The Experts below are selected from a list of 273 Experts worldwide ranked by ideXlab platform

Alan F Sved - One of the best experts on this subject based on the ideXlab platform.

  • Differentiating the Primary reinforcing and reinforcement-enhancing effects of varenicline
    Psychopharmacology, 2015
    Co-Authors: Rachel L. Schassburger, Melissa E Levin, Anthony R Caggiula, Matthew I. Palmatier, Eric C. Donny, Matthew T. Weaver, Alan F Sved
    Abstract:

    Rationale Varenicline (VAR), a smoking cessation aid that is a partial agonist at nicotinic receptors, mimics the reinforcement-enhancing effects of nicotine. Varenicline, when accompanied by non-drug cues, is self-administered by rats, though it is unclear whether this results from varenicline acting as a Primary Reinforcer or a reinforcement enhancer of the cues. Objectives This study sought to disentangle these two potential actions. Methods Rats were allowed to self-administer intravenous nicotine, saline, or varenicline during 1-h sessions in operant chambers equipped with two levers. Five groups had concurrent access to drug infusions and a moderately reinforcing visual stimulus (VS) for responding on separate levers. Meeting the reinforcement schedule on one lever was reinforced with VAR (0.01, 0.06, 0.1 mg/kg/infusion), nicotine (0.06 mg/kg/infusion), or saline, while meeting the same schedule on the other lever delivered the VS. Additional groups were reinforced for pressing a single “active” lever and received VAR paired with the VS, the VS with response-independent infusions of VAR, or VAR alone (0.1 mg/kg/infusion). Results Rats readily responded for VAR paired with VS on a single lever. However, when VAR was the only Reinforcer contingent on a response, rats did not respond more than for saline. Conclusions These findings show that VAR does not serve as a Primary Reinforcer in rats at doses that increase responding for non-drug Reinforcers. These data are consistent with research showing that the Primary reinforcing effects of VAR are weak, at best, and that the Primary reinforcing and reinforcement-enhancing actions of nicotinic drugs are pharmacologically distinct.

  • Behavioral mechanisms underlying nicotine reinforcement.
    Current topics in behavioral neurosciences, 2015
    Co-Authors: Laura E. Rupprecht, Alan F Sved, Rachel L. Schassburger, Tracy T. Smith, Deanne M. Buffalari, Eric C. Donny
    Abstract:

    Cigarette smoking is the leading cause of preventable deaths worldwide, and nicotine, the Primary psychoactive constituent in tobacco, drives sustained use. The behavioral actions of nicotine are complex and extend well beyond the actions of the drug as a Primary Reinforcer. Stimuli that are consistently paired with nicotine can, through associative learning, take on reinforcing properties as conditioned stimuli. These conditioned stimuli can then impact the rate and probability of behavior and even function as conditioning Reinforcers that maintain behavior in the absence of nicotine. Nicotine can also act as a conditioned stimulus (CS), predicting the delivery of other Reinforcers, which may allow nicotine to acquire value as a conditioned Reinforcer. These associative effects, establishing non-nicotine stimuli as conditioned stimuli with discriminative stimulus and conditioned reinforcing properties as well as establishing nicotine as a CS, are predicted by basic conditioning principles. However, nicotine can also act non-associatively. Nicotine directly enhances the reinforcing efficacy of other reinforcing stimuli in the environment, an effect that does not require a temporal or predictive relationship between nicotine and either the stimulus or the behavior. Hence, the reinforcing actions of nicotine stem both from the Primary reinforcing actions of the drug (and the subsequent associative learning effects) as well as the reinforcement enhancement action of nicotine which is non-associative in nature. Gaining a better understanding of how nicotine impacts behavior will allow for maximally effective tobacco control efforts aimed at reducing the harm associated with tobacco use by reducing and/or treating its addictiveness.

