Robert A. Boakes and Sadahiko Nakajima 10. Mechanisms of Overshadowing and Potentiation in Flavor-Aversion Conditioning W. Robert Batsell, Jr. and Gayla Y. Paschall 11. Representation-Mediated Food Aversions Peter C. Holland and Daniel S. Wheeler 12. Strain Differences in Taste Aversion Learning: Implications for Animal Models of Drug Abuse Anthony L. Riley, Catherine M. Davis, and Peter G. Roma 13. Taste, Disgust and Value: Taste Aversion Learning and Outcome Encoding in Instrumental Conditioning Bernard W. Balleine 14. Conditioned Taste Aversion Across the Lifespan from Prenascence to Senescence James R. Misanin, Matthew J. Anderson, and Charles F. Hinderliter Section III: Neural Analysis and Physiological Mechanisms 15. Central Gustatory System Lesions and Conditioned Taste Aversion Steve Reilly 16. Mapping Conditioned Taste Aversion Associations through Patterns of cFos Expression Ilene L. Bernstein, Emily E. Wilkins, and Sabiha K. Barot 17. Molecular Mechanisms of Taste Learning in the Insular Cortex and Amygdala Liza Barki-Harrington, Katya Belelovsky, Guy Doron, and Kobi Rosenblum 18. Hormonal Modulation of Conditioned Taste Avoidance: The Role of Estradiol Kathleen C. Chambers and Houri Hintiryan 19. Genetic Influences on Conditioned Taste Aversion Christopher L. Cunningham, Christina M. Gremel, and Peter A. Groblewski 20. Conditioned Taste Aversion Induced by Exposure to High Strength Static Magnetic Fields Thomas A. Houpt and James C. Smith Section IV: Clinical Application of Research and Target Populations 21. Chemical Aversion Treatment of Alcoholism Sam Revusky 22. Taste-Immune Associative Learning Gustavo Pacheco-Lopez, Harald Engler, Maj-Britt Niemi, and Manfred Schedlowski 23. Taste Aversions in Pregnancy Tracy M. Bayley , Louise Dye, and Andrew J. Hill 24. Role of Conditioned Taste Aversion on the Side Effects of Chemotherapy in Cancer Patients Giuseppe Scalera and Mario Bavieri
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effects of central and basolateral amygdala lesions on Conditioned Taste Aversion and latent inhibition
Behavioral Neuroscience, 2007Co-Authors: Justin St Andre, Steve ReillyAbstract:The present study examined the effects of neurotoxic lesions of the central nucleus (CNA) and basolateral complex (BLA) of the amygdala on Conditioned Taste Aversion (CTA) in a latent inhibition design. In Experiment 1, lesions of the CNA were found to have no affect on CTA acquisition regardless of whether the Taste Conditioned stimulus (CS) was novel or familiar. Lesions of the BLA, although having no influence on performance when the CS was familiar, retarded CTA acquisition when the CS was novel in Experiment 2. The pattern of results suggests that the CTA deficit in rats with BLA lesions may be a secondary consequence of a disruption of perceived stimulus novelty.
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Conditioned Taste Aversion and amygdala lesions in the rat: a critical review.
Neuroscience and biobehavioral reviews, 2005Co-Authors: Steve Reilly, Marina A. BornovalovaAbstract:Studies using permanent lesions implicate the amygdala, a recipient of gustatory and viscerosensory information, in Taste Aversion learning. Reviewing this literature with respect to the location of the lesions and the quality of the behavioral methodology reveals little, if any, involvement of the medial amygdala or central nucleus in Conditioned Taste Aversion. Although a disruption is found following damage to the basolateral region, the attenuated Conditioned Taste Aversion appears to be a consequence of a lesion-induced impairment of neophobia rather than an association formation deficit. The key to understanding the functional significance of the basolateral amygdala in Conditioned Taste Aversion reduces, we believe, to determining the role of this structure in gustatory neophobia.
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Medial versus lateral parabrachial nucleus lesions in the rat: Effects on mercaptoacetate-induced feeding and Conditioned Taste Aversion
Brain research bulletin, 2002Co-Authors: Radmila Trifunovic, Steve ReillyAbstract:Abstract The two experiments of the present study examined the influence of bilateral electrophysiologically-guided ibotenic acid lesions of the medial (gustatory) and lateral (viscerosensory) subdivisions of the parabrachial nucleus (PBN) on lipoprivic feeding and on the acquisition of a Conditioned Taste Aversion. In Experiment 1, mercaptoacetate (0, 400, 600, or 800 μ mol/kg) failed to enhance food intake in normal rats maintained and tested on standard laboratory chow. In the same procedure, rats with lesions of the medial or lateral PBN consumed less food during baseline but nonetheless were sensitive to the orexigenic action of mercaptoacetate. In Experiment 2, both types of PBN lesions prevented acquisition of a Conditioned Taste Aversion induced by the oral self administration of lithium chloride. The results suggest that PBN neurons essential for Conditioned Taste Aversion are not involved in the mercaptoacetate-induced feeding of rats maintained and tested on standard laboratory chow.
