Reciprocal changes in dopamine responsiveness in the nucleus accumbens shell and core and in the dorsal caudate–putamen in rats sensitized to morphine

Cadoni, C; Chiara, G. Di

doi:10.1016/s0306-4522(98)00466-7

Cited by 165 publications

(112 citation statements)

References 35 publications

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“…It is reasonable to assume that CNQX in the pVTA reduced the glutamatergic tone and excitation drive of dopaminergic neurons in this region, resulting in reduced dopaminergic secretion in the target areas of the pVTA, including the NAC medial shell (Ikemoto, 2007). Therefore, in accordance with the work by Cadoni and Di Chiara (1999), reduced DA levels in the medial NAC shell induced by CNQX injection to the pVTA were accompanied by hyperlocomotion already after the first exposure to opiates.…”

supporting

confidence: 55%

“…Interestingly, the hyperlocomotion was accompanied by increased DA levels in the NAC core but decreased DA levels in the NAC shell, whereas the hypolocomotion was accompanied by opposite effects on DA within the NAC (Cadoni and Di Chiara, 1999). It is reasonable to assume that CNQX in the pVTA reduced the glutamatergic tone and excitation drive of dopaminergic neurons in this region, resulting in reduced dopaminergic secretion in the target areas of the pVTA, including the NAC medial shell (Ikemoto, 2007).…”

mentioning

confidence: 99%

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Dissociation between Rewarding and Psychomotor Effects of Opiates: Differential Roles for Glutamate Receptors within Anterior and Posterior Portions of the Ventral Tegmental Area

Shabat-Simon¹,

Levy²,

Amir³

et al. 2008

J. Neurosci.

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The rewarding effects of drugs of abuse are thought to be dependent on the mesocorticolimbic dopamine system, which originates in the ventral tegmental area (VTA) and projects into the nucleus accumbens (NAC) and other forebrain regions. Heroin, by inhibiting GABAergic interneurons in the VTA, induces local dopaminergic activation and release in the NAC terminals. The role of other basic neurotransmitter systems, such as glutamate in the VTA, in mediating the rewarding effect of addictive drugs, is less established. We explored whether blockade of glutamate receptors in subregions of the VTA modulate the rewarding properties and/or the development of psychomotor changes induced by opiates. Administration of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; an AMPA/kainate receptor antagonist) into the anterior VTA blocked the rewarding effects of opiates in both the conditioned place preference and the selfadministration paradigms without affecting the gradual increase of the psychomotor response to opiates. In contrast, administration of CNQX into the posterior VTA did not affect the rewarding properties of opiates, but blocked the initial sedative effect of opiates and the gradual increase of the psychomotor response to the drug. These findings suggest a critical role for glutamate receptors in the VTA in opiate reward, as well as behavioral and anatomical dissociation between the rewarding and psychomotor effects of opiates.

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supporting

confidence: 55%

mentioning

confidence: 99%

Dissociation between Rewarding and Psychomotor Effects of Opiates: Differential Roles for Glutamate Receptors within Anterior and Posterior Portions of the Ventral Tegmental Area

Shabat-Simon¹,

Levy²,

Amir³

et al. 2008

J. Neurosci.

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“…The VTA provides dopaminergic inputs to the NAc (Fallon and Moore, 1978;Haglund et al, 1979;Swanson, 1982) and VP (Napier et al, 1991a;Klitenick et al, 1992;Mitrovic and Napier, 2002). Dopamine overflow in the NAc core occurs during expression of morphine-induced sensitization following long-term withdrawal (Cadoni and Di Chiara, 1999) and intra-VP morphine increases dopamine neurotransmission in the NAc (Anagnostakis and Spyraki, 1994). In light of this literature, the present findings indicate that sensitization-induced changes in VP m-opioid receptor function reduces GABAergic inhibition of VP GABAergic control over the VTA, leading to an increased number of active dopamine neurons in the VTA and increasing dopamine concentration and receptor activation in the NAc and VP.…”

Section: Discussionmentioning

confidence: 99%

The Ventral Pallidum is Critically Involved in the Development and Expression of Morphine-Induced Sensitization