  • Differentiating the Primary reinforcing and reinforcement-enhancing effects of varenicline.
    Psychopharmacology, 2014
    Co-Authors: Rachel L. Schassburger, Melissa E Levin, Anthony R Caggiula, Matthew I. Palmatier, Eric C. Donny, Matthew T. Weaver, Alan F Sved
    Abstract:

    Rationale Varenicline (VAR), a smoking cessation aid that is a partial agonist at nicotinic receptors, mimics the reinforcement-enhancing effects of nicotine. Varenicline, when accompanied by non-drug cues, is self-administered by rats, though it is unclear whether this results from varenicline acting as a Primary Reinforcer or a reinforcement enhancer of the cues.

  • Bupropion and nicotine enhance responding for nondrug Reinforcers via dissociable pharmacological mechanisms in rats
    Psychopharmacology, 2009
    Co-Authors: Matthew I. Palmatier, Melissa E Levin, Kara L Mays, Anthony R Caggiula, Eric C. Donny, Alan F Sved
    Abstract:

    Rationale Nicotine serves as a Primary Reinforcer but also potently enhances responding for nonnicotine stimuli with reinforcing properties. One of the most successful pharmacotherapies for smoking cessation, bupropion, also increases responding for nondrug Reinforcers such as food and brain stimulation rewards. Objective The present studies investigated whether treatment with bupropion and nicotine had similar effects on responding for a reinforcing visual stimulus (VS). They also investigated whether the effects of bupropion and nicotine depended on common pharmacological substrates. Results Nicotine (0.4 mg/kg base) enhanced responding for the VS, and this enhancing effect increased across testing sessions, replicating our previous findings. Bupropion (3, 10, and 30 mg/kg salt) dose-dependently increased responding for the VS. Treatment with 10 and 30 mg/kg bupropion resulted in a profile similar to nicotine; operant responding increased over repeated drug treatments. The reinforcement enhancing effect of nicotine, but not bupropion, was blocked by pretreatment with the nicotinic acetylcholine receptor antagonist mecamylamine. In contrast, the reinforcement enhancing effect of bupropion, but not nicotine, was blocked by pretreatment with the alpha noradrenergic antagonist prazosin. Conclusion The reinforcement enhancing effects of nicotine and bupropion increased over time and repeated treatments suggesting a shared mechanism of action. However, the reinforcement enhancing effects of nicotine are mediated by nicotinic acetylcholine receptors, whereas the reinforcement enhancing effects of bupropion were mediated by alpha noradrenergic receptors.

  • bupropion and nicotine enhance responding for nondrug Reinforcers via dissociable pharmacological mechanisms in rats
    Psychopharmacology, 2009
    Co-Authors: Matthew I. Palmatier, Melissa E Levin, Kara L Mays, Anthony R Caggiula, Eric C. Donny, Alan F Sved
    Abstract:

    Rationale Nicotine serves as a Primary Reinforcer but also potently enhances responding for nonnicotine stimuli with reinforcing properties. One of the most successful pharmacotherapies for smoking cessation, bupropion, also increases responding for nondrug Reinforcers such as food and brain stimulation rewards.

Eric C. Donny - One of the best experts on this subject based on the ideXlab platform.

  • Differentiating the Primary reinforcing and reinforcement-enhancing effects of varenicline
    Psychopharmacology, 2015
    Co-Authors: Rachel L. Schassburger, Melissa E Levin, Anthony R Caggiula, Matthew I. Palmatier, Eric C. Donny, Matthew T. Weaver, Alan F Sved
    Abstract:

    Rationale Varenicline (VAR), a smoking cessation aid that is a partial agonist at nicotinic receptors, mimics the reinforcement-enhancing effects of nicotine. Varenicline, when accompanied by non-drug cues, is self-administered by rats, though it is unclear whether this results from varenicline acting as a Primary Reinforcer or a reinforcement enhancer of the cues. Objectives This study sought to disentangle these two potential actions. Methods Rats were allowed to self-administer intravenous nicotine, saline, or varenicline during 1-h sessions in operant chambers equipped with two levers. Five groups had concurrent access to drug infusions and a moderately reinforcing visual stimulus (VS) for responding on separate levers. Meeting the reinforcement schedule on one lever was reinforced with VAR (0.01, 0.06, 0.1 mg/kg/infusion), nicotine (0.06 mg/kg/infusion), or saline, while meeting the same schedule on the other lever delivered the VS. Additional groups were reinforced for pressing a single “active” lever and received VAR paired with the VS, the VS with response-independent infusions of VAR, or VAR alone (0.1 mg/kg/infusion). Results Rats readily responded for VAR paired with VS on a single lever. However, when VAR was the only Reinforcer contingent on a response, rats did not respond more than for saline. Conclusions These findings show that VAR does not serve as a Primary Reinforcer in rats at doses that increase responding for non-drug Reinforcers. These data are consistent with research showing that the Primary reinforcing effects of VAR are weak, at best, and that the Primary reinforcing and reinforcement-enhancing actions of nicotinic drugs are pharmacologically distinct.

  • Behavioral mechanisms underlying nicotine reinforcement.
    Current topics in behavioral neurosciences, 2015
    Co-Authors: Laura E. Rupprecht, Alan F Sved, Rachel L. Schassburger, Tracy T. Smith, Deanne M. Buffalari, Eric C. Donny
    Abstract:

    Cigarette smoking is the leading cause of preventable deaths worldwide, and nicotine, the Primary psychoactive constituent in tobacco, drives sustained use. The behavioral actions of nicotine are complex and extend well beyond the actions of the drug as a Primary Reinforcer. Stimuli that are consistently paired with nicotine can, through associative learning, take on reinforcing properties as conditioned stimuli. These conditioned stimuli can then impact the rate and probability of behavior and even function as conditioning Reinforcers that maintain behavior in the absence of nicotine. Nicotine can also act as a conditioned stimulus (CS), predicting the delivery of other Reinforcers, which may allow nicotine to acquire value as a conditioned Reinforcer. These associative effects, establishing non-nicotine stimuli as conditioned stimuli with discriminative stimulus and conditioned reinforcing properties as well as establishing nicotine as a CS, are predicted by basic conditioning principles. However, nicotine can also act non-associatively. Nicotine directly enhances the reinforcing efficacy of other reinforcing stimuli in the environment, an effect that does not require a temporal or predictive relationship between nicotine and either the stimulus or the behavior. Hence, the reinforcing actions of nicotine stem both from the Primary reinforcing actions of the drug (and the subsequent associative learning effects) as well as the reinforcement enhancement action of nicotine which is non-associative in nature. Gaining a better understanding of how nicotine impacts behavior will allow for maximally effective tobacco control efforts aimed at reducing the harm associated with tobacco use by reducing and/or treating its addictiveness.

  • Differentiating the Primary reinforcing and reinforcement-enhancing effects of varenicline.
    Psychopharmacology, 2014
    Co-Authors: Rachel L. Schassburger, Melissa E Levin, Anthony R Caggiula, Matthew I. Palmatier, Eric C. Donny, Matthew T. Weaver, Alan F Sved
    Abstract:

    Rationale Varenicline (VAR), a smoking cessation aid that is a partial agonist at nicotinic receptors, mimics the reinforcement-enhancing effects of nicotine. Varenicline, when accompanied by non-drug cues, is self-administered by rats, though it is unclear whether this results from varenicline acting as a Primary Reinforcer or a reinforcement enhancer of the cues.

  • Bupropion and nicotine enhance responding for nondrug Reinforcers via dissociable pharmacological mechanisms in rats
    Psychopharmacology, 2009
    Co-Authors: Matthew I. Palmatier, Melissa E Levin, Kara L Mays, Anthony R Caggiula, Eric C. Donny, Alan F Sved
    Abstract:

    Rationale Nicotine serves as a Primary Reinforcer but also potently enhances responding for nonnicotine stimuli with reinforcing properties. One of the most successful pharmacotherapies for smoking cessation, bupropion, also increases responding for nondrug Reinforcers such as food and brain stimulation rewards. Objective The present studies investigated whether treatment with bupropion and nicotine had similar effects on responding for a reinforcing visual stimulus (VS). They also investigated whether the effects of bupropion and nicotine depended on common pharmacological substrates. Results Nicotine (0.4 mg/kg base) enhanced responding for the VS, and this enhancing effect increased across testing sessions, replicating our previous findings. Bupropion (3, 10, and 30 mg/kg salt) dose-dependently increased responding for the VS. Treatment with 10 and 30 mg/kg bupropion resulted in a profile similar to nicotine; operant responding increased over repeated drug treatments. The reinforcement enhancing effect of nicotine, but not bupropion, was blocked by pretreatment with the nicotinic acetylcholine receptor antagonist mecamylamine. In contrast, the reinforcement enhancing effect of bupropion, but not nicotine, was blocked by pretreatment with the alpha noradrenergic antagonist prazosin. Conclusion The reinforcement enhancing effects of nicotine and bupropion increased over time and repeated treatments suggesting a shared mechanism of action. However, the reinforcement enhancing effects of nicotine are mediated by nicotinic acetylcholine receptors, whereas the reinforcement enhancing effects of bupropion were mediated by alpha noradrenergic receptors.

  • bupropion and nicotine enhance responding for nondrug Reinforcers via dissociable pharmacological mechanisms in rats
    Psychopharmacology, 2009
    Co-Authors: Matthew I. Palmatier, Melissa E Levin, Kara L Mays, Anthony R Caggiula, Eric C. Donny, Alan F Sved
    Abstract:

    Rationale Nicotine serves as a Primary Reinforcer but also potently enhances responding for nonnicotine stimuli with reinforcing properties. One of the most successful pharmacotherapies for smoking cessation, bupropion, also increases responding for nondrug Reinforcers such as food and brain stimulation rewards.

Matthew I. Palmatier - One of the best experts on this subject based on the ideXlab platform.

  • Differentiating the Primary reinforcing and reinforcement-enhancing effects of varenicline
    Psychopharmacology, 2015
    Co-Authors: Rachel L. Schassburger, Melissa E Levin, Anthony R Caggiula, Matthew I. Palmatier, Eric C. Donny, Matthew T. Weaver, Alan F Sved
    Abstract:

    Rationale Varenicline (VAR), a smoking cessation aid that is a partial agonist at nicotinic receptors, mimics the reinforcement-enhancing effects of nicotine. Varenicline, when accompanied by non-drug cues, is self-administered by rats, though it is unclear whether this results from varenicline acting as a Primary Reinforcer or a reinforcement enhancer of the cues. Objectives This study sought to disentangle these two potential actions. Methods Rats were allowed to self-administer intravenous nicotine, saline, or varenicline during 1-h sessions in operant chambers equipped with two levers. Five groups had concurrent access to drug infusions and a moderately reinforcing visual stimulus (VS) for responding on separate levers. Meeting the reinforcement schedule on one lever was reinforced with VAR (0.01, 0.06, 0.1 mg/kg/infusion), nicotine (0.06 mg/kg/infusion), or saline, while meeting the same schedule on the other lever delivered the VS. Additional groups were reinforced for pressing a single “active” lever and received VAR paired with the VS, the VS with response-independent infusions of VAR, or VAR alone (0.1 mg/kg/infusion). Results Rats readily responded for VAR paired with VS on a single lever. However, when VAR was the only Reinforcer contingent on a response, rats did not respond more than for saline. Conclusions These findings show that VAR does not serve as a Primary Reinforcer in rats at doses that increase responding for non-drug Reinforcers. These data are consistent with research showing that the Primary reinforcing effects of VAR are weak, at best, and that the Primary reinforcing and reinforcement-enhancing actions of nicotinic drugs are pharmacologically distinct.