Fred O. Risinger - One of the best experts on this subject based on the ideXlab platform.
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ethanol induced Conditioned Taste Aversion in bxd recombinant inbred mice
Alcoholism: Clinical and Experimental Research, 1998Co-Authors: Fred O. Risinger, Christopher L. CunninghamAbstract:Genetic differences in sensitivity to ethanol's aversive effects may play an important role in the development of alcohol-seeking behavior and alcoholism. The present study examined the development of ethanol-induced Conditioned Taste Aversion in 20 BXD/Ty recombinant inbred strains of mice and their progenitor inbred strains, C57BL/6J (B6) and DBA/2J (D2). Adult male mice were given 1-hr access to a saccharin-flavored solution every 48 hr for 12 days. After all but the first and last saccharin access periods, they received ethanol injections (0, 2, or 4 g/kg, i.p.). Separate groups of unpaired control mice received 4 g/kg of ethanol 1 hr after water access. Saline control mice were also used for examining preference across a wide range of saccharin concentrations (0.019 to 4.864% w/v). As expected, saccharin consumption during Taste conditioning declined over conditioning trials in a dose-dependent manner, indicating development of ethanol-induced Conditioned Taste Aversion. Correlational analyses using strain means from recently published papers indicated no significant genetic correlation between Taste conditioning and two phenotypes thought to reflect ethanol reinforcement or reward (ethanol drinking, Conditioned place preference). However, there were significant genetic correlations between Taste conditioning at the high dose and sensitivity to ethanol-induced hypothermia, rotarod ataxia, and acute withdrawal. Quantitative trait locus (QTL) analyses of strain means indicated that Taste Aversion was associated (p < 0.01) with genetic markers on nine chromosomes (1, 2, 3, 4, 6, 7, 9, 11, and 17). These QTLs were located near several candidate genes, including genes encoding several different acetylcholine receptor subunits, the delta opioid receptor, and two serotonin receptors (1B and 1D). QTLs for saccharin preference were located on several of the same chromosomes (2, 3, 4, 6, and 11). Two of these saccharin QTLs overlap candidate genes influencing sensitivity to sweet or bitter Taste stimuli. In general, these findings support the conclusion that multiple genes influence ethanol-induced Conditioned Taste Aversion. Some of these genes appear to influence Taste sensitivity, whereas others appear to mediate sensitivity to aversive pharmacological effects of ethanol.
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Genetic differences in nicotine-induced Conditioned Taste Aversion
Life sciences, 1996Co-Authors: Fred O. Risinger, Miriam M. BrownAbstract:Abstract Genetic differences in nicotine-induced Conditioned Taste Aversion were examined using inbred mice. Adult male C57BL/6J, DBA/2J, BALB/cJ and C3H/heJ mice were adapted to a 2-h per day water access regimen. Subsequently, mice received nicotine injections (0.5, 1.0 or 2.0 mg/kg) immediately after 1-h access to a NaCl flavored solution. DBA and C3H mice developed dosedependent Aversions to the nicotine-paired flavor. BALB mice showed only minor reductions in intake with no difference between the nicotine dose groups. C57BL mice did not show development of nicotine-induced Conditioned Taste Aversion. These results demonstrate that nicotine's aversive motivational effect is strongly influenced by genotype. Further, genetic sensitivity (DBA mice) or insensitivity (C57BL mice) to nicotine-induced Conditioned Taste Aversion was similar to reports of genetic sensitivity to ethanol's aversive effect measured in this design.
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Genetic differences in ethanol-induced hyperglycemia and Conditioned Taste Aversion.
Life sciences, 1992Co-Authors: Fred O. Risinger, Christopher L. CunninghamAbstract:Genetic differences in the hyperglycemic response to acute ethanol exposure and ethanol-induced Conditioned Taste Aversion were examined using inbred mice. Adult male C57BL/6J and DBA/2J mice were injected with ethanol (0-6 g/kg, I.P.) and blood glucose levels determined over 4 h. C57 mice demonstrated greater dose-dependent elevations in blood glucose compared to DBA mice. In a Conditioned Taste Aversion procedure, water deprived mice received ethanol injections (1-4 g/kg, I.P.) immediately after access to a NaCl flavored solution. DBA mice developed Aversion to the ethanol-paired flavor at a lower dose (2 g/kg) than C57 mice. These results provide further support for a possible inverse genetic relationship between sensitivity to ethanol-induced hyperglycemia and sensitivity to Conditioned Taste Aversion.
Tayfun Uzbay - One of the best experts on this subject based on the ideXlab platform.
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Stimulus properties of venlafaxine in a Conditioned Taste Aversion procedure.
