Evidence for the coexistence of glutamate decar☐ylase and Met-enkephalin immunoreactivities in axon terminals of rat ventral pallidum

Zahm, Daniel S.; Záborszky, László; Alones, Vinessa; Heimer, Lennart

doi:10.1016/0006-8993(85)90331-2

Cited by 188 publications

(82 citation statements)

References 11 publications

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“…GABA projections from the VTA to the NAc shell contain presynaptic m-opioid receptors (Svingos et al, 1997). In addition, medium spiny neurons that project to the VTA from the NAc contain m-opioid receptors, suggesting that heroin could modulate these inhibitory fibers directly at the level of the NAc (Zahm et al, 1985). Activation of these receptors would hyperpolarize the GABAergic synapse, resulting in disinhibition of DA release in the NAc.…”

Section: Brain Sites Of Potentiationmentioning

confidence: 99%

Self-Administered Heroin and Cocaine Combinations in the Rat: Additive Reinforcing Effects—Supra-Additive Effects on Nucleus Accumbens Extracellular Dopamine

Smith

Coller

et al. 2005

Neuropsychopharmacol

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The concurrent use of cocaine and opiate combinations (speedball) has increased since the 1970s and now represents a growing subset of intravenous drug abusers. An isobolographic analysis was applied to the ascending limb of the dose-effect curves for rat selfadministration of cocaine, heroin, and their combination to determine the nature of the interaction. The addition of heroin to cocaine shifted the dose-effect curve for self-administration to the left, and the modulation in reinforcing efficacy of the combination of cocaine and heroin was found to be additive. A second experiment used microdialysis to determine the effects of this drug combination on nucleus accumbens (NAc) extracellular levels of dopamine ([DA] e ) in rats self-administering low doses of cocaine, heroin, or cocaine/ heroin combinations. These doses of cocaine and cocaine/heroin combinations significantly increased NAc [DA] e , while heroin alone did not. The ratio of the % baseline of [DA] e (or the dialysate concentrations of DA) to cocaine in the dialysate was higher during selfadministration of cocaine/heroin combinations than with cocaine alone. These data indicate that although the interaction between cocaine and heroin in maintaining self-administration is additive, a potentiation of NAc dopaminergic neurotransmission is present, suggesting that NAc [DA] e may not be a direct measure of reinforcing efficacy and/or it is not central to the mediation of the selfadministration of this drug combination.

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Section: Brain Sites Of Potentiationmentioning

confidence: 99%

Self-Administered Heroin and Cocaine Combinations in the Rat: Additive Reinforcing Effects—Supra-Additive Effects on Nucleus Accumbens Extracellular Dopamine

Smith

Coller

et al. 2005

Neuropsychopharmacol

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“…Several studies have shown a modulation of ACTH secretion by opioids [2,7,8]. Furthermore, ALP-opioid interaction have been reported at various levels in the central nervous system [7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Naloxone decreases the inhibitory effect of alprazolam on the release of adrenocorticotropin/cortisol induced by physical exercise in man

Coiro¹,

Volpi²,

Casti³

et al. 2011

Brit J Clinical Pharma

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• This study demonstrates a partial opioid influence in the inhibitory effect of ALP on the release of ACTH/cortisol during physical exercise. AIMSTo establish the possible involvement of alprazolam (ALP) and/or opiates in the mechanism underlying the ACTH/cortisol response to physical exercise. METHODSTests were carried out under basal conditions (exercise control test), exercise plus ALP (50 mg at time -90 min), naloxone (10 mg at time 0) or ALP plus naloxone. Plasma ACTH and serum cortisol concentrations were evaluated in blood samples taken before, during and after the bicycle ergometer tests. RESULTSACTH and cortisol concentrations rose significantly after physical exercise. Maximum peak at time 15 min (P Յ 0.01 vs. baseline) for ACTH and at time 30 min (P Յ 0.01 vs. baseline) for cortisol. In the presence of naloxone, the ACTH and cortisol responses were significantly increased (maximum peak at time 20 min, P Յ 0.02 vs. control test for ACTH, and at time 30 min (P Յ 0.01 vs. baseline) for cortisol) whereas they were abolished by ALP. When ALP and naloxone were given together, the inhibitory effect of ALP was partial. CONCLUSIONSThese data demonstrate an inhibitory effect of ALP in the regulation of the ACTH/cortisol response to physical exercise in man and suggest that GABAergic receptor activating benzodiazepines and opioids interact in the neuroendocrine secretion of ACTH/cortisol.British Journal of Clinical Pharmacology DOI:10.1111DOI:10. /j.1365DOI:10. -2125DOI:10. .2010 Br J Clin Pharmacol / 71:6 / 951-955 / 951

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“…One such structure, the ventral pallidum (VP), regulates the flow of information to and from the NAc and VTA, as well as inputting the motor outputs of the spinal cord (Zahm, 1989;Mogenson and Yang, 1991). Receiving converging inputs from the VTA dopaminergic neurons (Napier et al, 1991a;Klitenick et al, 1992;Maslowski-Cobuzzi and Napier, 1994;Mitrovic and Napier, 2002) and accumbal opioidergic (and GABAergic) inputs Zahm et al, 1985;Chrobak and Napier, 1993), we predicted that the VP is involved in opiate-induced sensitization. Thus, we revealed that blocking m-opioid receptors within the VP is sufficient to block the development of sensitized motor responding to systemically administered morphine (Johnson and Napier, 2000).…”

Section: Introductionmentioning

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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Evidence for the coexistence of glutamate decar☐ylase and Met-enkephalin immunoreactivities in axon terminals of rat ventral pallidum

Cited by 188 publications

References 11 publications

Self-Administered Heroin and Cocaine Combinations in the Rat: Additive Reinforcing Effects—Supra-Additive Effects on Nucleus Accumbens Extracellular Dopamine

Self-Administered Heroin and Cocaine Combinations in the Rat: Additive Reinforcing Effects—Supra-Additive Effects on Nucleus Accumbens Extracellular Dopamine

Naloxone decreases the inhibitory effect of alprazolam on the release of adrenocorticotropin/cortisol induced by physical exercise in man

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

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