Parametric analysis of brain stimulation reward in the rat: III. Effect of performance variables on the reward summation function.

Edmonds, Don E.; Gallistel, C. R.

doi:10.1037/h0037217

Cited by 200 publications

(117 citation statements)

References 8 publications

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“…The fact that rats with CHF demonstrated maximum response rates similar to baseline maximum rates indicates the absence of confounding motor/performance effects. This conclusion is consistent with other research employing curve shift paradigms for the analysis of selfstimulation (12,25). For instance, it has been suggested that changes in asymptotic performance in selfstimulation indicate that the manipulation in question has interfered with the animal's ability to perform the task, whereas a shift in the midpoint of the curve (i.e., the ECu 50 ) infers a change in the sensitivity to the rewarding properties of the stimulus (12).…”

Section: Discussionsupporting

confidence: 79%

Cytokine mediation of experimental heart failure-induced anhedonia

Grippo

Francis

Weiß

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Immune system dysfunction is hypothesized to influence several disease states, including cardiovascular disease and psychological depression. The comorbidity of depression and coronary artery disease may be influenced by immune system-brain interactions involving proinflammatory cytokines. The present studies evaluated an index of depression in a rodent model of heart failure by measuring responses to rewarding electrical brain stimulation, which provides an experimental procedure to operationally define anhedonia in rats. Heart failure led to a rightward shift in the current-response relationship in the brain stimulation paradigm, indicative of reduced rewarding properties of the brain stimulation (i.e., anhedonia). Acute treatment with a tumor necrosis factor antagonist, etanercept, reduced circulating tumor necrosis factor-α levels in rats with heart failure and restored responding for electrical brain stimulation. The current findings have implications for the study of pathophysiological mechanisms underlying the association of cardiovascular disease and depression.

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Section: Discussionsupporting

confidence: 79%

Cytokine mediation of experimental heart failure-induced anhedonia

Grippo

Francis

Weiß

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…A basic property of drugs of abuse is that they increase the rewarding efficacy of LH self-stimulation, an effect reflected in the shift of the rate-frequency function to the left (for review, see [60,61]). There is strong evidence, that the presently used intracranial self-stimulation paradigm provides reward-threshold estimates that are unaffected by performance effects of drug treatments or other experimental manipulations [17,38,39,45]. This is also evident in the present study.…”

Section: Discussionsupporting

confidence: 71%

WIN 55,212-2 decreases the reinforcing actions of cocaine through CB1 cannabinoid receptor stimulation

Vlachou

Nomikos

Panagis

2003

Behavioural Brain Research

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“…In contrast to SB-277011A or NGB 2904, the partial D 3 receptor agonist BP-897 produces a dose-dependent inhibition of both METH-enhanced BSR and BSR itself. This inhibition of BSR or METH-enhanced BSR is unlikely due to non-specific sedative effects, locomotor inhibition, or locomotor impairment, as none of the compounds significantly altered Ymax levels, a parameter highly sensitive to locomotor inhibition (Edmonds and Gallistel 1974;Miliaressis and Rompré 1987;Fouriezos et al 1990). These data suggest that selective blockade of DA D 3 receptors by relatively low doses of SB-277011A or NGB 2904 significantly inhibits the acute rewarding effects of METH, while these D 3 receptor antagonists themselves appear to have no intrinsic rewarding effects.…”

Section: Discussionmentioning

confidence: 96%

The selective dopamine D3 receptor antagonists SB-277011A and NGB 2904 and the putative partial D3 receptor agonist BP-897 attenuate methamphetamine-enhanced brain stimulation reward in rats

Spiller

Peng

et al. 2007

Psychopharmacology

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Rationale-We have previously reported that selective antagonism of brain D 3 receptors by SB-277011A or NGB 2904 significantly attenuates cocaine-or nicotine-enhanced brain stimulation reward (BSR).Objective-In the present study, we investigated whether the selective D 3 receptor antagonists SB-277011A and NGB 2904 and the putative partial D 3 agonist BP-897 similarly reduce methamphetamine (METH)-enhanced BSR.Materials and methods-Rats were trained to respond for rewarding electrical self-stimulation of the medial forebrain bundle. To assess the degree of drug-induced changes in BSR, a ratefrequency curve shift paradigm was used to measure brain-reward threshold (θ 0 ). © Springer-Verlag 2007Correspondence to: Zheng-Xiong Xi. Conflict of interest statementThere are no personal financial holdings that could be perceived as constituting a potential conflict of interest. NIH Public AccessAuthor Manuscript Psychopharmacology (Berl). Author manuscript; available in PMC 2013 July 17. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptResults-METH (0.1-0.65 mg/kg, i.p.) dose-dependently lowered (~10-50%) BSR thresholds, producing an enhancement of BSR. Pretreatment with SB-277011A (12 mg/kg, but not 24 mg/kg, i.p.) significantly attenuated METH-enhanced BSR. NGB 2904 (0.1-1.0 mg/kg, but not 10 mg/kg) also attenuated METH-enhanced BSR. SB-277011A or NGB 2904 alone, at the doses tested, had no effect on BSR. Pretreatment with BP-897 (0.1-5 mg/kg) dose-dependently attenuated METHenhanced BSR. However, when the dose was increased to 10 mg/kg, BP-897 shifted the stimulation-response curve to the right (inhibited BSR itself) in the presence or absence of METH.Conclusions-Selective antagonism of D 3 receptors by SB-277011A or NGB 2904 attenuates METH-enhanced BSR in rats, while the METH-enhanced BSR attenuation produced by BP-897 may involve both D 3 and non-D 3 receptors. These findings support a potential use of selective D 3 receptor antagonists for the treatment of METH addiction.

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Parametric analysis of brain stimulation reward in the rat: III. Effect of performance variables on the reward summation function.

Cited by 200 publications

References 8 publications

Cytokine mediation of experimental heart failure-induced anhedonia

Cytokine mediation of experimental heart failure-induced anhedonia

WIN 55,212-2 decreases the reinforcing actions of cocaine through CB1 cannabinoid receptor stimulation

The selective dopamine D3 receptor antagonists SB-277011A and NGB 2904 and the putative partial D3 receptor agonist BP-897 attenuate methamphetamine-enhanced brain stimulation reward in rats

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