European Journal of Pharmacology, 2008Co-Authors: Hakan Kayir, Tevfik Alici, Gokhan Goktalay, Murat Yildirim, Gokhan Ulusoy, Mert Ceyhan, Turgay Celik, Tayfun UzbayAbstract:Abstract Conditioned stimulus properties of venlafaxine are still unknown. In the present study, the discriminative stimulus properties of venlafaxine by using a Conditioned Taste Aversion procedure were investigated. Swiss Webster mice were allowed to reach water from 2 pipettes for 20 min (09:00–11:30 h), plus 30 min (15:30–16:00 h), daily. During the 4 days, the test drugs [fluoxetine, escitalopram, tianeptine, reboxetine, and N ω-nitro- l -arginine methyl ester ( l -NAME)] were injected to mice at least 1 h after they had first water session. On day 5, they consumed glucose solution (5% w/v) and immediately injected with conditioning drug (venlafaxine 32 mg/kg). On day 8, mice were allowed to make a choice between water and glucose solution. The amount of glucose consumption as a percentage of total fluid intakes was calculated for each animal. Significant reduction in glucose choice was defined as Conditioned Taste Aversion. Venlafaxine (32 mg/kg) induced a robust Conditioned Taste Aversion in mice. Pre-exposure to tianeptine (2.5–10 mg/kg), fluoxetine (10 mg/kg), escitalopram (32 mg/kg), and reboxetine (5 mg/kg) substituted for venlafaxine by preventing the Conditioned Taste Aversion induced by venlafaxine. l -NAME did not substitute for venlafaxine. Substitution of venlafaxine by fluoxetine, tianeptine, escitalopram, and reboxetine provides further evidence that both 5-HT and noradrenaline reuptake inhibition may play an important role in the stimulus effect of venlafaxine.
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Stimulus properties of venlafaxine in a Conditioned Taste Aversion procedure.
European journal of pharmacology, 2008Co-Authors: Hakan Kayir, Tevfik Alici, Gokhan Goktalay, Murat Yildirim, Mert Ceyhan, Turgay Celik, Gökhan K Ulusoy, Tayfun UzbayAbstract:Conditioned stimulus properties of venlafaxine are still unknown. In the present study, the discriminative stimulus properties of venlafaxine by using a Conditioned Taste Aversion procedure were investigated. Swiss Webster mice were allowed to reach water from 2 pipettes for 20 min (09:00-11:30 h), plus 30 min (15:30-16:00 h), daily. During the 4 days, the test drugs [fluoxetine, escitalopram, tianeptine, reboxetine, and Nomega-nitro-L-arginine methyl ester (L-NAME)] were injected to mice at least 1 h after they had first water session. On day 5, they consumed glucose solution (5% w/v) and immediately injected with conditioning drug (venlafaxine 32 mg/kg). On day 8, mice were allowed to make a choice between water and glucose solution. The amount of glucose consumption as a percentage of total fluid intakes was calculated for each animal. Significant reduction in glucose choice was defined as Conditioned Taste Aversion. Venlafaxine (32 mg/kg) induced a robust Conditioned Taste Aversion in mice. Pre-exposure to tianeptine (2.5-10 mg/kg), fluoxetine (10 mg/kg), escitalopram (32 mg/kg), and reboxetine (5 mg/kg) substituted for venlafaxine by preventing the Conditioned Taste Aversion induced by venlafaxine. L-NAME did not substitute for venlafaxine. Substitution of venlafaxine by fluoxetine, tianeptine, escitalopram, and reboxetine provides further evidence that both 5-HT and noradrenaline reuptake inhibition may play an important role in the stimulus effect of venlafaxine.
Miriam M. Brown - One of the best experts on this subject based on the ideXlab platform.
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Genetic differences in nicotine-induced Conditioned Taste Aversion
Life sciences, 1996Co-Authors: Fred O. Risinger, Miriam M. BrownAbstract:Abstract Genetic differences in nicotine-induced Conditioned Taste Aversion were examined using inbred mice. Adult male C57BL/6J, DBA/2J, BALB/cJ and C3H/heJ mice were adapted to a 2-h per day water access regimen. Subsequently, mice received nicotine injections (0.5, 1.0 or 2.0 mg/kg) immediately after 1-h access to a NaCl flavored solution. DBA and C3H mice developed dosedependent Aversions to the nicotine-paired flavor. BALB mice showed only minor reductions in intake with no difference between the nicotine dose groups. C57BL mice did not show development of nicotine-induced Conditioned Taste Aversion. These results demonstrate that nicotine's aversive motivational effect is strongly influenced by genotype. Further, genetic sensitivity (DBA mice) or insensitivity (C57BL mice) to nicotine-induced Conditioned Taste Aversion was similar to reports of genetic sensitivity to ethanol's aversive effect measured in this design.