Mickiewicz

Dallimore

Napier

2008

Neuropsychopharmacol

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Repeated, intermittent exposure to drugs of abuse results in response enhancements to subsequent drug treatments, a phenomenon referred to as sensitization. As persistent neuronal sensitization may contribute to the long-lasting consequences of drug abuse, characterizing the neuroanatomical substrates of sensitization is providing insights into addiction. It is known that the ventral tegmental area (VTA) is necessary for induction, and expression involves the nucleus accumbens (NAc). We reveal here that the ventral pallidum (VP), a brain region reciprocally innervated by the VTA and the NAc, is a critical mediator of opiate-induced behavioral sensitization. Blockade of VP m-opioid receptors (via intra-VP CTOP injections) negated the ability of systemic administration of the opiate, morphine to induce motor sensitization, and for sensitized rats to subsequently express enhanced responding to a morphine challenge. Intra-VP morphine was sufficient to induce motor sensitization, and this sensitization was expressed following 17 days of withdrawal. Rats with a treatment history of intra-VP morphine demonstrated cross-sensitization to a challenge injection of systemically administered morphine. Conversely, repeated systemic treatments of morphine cross-sensitized to an intra-VP morphine challenge. These results indicate that activation of VP m-opioid receptors is sufficient to evoke behavioral sensitization and that these receptors are necessary for sensitized responding to systemic morphine. The study pioneers the concept that both development and expression of drug-induced sensitization are regulated by the VP. Thus, the VP is likely an important contributor to neuronal adaptations that underlie addiction.

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“…Drugs of abuse stimulate the activity of mesoaccumbal DA neurons and this effect increases upon repeated drug exposure. Sensitization of the mesoaccumbal DA system after repeated drug administration has been demonstrated for most drugs of abuse, including psychostimulants (Kalivas and Duffy, 1993a;Cadoni et al, 2000b;Zapata et al, 2003), opiates (Cadoni and Di Chiara, 1999), and nicotine (Reid et al, 1996;Cadoni and Di Chiara, 2000a). This enhanced accumbens DA response after repeated drug experience has been proposed to be one neuroadaptation important for the maintenance and reinstatement of compulsive drug-seeking behavior (Robinson and Berridge, 1993).…”

Section: Introductionmentioning

confidence: 99%

Repeated Ethanol Intoxication Induces Behavioral Sensitization in the Absence of a Sensitized Accumbens Dopamine Response in C57BL/6J and DBA/2J Mice

Zapata

Gonzales

Shippenberg

2005

Neuropsychopharmacol

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Repeated exposure to drugs of abuse results in an increased sensitivity to their behavioral effects, a phenomena referred to as behavioral sensitization. It has been suggested that the same neuroadaptations underlying behavioral sensitization contribute to the maintenance and reinstatement of addiction. Dysregulation of dopamine (DA) neurotransmission in the mesoaccumbens system is one neuroadaptation that is thought to lead to the compulsive drug-seeking that characterizes addiction. Evidence that sensitization to psychostimulants and opiates is associated with an enhancement of drug-evoked DA levels in the nucleus accumbens has also been obtained. Like other drugs of abuse, the acute administration of ethanol (ETOH) stimulates DA release in this brain region. Moreover, repeated ETOH experience results in an enhanced behavioral response to a subsequent ethanol challenge. Data regarding the influence of repeated ethanol intoxication and withdrawal upon mesoaccumbal DA neurotransmission is limited. Studies examining ETOH-evoked alterations in mesoaccumbal DA neurotransmission as a function of withdrawal duration are lacking. The present experiments quantified basal and ethanol-evoked DA levels 14 days and 24 h following the cessation of a repeated ETOH intoxication protocol, which results in sensitization to the locomotor activating effects of ethanol. Locomotor activity was assessed in parallel groups of animals. Studies were conducted in two mouse strains, C57BL/6J and DBA/2J, which differ in their behavioral responses to ETOH. The results indicate the development of transient tolerance to both ETOH-induced behavioral activation and evoked accumbens DA release at early withdrawal. Moreover, no enhanced DA response to a subsequent ETOH challenge could be demonstrated in ETOH experienced animals 2 weeks after withdrawal, in spite of the observation of clear behavioral sensitization at this time point. These results suggest that, at least in the case of ethanol, sensitization of the DA mesolimbic system may not be necessary for the development of behavioral sensitization.

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Reciprocal changes in dopamine responsiveness in the nucleus accumbens shell and core and in the dorsal caudate–putamen in rats sensitized to morphine

Cited by 165 publications

References 35 publications

Dissociation between Rewarding and Psychomotor Effects of Opiates: Differential Roles for Glutamate Receptors within Anterior and Posterior Portions of the Ventral Tegmental Area

Dissociation between Rewarding and Psychomotor Effects of Opiates: Differential Roles for Glutamate Receptors within Anterior and Posterior Portions of the Ventral Tegmental Area

The Ventral Pallidum is Critically Involved in the Development and Expression of Morphine-Induced Sensitization

Repeated Ethanol Intoxication Induces Behavioral Sensitization in the Absence of a Sensitized Accumbens Dopamine Response in C57BL/6J and DBA/2J Mice

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