On the role of ascending catecholaminergic systems in intravenous self-administration of cocaine

Roberts, David C. S.; Corcoran, Michael E.; Fibiger, Hans C.

doi:10.1016/0091-3057(77)90084-3

Cited by 700 publications

(323 citation statements)

References 37 publications

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“…Two studies (Goldberg and Gonzalez, 1976;Harris et al, 1996) demonstrated a decrease in cocaine SA following treatment with propanolol, a b-antagonist, but there was a concomitant decrease in responding for food in the latter study, suggesting a nonspecific effect on task performance. Although 6-OHDA lesions of DA produce a long-lasting reduction in SA of cocaine, lesions of both the dorsal and VNBs fail to alter responding (Roberts et al, 1977). Furthermore, while selective DA reuptake inhibitors themselves are readily self-administered and alter psychostimulant SA, selective NET inhibitors possess neither property (Woolverton, 1987;Howell and Byrd, 1991;Skjoldager et al, 1993;Tella, 1995;Wee et al, 2006).…”

Section: Ne and Psychostimulant Samentioning

confidence: 99%

There and Back Again: A Tale of Norepinephrine and Drug Addiction

Weinshenker

Schroeder

2006

Neuropsychopharmacol

322

277

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Fueled by anatomical, electrophysiological, and pharmacological analyses of endogenous brain reward systems, norepinephrine (NE) was identified as a key mediator of both natural and drug-induced reward in the late 1960s and early 1970s. However, reward experiments from the mid-1970s that could distinguish between the noradrenergic and dopaminergic systems resulted in the prevailing view that dopamine (DA) was the primary 'reward transmitter' (a belief holding some sway still today), thereby pushing NE into the background. Most damaging to the NE hypothesis of reward were studies demonstrating that NE receptor antagonists and NE reuptake inhibitors failed to impact drug self-administration. In recent years new tools, such as genetically engineered mice, and new experimental paradigms, such as reinstatement of drug seeking following withdrawal, have propelled NE back into the awareness of addiction researchers. Of particular interest is disulfiram, an inhibitor of the NE biosynthetic enzyme dopamine b-hydroxylase, which has demonstrated promising efficacy in the treatment of cocaine dependence in preliminary clinical trials. The purpose of this review is to synthesize the new data linking NE to critical aspects of DA signaling and drug addiction, with a focus on psychostimulants (eg, cocaine), opiates (eg, morphine), and alcohol.

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Section: Ne and Psychostimulant Samentioning

confidence: 99%

There and Back Again: A Tale of Norepinephrine and Drug Addiction

Weinshenker

Schroeder

2006

Neuropsychopharmacol

322

277

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“…The dopamine (DA) system is an obvious starting point in the search for neuroadaptations responsible for the addictive process. Pharmacological, neurochemical, and lesion experiments indicate that cocaine acts as an indirect agonist at DA synapses by blocking the reuptake of DA into the presynaptic terminal in the nucleus accumbens (NAc) and other projection areas of the ventral tegmental area (Heikkila et al, 1975;Ritz et al, 1987, Roberts et al, 1977Koob et al, 1994;Volkow et al, 1997;Bardo, 1998;Di Chiara, 1999). Despite the evidence for the role of DA neurotransmission in the acute reinforcing effects of cocaine, it remains to be determined whether changes in the physiology of this system account for motivational changes associated with cocaine addiction.…”

Section: Introductionmentioning

confidence: 99%

Reduced Dopamine Terminal Function and Insensitivity to Cocaine Following Cocaine Binge Self-Administration and Deprivation

Mateo

Läck

Morgan

et al. 2005

Neuropsychopharmacol

124

139

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Despite large numbers of studies describing neuroadaptations caused by chronic cocaine exposure, there remains considerable uncertainty as to whether alterations in dopamine (DA) neurotransmission are responsible for progression into an addicted state. Highintake, 24-h access cocaine self-administration (SA, 10 days) followed by an extended (7 days), but not 1 day deprivation period produces an increased motivation to SA cocaine as measured by a progressive ratio protocol. Following binge cocaine SA and deprivation, the status of DA terminals in the nucleus accumbens (NAc) was investigated using microdialysis in freely moving rats and voltammetry in brain slices. At 1 and 7 days following binge cocaine SA, baseline extracellular DA concentrations in the NAc core were decreased by 40 and 55% of control levels, in the 1 and 7 day deprivation groups, respectively. Acute cocaine (1.5 mg/kg, i.v.) administration increased extracellular DA (350%) in the NAc core of naïve animals but failed to significantly increase DA at 1 or 7 days following binge cocaine SA. The shell of the NAc showed a similar lack of effect of cocaine. Analysis of DA terminals in brain slices showed that cocaine was markedly less effective in inhibiting DA uptake at 1 and 7 days of cocaine deprivation (max. effect 40% of control). Electrically stimulated DA release was decreased at 1 day and further decreased at 7 days of deprivation (67 and 49% of control, respectively). The rate of DA uptake was increased (150% of control) following binge SA, irrespective of deprivation period. Finally, presynaptic autoreceptors were subsensitive at both time points, as measured by the ability of quinpirole, a D2-like DA receptor agonist, to inhibit DA release. Thus, the NAc was hypodopaminergic and DA terminals were less sensitive to cocaine following binge cocaine SA and deprivation.

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“…1 Rats readily engage in intravenous self-administration (IVSA) of d-AMPH and given continuous access, will engage in a cyclic IVSA pattern of binge, abstinence, and relapse, 2 reflecting the typical use pattern of human drug abusers. 3 Understanding the neurobiological substrates mediating the transition from one behavioral phase to the next is critical to the development of more effective treatment strategies.…”

Section: Introductionmentioning

confidence: 99%

Distinct proteomic profiles of amphetamine self-administration transitional states

et al. 2005

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In the rat, continuous access to d-amphetamine (d-AMPH) leads to lengthy bouts of self-administration, voluntary abstinence, and relapse to selfadministration. Previous studies have revealed that the progression from psychostimulant self-administration to abstinence to relapse is mediated in part by the ventral hippocampus. Stimulation of the ventral subiculum (vSub) during voluntary abstinence from d-AMPH self-administration reinstates self-administration and increases nucleus accumbens (NAc) dopamine efflux. Quantitative proteomic examination of the hippocampus from rats naïve to amphetamine, during a self-administration session 'Binge', during voluntarily abstinence 'Abstinent', and after reinstatement of selfadministration 'Relapse', revealed a differential proteomic state during abstinence. Actin-and cytoskeletal-related proteins were over-represented in the changes occurring during abstinence and suggest a decrease in actin filament polymerization. These changes may underlie alterations in neuronal tone during abstinence that could affect both neurotransmission and behavior. These data provide the first classification of addiction-related behaviors based on clustering of quantitative proteomic measurements.

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On the role of ascending catecholaminergic systems in intravenous self-administration of cocaine

Cited by 700 publications

References 37 publications

There and Back Again: A Tale of Norepinephrine and Drug Addiction

There and Back Again: A Tale of Norepinephrine and Drug Addiction

Reduced Dopamine Terminal Function and Insensitivity to Cocaine Following Cocaine Binge Self-Administration and Deprivation

Distinct proteomic profiles of amphetamine self-administration transitional states

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