Effects of the AMPA/kainate receptor antagonist DNQX in the nucleus accumbens on drug-induced conditioned place preference

Layer, Richard T.; Uretsky, Norman J.; Wallace, Lane J.

doi:10.1016/0006-8993(93)91094-9

Cited by 78 publications

(47 citation statements)

References 28 publications

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“…In fact, baclofen may have acted directly on processes responsible for initiating behavioral activity in a manner that superseded the control exerted by conditioned stimuli. This interpretation would be consistent with a substantial body of evidence implicating the NAc in the expression of both conditioned and unconditioned locomotor responses (DiCiano et al 1998a,b;Gold et al 1988;Gratton and Wise 1994;Kelly and Iverson 1976;Kiyatkin and Stein 1996;Layer et al 1993;Neisewander et al 2000;Pijnenburg et al 1975).…”

Section: Discussionsupporting

confidence: 83%

Involvement of the Nucleus Accumbens and Medial Prefrontal Cortex in the Expression of Conditioned Hyperactivity to a Cocaine-Associated Environment in Rats

Franklin

Druhan

2000

Neuropsychopharmacology

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This study examined the roles of the nucleus accumbens (NAc), medial prefrontal cortex, basolateral amygdala, and ventral subiculum of the hippocampus in the expression of Pavlovian conditioned hyperactivity responses to cocainerelated stimuli. This was accomplished by pharmacologically inhibiting these regions prior to drug-free tests for conditioned hyperactivity in an environment previously associated with cocaine. The results indicate that conditioned hyperactivity could be disrupted by infusions of the baclofen (0.2 nmol/0.5 l/side) Environmental stimuli associated with cocaine use can elicit a variety of conditioned physiological and subjective responses in abstinent cocaine addicts (Childress et al. 1999;Newlin 1992). These Pavlovian conditioned responses may contribute to the maintenance of drug-taking habits in active cocaine users, and promote relapse in detoxified addicts. In rats, environments associated with cocaine evoke conditioned locomotor activation in the absence of the drug (Barr et al. 1983;Cervo and Samanin 1996;DiCiano et al. 1998a;Stewart et al. 1984). This Pavlovian conditioned behavioral activation may be analogous to some of the conditioned subjective and physiological responses elicited by cocaine-related stimuli in human drug addicts (Pert 1994). Accordingly, studies of the neurobiological mechanisms underlying conditioned behavioral activation in rats may provide valuable information that could facilitate the development of pharmacological treatments for cocaine addiction.Several lines of evidence suggest that the nucleus accumbens (NAc) may regulate the expression of conditioned responses to stimuli associated with cocaine or other psychostimulants. For example, 6-OHDA lesions of mesoaccumbens dopamine terminals post-conditioning can interfere with conditioned hyperactivity elicited NO . 6 by an environment repeatedly paired with amphetamine (Gold et al. 1988). Moreover, exposure to cocaine-or amphetamine-related cues increases dopamine release within the NAc (DiCiano et al. 1998a,b;Fontana et al. 1993;Gratton and Wise 1994), alters NAc cell firing (Bowman et al. 1996;Giampoala et al. 1999), and induces conditioned increases in Fos-related protein within the caudal NAc (Franklin and Druhan 2000;Neisewander et al. 2000; although see Brown and Fibiger 1992). Together, these studies suggest that the NAc may be important for the expression of conditioned hyperactivity responses to psychostimulantpaired stimuli.Cortical and limbic regions that project to the NAc also may regulate conditioned responses to psychostimulant-related cues. Indeed, lesions or pharmacological manipulations of the medial prefrontal cortex (mPFC), the basolateral amygdala (Bl), and the ventral subiculum of the hippocampus (vSub) disrupt the stimulus control of operant drug-seeking responses measured in place-preference, conditioned reinforcement, or self-administration procedures (Brown and Fibiger 1993; Hiroi and White 1991; Phillips 1997, 1998;Isaac et al. 1989;Tzschentke and Schmidt 1998;Whitelaw et al...

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Section: Discussionsupporting

confidence: 83%

Involvement of the Nucleus Accumbens and Medial Prefrontal Cortex in the Expression of Conditioned Hyperactivity to a Cocaine-Associated Environment in Rats

Franklin

Druhan

2000

Neuropsychopharmacology

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“…Within this framework, the attenuation of glutamate (and potentially dopamine) transmission by intra-NAc LY379268 injections is hypothesized to decrease an incentive motivational state, induced by exposure to the contextual cues, which leads to reinstatement of heroin seeking. The findings that blockade of ionotropic excitatory glutamate receptors in the NAc attenuates the expression of conditioned place preference for morphine (Layer et al, 1993) is in agreement with this interpretation. The conditioned place preference procedure is commonly used to assess the incentive motivational effects of opiates and other drugs (Stewart et al, 1984;Phillips and Fibiger, 1987;Bardo and Bevins, 2000).…”

Section: Psychological Mechanisms Underlying the Effect Of Ly379268 Nsupporting

confidence: 84%

“…There is also evidence that glutamate transmission in the NAc is involved in conditioned drug effects. Blockade of NAc AMPA/kainate receptors attenuates conditioned place preference induced by morphine, cocaine, or amphetamine (Layer et al, 1993;Kaddis et al, 1995) and exposure to environmental cues previously paired with cocaine injections increases glutamate release in the NAc ).…”

