Endogenous opioids are necessary for benzodiazepine palatability enhancement: Naltrexone blocks diazepam-induced increase of sucrose-‘liking’

Richardson, Derek; Reynolds, Sheila M.; Cooper, Steven J.; Berridge, Kent

doi:10.1016/j.pbb.2005.05.006

Cited by 33 publications

(15 citation statements)

References 62 publications

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“…Thus, the effects of FG 7142 on feeding microstructure more resemble the effects of a moderate dose of naltrexone (1 mg/kg) (Carrillo et al, 2001) an opioid receptor antagonist whose actions are proposed to result from decrements in the hedonic valuation of food (Cooper and Kirkham, 1993;Li et al, 2003;Kelley et al, 2000Kelley et al, , 2005. Consistent with this parallel in the feeding microstructure mode of action of FG 7142 and naltrexone, recent taste reactivity studies likewise suggest similarity and cross-talk between opioid and GABAergic systems in modulating the hedonic impact of natural taste reward (Richardson et al, 2005). In addition, a very recent study that used a cyclic-ratio operant schedule paradigm similarly found that orexigenic properties of benzodiazepine receptor agonists appeared to be mediated through a mechanism affecting perceived palatability rather than through homeostatic, regulatory effects on food intake (O'Hare et al, 2006).…”

Section: Discussionmentioning

confidence: 91%

“…For example, benzodiazepine receptor agonists increase break points for food reinforcement under progressive-ratio responding schedules, enhance opioid-dependent positive, but not negative, hedonic evaluations in taste reactivity tests, and facilitate food-reinforced incentive learning (Cooper, 2005;Richardson et al, 2005). Conversely, benzodiazepine receptor inverse agonists reduce preference for favored sweet and salty solutions and reduce sham intake of sucrose in gastric-fistulated rats (Cooper, 2005).…”

Section: Introductionmentioning

confidence: 99%

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FG 7142 Specifically Reduces Meal Size and the Rate and Regularity of Sustained Feeding in Female Rats: Evidence that Benzodiazepine Inverse Agonists Reduce Food Palatability

Cottone

Sabino

Steardo

et al. 2006

Neuropsychopharmacol

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Benzodiazepine receptor inverse agonists reduce food intake in males, but their actions in females, in whom stress-related eating disorders are more common, as well as their behavioral mode of action remain unclear. The consummatory effects of benzodiazepine receptor ligands have alternately been hypothesized to reflect changes in the hedonic evaluation of food or secondary effects of anxietyrelated or cognitive properties. To test the anorectic mode of action of benzodiazepine inverse agonists, the effects of FG 7142 on feeding microstructure were studied in nondeprived female Wistar rats (n ¼ 32). Microstructure analysis used a novel meal definition that recognizes prandial drinking. On pharmacologically synchronized diestrus I, rats were pretreated (À30 min dark onset) with the benzodiazepine partial inverse agonist FG 7142 (i.p. 0, 3.75, 7.5, 15 mg/kg) in a between-subjects design. FG 7142 delayed the onset of (16-541%), decreased the amount eaten (36-52%) and drunk (63-87%), and reduced the time spent drinking (59-87%) within the first nocturnal meal. Dose-dependent incremental anorexia continued 6 h into the dark cycle, whereas FG 7142 did not suppress the quantity, duration or rate of drinking past the first meal. Treated rats ate smaller meals (17-42%) of normal duration. This reflected that FG 7142 slowed feeding within meals (9-38%) by decreasing the regularity and maintenance of feeding from pellet-to-pellet. FG 7142 did not influence postprandial satiety; meal frequency and inter-meal intervals were unaffected. FG 7142 anorexia was blocked by the benzodiazepine receptor antagonist flumazenil in a 2:1 molar ratio (n ¼ 17 rats). The very early, nonspecific ( + 10 min), but not subsequent (2.5, 4.5 h) feeding-specific phase, of FG 7142 anorexia was mirrored by anxiogenic-like behavior in FG 7142-treated (7.5 mg/ kg) female rats (n ¼ 48) in the elevated plus-maze. Thus, benzodiazepine receptor inverse agonists preferentially lessen the maintenance of feeding in female rats, effects opposite to those of palatable food.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

FG 7142 Specifically Reduces Meal Size and the Rate and Regularity of Sustained Feeding in Female Rats: Evidence that Benzodiazepine Inverse Agonists Reduce Food Palatability

Cottone

Sabino

Steardo

et al. 2006

Neuropsychopharmacol

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“…In the RDoC Positive Valence system, this aligns with initial responsiveness to reward. Traditionally researchers have focused on the neurotransmitter dopamine (DA) as a primary substrate of liking (Berridge 2004), but more recent research instead suggests that hedonic responses (at least to primary sensory stimuli) seem to be mediated by activation of the opioid and GABA-ergic systems in the nucleus accumbens shell and its projections to the ventral pallidum, as well as in the orbital frontal cortex (OFC) (Richardson et al 2005;Burgdorf and Panksepp 2006;Pecina et al 2006;Smith and Berridge 2007;Berridge et al 2009). For more information on the neurobiology of liking and the role of liking in motivated behaviors, see Robinson et al in this volume. A second component, reward prediction and wanting (component 2 in Fig.…”