  • Differentiating the Primary reinforcing and reinforcement-enhancing effects of varenicline.
    Psychopharmacology, 2014
    Co-Authors: Rachel L. Schassburger, Melissa E Levin, Anthony R Caggiula, Matthew I. Palmatier, Eric C. Donny, Matthew T. Weaver, Alan F Sved
    Abstract:

    Rationale Varenicline (VAR), a smoking cessation aid that is a partial agonist at nicotinic receptors, mimics the reinforcement-enhancing effects of nicotine. Varenicline, when accompanied by non-drug cues, is self-administered by rats, though it is unclear whether this results from varenicline acting as a Primary Reinforcer or a reinforcement enhancer of the cues.

  • Bupropion and nicotine enhance responding for nondrug Reinforcers via dissociable pharmacological mechanisms in rats
    Psychopharmacology, 2009
    Co-Authors: Matthew I. Palmatier, Melissa E Levin, Kara L Mays, Anthony R Caggiula, Eric C. Donny, Alan F Sved
    Abstract:

    Rationale Nicotine serves as a Primary Reinforcer but also potently enhances responding for nonnicotine stimuli with reinforcing properties. One of the most successful pharmacotherapies for smoking cessation, bupropion, also increases responding for nondrug Reinforcers such as food and brain stimulation rewards. Objective The present studies investigated whether treatment with bupropion and nicotine had similar effects on responding for a reinforcing visual stimulus (VS). They also investigated whether the effects of bupropion and nicotine depended on common pharmacological substrates. Results Nicotine (0.4 mg/kg base) enhanced responding for the VS, and this enhancing effect increased across testing sessions, replicating our previous findings. Bupropion (3, 10, and 30 mg/kg salt) dose-dependently increased responding for the VS. Treatment with 10 and 30 mg/kg bupropion resulted in a profile similar to nicotine; operant responding increased over repeated drug treatments. The reinforcement enhancing effect of nicotine, but not bupropion, was blocked by pretreatment with the nicotinic acetylcholine receptor antagonist mecamylamine. In contrast, the reinforcement enhancing effect of bupropion, but not nicotine, was blocked by pretreatment with the alpha noradrenergic antagonist prazosin. Conclusion The reinforcement enhancing effects of nicotine and bupropion increased over time and repeated treatments suggesting a shared mechanism of action. However, the reinforcement enhancing effects of nicotine are mediated by nicotinic acetylcholine receptors, whereas the reinforcement enhancing effects of bupropion were mediated by alpha noradrenergic receptors.

  • bupropion and nicotine enhance responding for nondrug Reinforcers via dissociable pharmacological mechanisms in rats
    Psychopharmacology, 2009
    Co-Authors: Matthew I. Palmatier, Melissa E Levin, Kara L Mays, Anthony R Caggiula, Eric C. Donny, Alan F Sved
    Abstract:

    Rationale Nicotine serves as a Primary Reinforcer but also potently enhances responding for nonnicotine stimuli with reinforcing properties. One of the most successful pharmacotherapies for smoking cessation, bupropion, also increases responding for nondrug Reinforcers such as food and brain stimulation rewards.

  • the motivation to obtain nicotine conditioned Reinforcers depends on nicotine dose
    Neuropharmacology, 2008
    Co-Authors: Matthew I. Palmatier, Anthony R Caggiula, Eric C. Donny, Sarah Coddington, Alan F Sved
    Abstract:

    Abstract Stimuli associated with nicotine (NIC) can acquire new meaning via Pavlovian conditioning. If a stimulus is associated with the Primary reinforcing effects of NIC, the new conditional properties of the stimulus should make it a more valuable Reinforcer (i.e., increase the motivation to obtain the stimulus), and this value should be based, in part, on the strength or intensity of the Primary Reinforcer (i.e., NIC dose). The purpose of the present study was to investigate whether NIC-conditioned reinforcement increased motivation to obtain non-NIC stimuli, as reflected by performance on a progressive ratio (PR) reinforcement schedule, and whether this increased motivation was systematically related to NIC dose. Two Paired groups were allowed to nose-poke for NIC (0.03 or 0.09 mg/kg/infusion, IV) accompanied by 15-s illumination of a stimulus light (conditional stimulus or CS). Two Unpaired groups (0.03 or 0.09 mg/kg/infusion) could also make a nose-poke response for the CS; however their NIC infusions were controlled by the Paired group (i.e., yoked design). A fifth group (CS-Only) was allowed to nose-poke for CS presentations and saline infusions. After 29 conditioning sessions the nose-poke operant was prevented by obscuring the receptacle and the CS (accompanied by saline infusion for all groups) was made contingent upon a novel operant response (lever press). During the acquisition of this novel response, each CS/saline infusion earned increased the number of responses required to earn the next CS/saline infusion. Pairings with the Primary reinforcing effects of NIC resulted the acquisition of a novel response for the CS. Motivation to obtain the CS depended on salience (dose) of the Primary reinforcement (NIC).