Section: Introductionmentioning

confidence: 99%

Activation of Group II Metabotropic Glutamate Receptors in the Nucleus Accumbens Shell Attenuates Context-Induced Relapse to Heroin Seeking

Bossert

Gray

Lü

et al. 2005

Neuropsychopharmacol

215

173

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Using a rat relapse model, we previously reported that re-exposing rats to a drug-associated context, following extinction of operant responding in a different context, reinstates heroin seeking. In an initial pharmacological characterization, we found that the mGluR 2/3 agonist LY379268, which acts centrally to reduce evoked glutamate release, attenuates context-induced reinstatement of heroin seeking when injected systemically or into the ventral tegmental area, the cell body region of the mesolimbic dopamine system. Here, we tested whether injections of LY379268 into the nucleus accumbens (NAc), a terminal region of the mesolimbic dopamine system, would also attenuate context-induced reinstatement of heroin seeking. Rats were trained to self-administer heroin; drug infusions were paired with a discrete tone-light cue. Subsequently, lever pressing was extinguished in the presence of the discrete cue in a context that differed from the drug self-administration context in terms of visual, auditory, tactile, and circadian cues. After extinction of responding, LY379268 was injected to different groups of rats into the NAc core or shell or into the caudate-putamen, a terminal region of the nigrastriatal dopamine system. Injections of LY379268 into the NAc shell (0.3 or 1.0 mg) dose-dependently attenuated context-induced reinstatement of heroin seeking. Injections of 1.0 mg of LY379268 into the NAc core had no effect, while a higher dose (3.0 mg) decreased this reinstatement. Injections of LY379268 (3.0 mg) 1.5 mm dorsal from the NAc core into the caudate-putamen were ineffective. Results suggest an important role of glutamate transmission in the NAc shell in context-induced reinstatement of heroin seeking.

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“…In addition, the Acb also receives a major projection from ventral tegmental area (VTA) afferents containing the catecholamine neuromodulator dopamine (French and Totterdell 2004;Gerfen et al 1987;Kalivas and Volkow 2005). Nucleus accumbens glutamate and dopamine influence reward through actions on the ionotropic AMPA-type glutamate and the G-protein-coupled D1R receptors, respectively (Kelz et al 1999;Layer et al 1993;Shippenberg et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Chronic administration of morphine is associated with a decrease in surface AMPA GluR1 receptor subunit in dopamine D1 receptor expressing neurons in the shell and non-D1 receptor expressing neurons in the core of the rat nucleus accumbens

Glass

Lane

Colago

et al. 2008

Experimental Neurology

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The nucleus accumbens (Acb) is an extensively studied neuroanatomical substrate of opiate reward and the neural plasticity associated with chronic opioid use. The cellular mechanisms mediating opioid-dependent plasticity are uncertain, however AMPA-type glutamate receptor trafficking in dopamine D1 dopamine receptor (D1R) expressing neurons may be a potential cellular pathway for these adaptations, although there is no evidence for this possibility. Immunogold electron microscopy was used to quantify the surface expression of the AMPA GluR1 subunit in dendritic profiles of neurons in the Acb in response to intermittent 14-day non-contingent injections of escalating doses of morphine, a model that parallels opioid self-administration. To determine if changes in GluR1 trafficking occurred in neurons potentially sensitive to dopamine-induced D1R activation, immunoperoxidase labeling of D1R was combined with immunogold labeling of GluR1.Immunogold quantification was performed in two distinct Acb subregions, the shell, an area involved in processing incentive salience related to rewarding stimuli, and the core, an area involved in rewardseeking behaviors. We provide the first report that chronic morphine administration is associated with a receptor-phenotypic decrease in surface trafficking of GluR1 in Acb subregions. When compared to saline injected animals, morphine produced a decrease in plasma membrane GluR1 labeling in medium-and large-size D1R expressing dendritic profiles in the Acb shell. In contrast, in the Acb core, surface GluR1 was decreased in small-size dendrites that did not express the dopamine receptor. These results indicate that chronic intermittent injection of escalating doses of morphine is accompanied by ultrastructural plasticity of GluR1 in neurons that are responsive to glutamate and dopamine-induced D1R activation in the Acb shell, and neurons capable of responding to glutamate but not D1R receptor stimulation in the Acb core. Thus, AMPA receptor trafficking associated with chronic opiate exposure in functionally distinct areas of the Acb may be distinguished by D1R receptor activation, suggesting the potential for differing neural substrates of reward and motor aspects of addictive processes involving glutamate and dopamine signaling.

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Effects of the AMPA/kainate receptor antagonist DNQX in the nucleus accumbens on drug-induced conditioned place preference

Cited by 78 publications

References 28 publications

Involvement of the Nucleus Accumbens and Medial Prefrontal Cortex in the Expression of Conditioned Hyperactivity to a Cocaine-Associated Environment in Rats

Involvement of the Nucleus Accumbens and Medial Prefrontal Cortex in the Expression of Conditioned Hyperactivity to a Cocaine-Associated Environment in Rats

Activation of Group II Metabotropic Glutamate Receptors in the Nucleus Accumbens Shell Attenuates Context-Induced Relapse to Heroin Seeking

Chronic administration of morphine is associated with a decrease in surface AMPA GluR1 receptor subunit in dopamine D1 receptor expressing neurons in the shell and non-D1 receptor expressing neurons in the core of the rat nucleus accumbens

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