Section: Translating Hedonic Experience Into Motivated Behaviormentioning

confidence: 99%

Mechanisms Underlying Motivational Deficits in Psychopathology: Similarities and Differences in Depression and Schizophrenia

Deanna¹,

Pagliaccio²,

Luking³

2015

Current Topics in Behavioral Neurosciences

188

151

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Motivational and hedonic impairments are core aspects of a variety of types of psychopathology. These impairments cut across diagnostic categories and may be critical to understanding major aspects of the functional impairments accompanying psychopathology. Given the centrality of motivational and hedonic systems to psychopathology, the Research Domain Criteria (RDoC) initiative includes a "positive valence" systems domain that outlines a number of constructs that may be key to understanding the nature and mechanisms of motivational and hedonic impairments in psychopathology. These component constructs include initial responsiveness to reward, reward anticipation or expectancy, incentive or reinforcement learning, effort valuation, and action selection. Here, we review behavioral and neuroimaging studies providing evidence for impairments in these constructs in individuals with psychosis versus in individuals with depressive pathology. There are important differences in the nature of reward-related and hedonic deficits associated with psychosis versus depression that have major implications for our understanding of etiology and treatment development. In particular, the literature strongly suggests the presence of impairments in in-the-moment hedonics or "liking" in individuals with depressive pathology, particularly among those who experience anhedonia. Such deficits may propagate forward and contribute to impairments in other constructs that are dependent on hedonic responses, such as anticipation, learning, effort, and action selection. Such hedonic impairments could reflect alterations in dopamine and/or opioid signaling in the striatum related to depression or specifically to anhedonia in depressed populations. In contrast, the literature points to relatively intact in-the-moment hedonic processing in psychosis, but provides much evidence for impairments in other components involved in translating reward to action selection. Particularly, individuals with schizophrenia exhibit altered reward prediction and associated striatal and prefrontal activation, impaired reward learning, and impaired reward-modulated action selection.

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“…24 Instead, hedonic responses (at least to primary sensory stimuli) seem to be mediated by activation of the opioid and gamma amino butyric acidergic systems in the nucleus accumbens shell and its projections to the ventral pallidum as well as in the orbital frontal cortex (OFC). [30][31][32][33] A second component, called ''reward prediction and wanting,'' is thought to be mediated by the midbrain DA system, particularly the projections to ventral and dorsal striatal regions of the basal ganglia. 24,29 Many DA neurons in the substantia nigra and ventral tegmental area respond to stimuli that predict reward as well as to food and liquid rewards themselves.…”

Section: Components Of the Systems Linking Experienced Or Anticipatedmentioning

confidence: 99%

Goal Representations and Motivational Drive in Schizophrenia: The Role of Prefrontal-Striatal Interactions

Deanna

Dowd

2010

Schizophrenia Bulletin

424

325

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The past several years have seen a resurgence of interest in understanding the psychological and neural bases of what are often referred to as ''negative symptoms'' in schizophrenia. These aspects of schizophrenia include constructs such as asociality, avolition (a reduction in the motivation to initiate or persist in goal-directed behavior), and anhedonia (a reduction in the ability to experience pleasure). We believe that these dimensions of impairment in individuals with schizophrenia reflect difficulties using internal representations of emotional experiences, previous rewards, and motivational goals to drive current and future behavior in a way that would allow them to obtain desired outcomes, a deficit that has major clinical significance in terms of functional capacity. In this article, we review the major components of the systems that link experienced and anticipated rewards with motivated behavior that could potentially be impaired in schizophrenia. We conclude that the existing evidence suggests relatively intact hedonics in schizophrenia, but impairments in some aspects of reinforcement learning, reward prediction, and prediction error processing, consistent with an impairment in ''wanting.'' As of yet, there is only indirect evidence of impairment in anterior cingulate and orbital frontal function that may support value and effort computations. However, there are intriguing hints that individuals with schizophrenia may not be able to use reward information to modulate cognitive control and dorsolateral prefrontal cortex function, suggesting a potentially important role for cortical-striatal interactions in mediating impairment in motivated and goal-directed behavior in schizophrenia.

show abstract

Endogenous opioids are necessary for benzodiazepine palatability enhancement: Naltrexone blocks diazepam-induced increase of sucrose-‘liking’

Cited by 33 publications

References 62 publications

FG 7142 Specifically Reduces Meal Size and the Rate and Regularity of Sustained Feeding in Female Rats: Evidence that Benzodiazepine Inverse Agonists Reduce Food Palatability

FG 7142 Specifically Reduces Meal Size and the Rate and Regularity of Sustained Feeding in Female Rats: Evidence that Benzodiazepine Inverse Agonists Reduce Food Palatability

Mechanisms Underlying Motivational Deficits in Psychopathology: Similarities and Differences in Depression and Schizophrenia

Goal Representations and Motivational Drive in Schizophrenia: The Role of Prefrontal-Striatal Interactions

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