Anthony R Caggiula - One of the best experts on this subject based on the ideXlab platform.

  • Differentiating the Primary reinforcing and reinforcement-enhancing effects of varenicline
    Psychopharmacology, 2015
    Co-Authors: Rachel L. Schassburger, Melissa E Levin, Anthony R Caggiula, Matthew I. Palmatier, Eric C. Donny, Matthew T. Weaver, Alan F Sved
    Abstract:

    Rationale Varenicline (VAR), a smoking cessation aid that is a partial agonist at nicotinic receptors, mimics the reinforcement-enhancing effects of nicotine. Varenicline, when accompanied by non-drug cues, is self-administered by rats, though it is unclear whether this results from varenicline acting as a Primary Reinforcer or a reinforcement enhancer of the cues. Objectives This study sought to disentangle these two potential actions. Methods Rats were allowed to self-administer intravenous nicotine, saline, or varenicline during 1-h sessions in operant chambers equipped with two levers. Five groups had concurrent access to drug infusions and a moderately reinforcing visual stimulus (VS) for responding on separate levers. Meeting the reinforcement schedule on one lever was reinforced with VAR (0.01, 0.06, 0.1 mg/kg/infusion), nicotine (0.06 mg/kg/infusion), or saline, while meeting the same schedule on the other lever delivered the VS. Additional groups were reinforced for pressing a single “active” lever and received VAR paired with the VS, the VS with response-independent infusions of VAR, or VAR alone (0.1 mg/kg/infusion). Results Rats readily responded for VAR paired with VS on a single lever. However, when VAR was the only Reinforcer contingent on a response, rats did not respond more than for saline. Conclusions These findings show that VAR does not serve as a Primary Reinforcer in rats at doses that increase responding for non-drug Reinforcers. These data are consistent with research showing that the Primary reinforcing effects of VAR are weak, at best, and that the Primary reinforcing and reinforcement-enhancing actions of nicotinic drugs are pharmacologically distinct.

  • Differentiating the Primary reinforcing and reinforcement-enhancing effects of varenicline.
    Psychopharmacology, 2014
    Co-Authors: Rachel L. Schassburger, Melissa E Levin, Anthony R Caggiula, Matthew I. Palmatier, Eric C. Donny, Matthew T. Weaver, Alan F Sved
    Abstract:

    Rationale Varenicline (VAR), a smoking cessation aid that is a partial agonist at nicotinic receptors, mimics the reinforcement-enhancing effects of nicotine. Varenicline, when accompanied by non-drug cues, is self-administered by rats, though it is unclear whether this results from varenicline acting as a Primary Reinforcer or a reinforcement enhancer of the cues.

  • Bupropion and nicotine enhance responding for nondrug Reinforcers via dissociable pharmacological mechanisms in rats
    Psychopharmacology, 2009
    Co-Authors: Matthew I. Palmatier, Melissa E Levin, Kara L Mays, Anthony R Caggiula, Eric C. Donny, Alan F Sved
    Abstract:

    Rationale Nicotine serves as a Primary Reinforcer but also potently enhances responding for nonnicotine stimuli with reinforcing properties. One of the most successful pharmacotherapies for smoking cessation, bupropion, also increases responding for nondrug Reinforcers such as food and brain stimulation rewards. Objective The present studies investigated whether treatment with bupropion and nicotine had similar effects on responding for a reinforcing visual stimulus (VS). They also investigated whether the effects of bupropion and nicotine depended on common pharmacological substrates. Results Nicotine (0.4 mg/kg base) enhanced responding for the VS, and this enhancing effect increased across testing sessions, replicating our previous findings. Bupropion (3, 10, and 30 mg/kg salt) dose-dependently increased responding for the VS. Treatment with 10 and 30 mg/kg bupropion resulted in a profile similar to nicotine; operant responding increased over repeated drug treatments. The reinforcement enhancing effect of nicotine, but not bupropion, was blocked by pretreatment with the nicotinic acetylcholine receptor antagonist mecamylamine. In contrast, the reinforcement enhancing effect of bupropion, but not nicotine, was blocked by pretreatment with the alpha noradrenergic antagonist prazosin. Conclusion The reinforcement enhancing effects of nicotine and bupropion increased over time and repeated treatments suggesting a shared mechanism of action. However, the reinforcement enhancing effects of nicotine are mediated by nicotinic acetylcholine receptors, whereas the reinforcement enhancing effects of bupropion were mediated by alpha noradrenergic receptors.

  • bupropion and nicotine enhance responding for nondrug Reinforcers via dissociable pharmacological mechanisms in rats
    Psychopharmacology, 2009
    Co-Authors: Matthew I. Palmatier, Melissa E Levin, Kara L Mays, Anthony R Caggiula, Eric C. Donny, Alan F Sved
    Abstract:

    Rationale Nicotine serves as a Primary Reinforcer but also potently enhances responding for nonnicotine stimuli with reinforcing properties. One of the most successful pharmacotherapies for smoking cessation, bupropion, also increases responding for nondrug Reinforcers such as food and brain stimulation rewards.

  • the motivation to obtain nicotine conditioned Reinforcers depends on nicotine dose
    Neuropharmacology, 2008
    Co-Authors: Matthew I. Palmatier, Anthony R Caggiula, Eric C. Donny, Sarah Coddington, Alan F Sved
    Abstract:

    Abstract Stimuli associated with nicotine (NIC) can acquire new meaning via Pavlovian conditioning. If a stimulus is associated with the Primary reinforcing effects of NIC, the new conditional properties of the stimulus should make it a more valuable Reinforcer (i.e., increase the motivation to obtain the stimulus), and this value should be based, in part, on the strength or intensity of the Primary Reinforcer (i.e., NIC dose). The purpose of the present study was to investigate whether NIC-conditioned reinforcement increased motivation to obtain non-NIC stimuli, as reflected by performance on a progressive ratio (PR) reinforcement schedule, and whether this increased motivation was systematically related to NIC dose. Two Paired groups were allowed to nose-poke for NIC (0.03 or 0.09 mg/kg/infusion, IV) accompanied by 15-s illumination of a stimulus light (conditional stimulus or CS). Two Unpaired groups (0.03 or 0.09 mg/kg/infusion) could also make a nose-poke response for the CS; however their NIC infusions were controlled by the Paired group (i.e., yoked design). A fifth group (CS-Only) was allowed to nose-poke for CS presentations and saline infusions. After 29 conditioning sessions the nose-poke operant was prevented by obscuring the receptacle and the CS (accompanied by saline infusion for all groups) was made contingent upon a novel operant response (lever press). During the acquisition of this novel response, each CS/saline infusion earned increased the number of responses required to earn the next CS/saline infusion. Pairings with the Primary reinforcing effects of NIC resulted the acquisition of a novel response for the CS. Motivation to obtain the CS depended on salience (dose) of the Primary reinforcement (NIC).

Rachel L. Schassburger - One of the best experts on this subject based on the ideXlab platform.

