Possible role of dopamine D1-like and D2-like receptors in behavioural activation and “contingent” reward evaluation in sodium-replete and sodium-depleted rats licking for NaCl solutions

D’Aquila, Paolo S.; Rossi, Roberta; Rizzi, Antonella; Galistu, Adriana

doi:10.1016/j.pbb.2011.12.004

Cited by 23 publications

(21 citation statements)

References 32 publications

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“…These response patterns are paralleled by similar ones induced by either D2-like (extinction mimicry) or D1-like (different activation level) receptor antagonism [8, 9]. Thus, these observations might bear relevance in relation to the ongoing debate on the role of dopamine on goal-directed behaviour [3, 6, 8, 9, 17, 19, 20, 23–25, 35–39]. Moreover, this contribution to the characterisation of the analysis of licking microstructure might help to better define the experimental measures in behaviourally (and psychologically) meaningful functional terms.…”

Section: Discussionmentioning

confidence: 73%

“…It is worth noting that its effect on the burst number within-session time course is apparent since the very beginning of the sessions, thus differing substantially from the effect of dopamine D2 receptor blockade [8,9]. Consistent results were obtained examining the effect of dopamine D1- and D2-like receptor antagonists in sodium-replete [9, 23–25] and sodium-depleted [23] rats licking for NaCl solutions.…”

Section: Introductionmentioning

confidence: 66%

“…However, very small changes of this parameter had been previously observed in response to experimental manipulations not involving drugs (which can have direct effects on CPG neurons). For example, in rats licking for NaCl solutions, the intra-burst lick rate was influenced by NaCl concentration and by sodium-depletion [23]. It might be worth noting that such effects are very small and have, if any, negligible effects on intake.…”

Section: Discussionmentioning

confidence: 99%

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Within-session decrement of the emission of licking bursts following reward devaluation in rats licking for sucrose

D’Aquila

Galistu

2017

PLoS ONE

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We previously observed that dopamine D2-like receptor blockade in rats licking for sucrose produced a within-session decrement of the emission of licking bursts similar to the effect of either reward devaluation, or neuroleptics, on operant responding for different rewards, which, accordingly, we interpreted as an extinction-like effect. This implies that exposing animals to reward devaluation would result in a drop of burst number taking place only after the contact with the devalued reward. To test this prediction, we compared the difference in the within-session time course of burst number in response to high (10%) versus low (2%) concentration sucrose solutions, either in a condition of reward devaluation (exposure to 2% after daily 10%), or in a condition which does not involve changes in the reward value (two groups of subjects each repeatedly exposed to only one of the two concentrations). Reward devaluation resulted in a within-session decrement of the burst number, with the response rate dropping only after the contact with the devalued reward, as predicted. This response pattern was reliably observed only in subjects at their first devaluation experience. In contrast, exposure of separate groups of animals to the two different concentrations yielded lower levels of burst number in the low concentration group apparent since the beginning of the session, as previously observed with dopamine D1-like receptor blockade. These results show that the analysis of burst number, but not of burst size, reveals a specific activation pattern in response to reward devaluation, which differs from the pattern observed comparing the response to two different sucrose concentrations in separate groups of subjects, i.e. in a condition not involving reward devaluation. Finally, the characterisation of the experimental measures of the analysis of licking microstructure in behaviourally (and psychologically) meaningful functional terms, might be relevant for the investigation of the mechanisms underlying behavioural activation and the related evaluation processes.

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Section: Discussionmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 99%

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Within-session decrement of the emission of licking bursts following reward devaluation in rats licking for sucrose

D’Aquila

Galistu

2017

PLoS ONE

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“…Specifically, sodium depletion substantially elevates the palatability of sodium chloride (assessed using initial lick rate) relative to sodium replete rats (Breslin, Kaplan, Spector, Zambito, Grill, 1993; Breslin, Spector, Grill, 1993; D’Aquila, Rossi, Rizzi, & Galistu, 2012). Similarly, benzodiazepines enhance taste palatability as revealed by increases in both initial rates of licking and lick cluster size (e.g., Higgs & Cooper, 1996, 1997, 1998, 2000).…”

Section: Lick Pattern Analysis and Palatabilitymentioning

confidence: 99%

Conditioned taste aversion, drugs of abuse and palatability

Lin

Arthurs

Reilly

2014

Neuroscience & Biobehavioral Reviews

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LIN, J.-Y., J. Arthurs and S. Reilly. Conditioned taste aversion: Palatability and drugs of abuse. NEUROSCI BIOBEHAV REV XX(x) XXX-XXX, 2014. – We consider conditioned taste aversion to involve a learned reduction in the palatability of a taste (and hence in amount consumed) based on the association that develops when a taste experience is followed by gastrointestinal malaise. The present article evaluates the well-established finding that drugs of abuse, at doses that are otherwise considered rewarding and self-administered, cause intake suppression. Our recent work using lick pattern analysis shows that drugs of abuse also cause a palatability downshift and, therefore, support conditioned taste aversion learning.

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“…AD patients exhibit a loss of dopamine receptors in the olfactory bulb (Loopuijt and Sebens 1990). Dopamine also plays a major role in mediating motor activity (D'Aquila et al 2010;Drucker-Colín and García-Hernández 1991;Stiles et al 2012;Yehuda and Sheleff 1985), eating behaviors The protecting effects of fatty acid treatments from the immunological long term effects of OBX. EFA Essential fatty acid treatment, OBX olfactory bulbectomy.…”

Section: Discussionmentioning

confidence: 99%

Fatty acids rehabilitated long-term neurodegenerative: like symptoms in olfactory bulbectomized rats

Yehuda

Rabinovitz

2014

J Neural Transm

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Our previous study demonstrated that an olfactory bulbectomy in rats induced short-term, multifaceted, devastating Alzheimer's-like effects, which included cognitive impairment, hyperactivity, hyperthermia, and increased levels of homocysteine and pro-inflammatory cytokines, including IL-17A. In addition, the rats exhibited an increase in the hyperphosphorylation of brain Tau proteins and in the number of neurofibrillary tangles. Here, we examined the long-term effects of the surgery and found that olfactory bulbectomy also rendered the rats to become anemic with brain iron overload. Additionally, a significant reduction in the membrane fluidity index in frontal cortex synaptosomes was found. Treatment with a mixture of n - 3/n - 6 of fatty acids restored the unwanted effect. The beneficial effects of fatty acids are mediated via the effects of fatty acids on the neuronal membrane structure and fluidity. These findings are similar to Alzheimer's symptoms, which suggest this model can be used as an animal model for Alzheimer's disease. We recommend using this model to scan potential new anti-Alzheimer's drugs.

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Possible role of dopamine D1-like and D2-like receptors in behavioural activation and “contingent” reward evaluation in sodium-replete and sodium-depleted rats licking for NaCl solutions

Cited by 23 publications

References 32 publications

Within-session decrement of the emission of licking bursts following reward devaluation in rats licking for sucrose

Within-session decrement of the emission of licking bursts following reward devaluation in rats licking for sucrose

Conditioned taste aversion, drugs of abuse and palatability

Fatty acids rehabilitated long-term neurodegenerative: like symptoms in olfactory bulbectomized rats

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