Analysis of licking microstructure provides no evidence for a reduction in reward value following acute or sub-chronic phencyclidine administration

Lydall, Emma Sian; Gilmour, Gary; Dwyer, Dominic M.

doi:10.1007/s00213-010-1779-x

Cited by 26 publications

(26 citation statements)

References 54 publications

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“…23,36,53,56,70); changes seen occasionally in this parameter are rarely of the magnitude seen here and typically occur with drugs that produce overt motor disturbances (e.g., Refs. 19,20,34), which were not observed in this study with Ex4. That the ILI was affected to such a notable degree by Ex4 suggests that GLP-1-receptor activation might directly or indirectly act on premotor or motoneurons in the brain stem that control oromotor function (see Refs.…”

Section: The Effects Of Glp-1-receptor Modulation On Responsiveness Tcontrasting

confidence: 79%

Roux-en-Y gastric bypass in rats increases sucrose taste-related motivated behavior independent of pharmacological GLP-1-receptor modulation

Mathes

Bueter

Smith

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Roux-en-Y gastric bypass (RYGB) surgery has been shown to decrease consummatory responsiveness of rats to high sucrose concentrations, and genetic deletion of glucagon-like peptide-1 receptors (GLP-1R) has been shown to decrease consummatory responsiveness of mice to low-sucrose concentrations. Here we assessed the effects of RYGB and pharmacological GLP-1R modulation on sucrose licking by chow-fed rats in a brief-access test that assessed consummatory and appetitive behaviors. Rats were tested while fasted presurgically and postsurgically and while nondeprived postsurgically and 5 h after intraperitoneal injections with the GLP-1R antagonist exendin-3(9-39) (30 μg/kg), agonist exendin-4 (1 μg/kg), and vehicle in 30-min sessions during which a sucrose concentration series (0.01-1.0 M) was presented in 10-s trials. Other rats were tested postsurgically or 15 min after peptide or vehicle injection while fasted and while nondeprived. Independent of food-deprivation state, sucrose experience, or GLP-1R modulation, RYGB rats took 1.5-3× as many trials as sham-operated rats, indicating increased appetitive behavior. Under nondeprived conditions, RYGB rats with presurgical sucrose experience licked more to sucrose relative to water compared with sham-operated rats. Exendin-4 and exendin-3(9-39) impacted 0.3 M sucrose intake in a one-bottle test, but never interacted with surgical group to affect brief-access responding. Unlike prior reports in both clearly obese and relatively leaner rats given RYGB and in GLP-1R knockout mice, we found that neither RYGB nor GLP-1R blockade decreased consummatory responsiveness to sucrose in our less obese chow-fed rats. Collectively, these results highlight the fact that changes in taste-driven motivated behavior to sucrose after RYGB and/or GLP-1R modulation are very model and measure dependent.

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Section: The Effects Of Glp-1-receptor Modulation On Responsiveness Tcontrasting

confidence: 79%

Roux-en-Y gastric bypass in rats increases sucrose taste-related motivated behavior independent of pharmacological GLP-1-receptor modulation

Mathes

Bueter

Smith

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Recently, Lydall and colleagues showed that sub-chronic treatment with PCP does not reduce the value of a reward which is of high value for rats (sucrose) (Lydall et al, 2010). They conclude (as do we, reviewed in Neill et al 2014) that scPCP does not induce anhedonia per se.…”

Section: Discussionmentioning

confidence: 85%

“…We have demonstrated that these deficits are reversed by several novel targets and low doses of atypical antipsychotics (Grayson et al 2015, Neill et al 2010, 2014. When it comes to investigating negative symptoms, we and others have shown that sc PCP induces social withdrawal but not anhedonia in rodents (Lydall et al, 2010;Neill et al, 2014) with the growing consensus that anhedonia per se. is not a feature of negative symptoms (Barnes et al, 2014a;Foussias et al, 2014) lending further support for the validity of this model.…”

Section: Introductionmentioning

confidence: 95%

Towards the development of improved tests for negative symptoms of schizophrenia in a validated animal model

Şahin

Doostdar

Neill

2016

Behavioural Brain Research

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Negative symptoms in schizophrenia remain an unmet clinical need. There is no licensed treatment specifically for this debilitating aspect of the disorder and effect sizes of new therapies are too small to make an impact on quality of life and function. Negative symptoms are multifactorial but often considered in terms of two domains, expressive deficit incorporating blunted affect and poverty of speech and avolition incorporating asociality and lack of drive. There is a clear need for improved understanding of the neurobiology of negative symptoms which can be enabled through the use of carefully validated animal models. While there are several tests for assessing sociability in animals, tests for blunted affect in schizophrenia are currently lacking. Two paradigms have recently been developed for assessing negative affect of relevance to depression in rats. Here we assess their utility for studying negative symptoms in schizophrenia using our well validated model for schizophrenia of sub-chronic (sc) treatment with Phencyclidine (PCP) in adult female rats. Results demonstrate that sc PCP treatment produces a significant negative affect bias in response to a high value reward in the optimistic and affective bias tests. Our results are not easily explained by the known cognitive deficits induced by sc PCP and support the hypothesis of a negative affective bias in this model. We suggest that further refinement of these two tests will provide a means to investigate the neurobiological basis of negative affect in schizophrenia, thus supporting the assessment of efficacy of new targets for this currently untreated symptom domain.

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“…It has been suggested that assays of licking microstructure can reveal changes in reward. However, this is not always the case, as neuroleptic drugs, such as PCP, cause anhedonia in humans, but do not change lick microstructure during sucrose intake in animals, at doses that do not cause motor impairment 30 . The design of our choice assay is based on the neuroeconomic principle that, if animals choose between two options that require the same of work, the option chosen provides a measure of the value of that option 9,31,32 .…”

Section: Discussionmentioning

confidence: 99%

Leptin regulates the reward value of nutrient

et al. 2011

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We developed an assay for quantifying the reward value of nutrient and used it to analyze the effects of metabolic state and leptin. In this assay, mice chose between two sippers, one of which dispensed water and was coupled to optogenetic activation of dopaminergic (DA) neurons and the other of which dispensed natural or artificial sweeteners. This assay measured the reward value of sweeteners relative to lick-induced optogenetic activation of DA neurons. Mice preferred optogenetic stimulation of DA neurons to sucralose, but not to sucrose. However, the mice preferred sucralose plus optogenetic stimulation versus sucrose. We found that food restriction increased the value of sucrose relative to sucralose plus optogenetic stimulation, and that leptin decreased it. Our data suggest that leptin suppresses the ability of sucrose to drive taste-independent DA neuronal activation and provide new insights into the mechanism of leptin's effects on food intake.

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Analysis of licking microstructure provides no evidence for a reduction in reward value following acute or sub-chronic phencyclidine administration

Cited by 26 publications

References 54 publications

Roux-en-Y gastric bypass in rats increases sucrose taste-related motivated behavior independent of pharmacological GLP-1-receptor modulation

Roux-en-Y gastric bypass in rats increases sucrose taste-related motivated behavior independent of pharmacological GLP-1-receptor modulation

Towards the development of improved tests for negative symptoms of schizophrenia in a validated animal model

Leptin regulates the reward value of nutrient

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