  • Differentiating the Primary reinforcing and reinforcement-enhancing effects of varenicline
    Psychopharmacology, 2015
    Co-Authors: Rachel L. Schassburger, Melissa E Levin, Anthony R Caggiula, Matthew I. Palmatier, Eric C. Donny, Matthew T. Weaver, Alan F Sved
    Abstract:

    Rationale Varenicline (VAR), a smoking cessation aid that is a partial agonist at nicotinic receptors, mimics the reinforcement-enhancing effects of nicotine. Varenicline, when accompanied by non-drug cues, is self-administered by rats, though it is unclear whether this results from varenicline acting as a Primary Reinforcer or a reinforcement enhancer of the cues. Objectives This study sought to disentangle these two potential actions. Methods Rats were allowed to self-administer intravenous nicotine, saline, or varenicline during 1-h sessions in operant chambers equipped with two levers. Five groups had concurrent access to drug infusions and a moderately reinforcing visual stimulus (VS) for responding on separate levers. Meeting the reinforcement schedule on one lever was reinforced with VAR (0.01, 0.06, 0.1 mg/kg/infusion), nicotine (0.06 mg/kg/infusion), or saline, while meeting the same schedule on the other lever delivered the VS. Additional groups were reinforced for pressing a single “active” lever and received VAR paired with the VS, the VS with response-independent infusions of VAR, or VAR alone (0.1 mg/kg/infusion). Results Rats readily responded for VAR paired with VS on a single lever. However, when VAR was the only Reinforcer contingent on a response, rats did not respond more than for saline. Conclusions These findings show that VAR does not serve as a Primary Reinforcer in rats at doses that increase responding for non-drug Reinforcers. These data are consistent with research showing that the Primary reinforcing effects of VAR are weak, at best, and that the Primary reinforcing and reinforcement-enhancing actions of nicotinic drugs are pharmacologically distinct.

  • Behavioral mechanisms underlying nicotine reinforcement.
    Current topics in behavioral neurosciences, 2015
    Co-Authors: Laura E. Rupprecht, Alan F Sved, Rachel L. Schassburger, Tracy T. Smith, Deanne M. Buffalari, Eric C. Donny
    Abstract:

    Cigarette smoking is the leading cause of preventable deaths worldwide, and nicotine, the Primary psychoactive constituent in tobacco, drives sustained use. The behavioral actions of nicotine are complex and extend well beyond the actions of the drug as a Primary Reinforcer. Stimuli that are consistently paired with nicotine can, through associative learning, take on reinforcing properties as conditioned stimuli. These conditioned stimuli can then impact the rate and probability of behavior and even function as conditioning Reinforcers that maintain behavior in the absence of nicotine. Nicotine can also act as a conditioned stimulus (CS), predicting the delivery of other Reinforcers, which may allow nicotine to acquire value as a conditioned Reinforcer. These associative effects, establishing non-nicotine stimuli as conditioned stimuli with discriminative stimulus and conditioned reinforcing properties as well as establishing nicotine as a CS, are predicted by basic conditioning principles. However, nicotine can also act non-associatively. Nicotine directly enhances the reinforcing efficacy of other reinforcing stimuli in the environment, an effect that does not require a temporal or predictive relationship between nicotine and either the stimulus or the behavior. Hence, the reinforcing actions of nicotine stem both from the Primary reinforcing actions of the drug (and the subsequent associative learning effects) as well as the reinforcement enhancement action of nicotine which is non-associative in nature. Gaining a better understanding of how nicotine impacts behavior will allow for maximally effective tobacco control efforts aimed at reducing the harm associated with tobacco use by reducing and/or treating its addictiveness.

  • Differentiating the Primary reinforcing and reinforcement-enhancing effects of varenicline.
    Psychopharmacology, 2014
    Co-Authors: Rachel L. Schassburger, Melissa E Levin, Anthony R Caggiula, Matthew I. Palmatier, Eric C. Donny, Matthew T. Weaver, Alan F Sved
    Abstract:

    Rationale Varenicline (VAR), a smoking cessation aid that is a partial agonist at nicotinic receptors, mimics the reinforcement-enhancing effects of nicotine. Varenicline, when accompanied by non-drug cues, is self-administered by rats, though it is unclear whether this results from varenicline acting as a Primary Reinforcer or a reinforcement enhancer of the cues.