Examinando por Autor "Papini, Mauricio R."
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Ítem Flexible behavioral adjustment to frustrative nonreward in anticipatory behavior, but not in consummatory behavior, requires the dorsal hippocampus.(Wiley-Liss Inc., 2024-09-20) Hagen, Christopher; Hoxha, Megi; Chitale, Saee; White, Andre O.; Ogállar, Pedro; Navarro-Expósito, Alejandro; Agüera, Antonio ; Torres-Bares, Carmen; Papini, Mauricio R.; Sabariego, MartaThe hippocampus (HC) is recognized for its pivotal role in memory-related plasticity and facilitating adaptive behavioral responses to reward shifts. However, the nature of its involvement in the response to reward downshifts remains to be determined. To bridge this knowledge gap, we explored the HC's function through a series of experiments in various tasks involving reward downshifts and using several neural manipulations in rats. In Experiment 1, complete excitotoxic lesions of the HC impaired choice performance in a modified T-maze after reducing the quantity of sugar pellet rewards. In Experiment 2, chemogenetic inhibition of the dorsal HC (dHC) disrupted anticipatory behavior following a food-pellet reward reduction. Experiments 3-5 impaired HC function by using peripheral lipopolysaccharide (LPS) administration. This treatment, which induces peripheral inflammation affecting HC function, significantly increased cytokine levels in the dHC (Experiment 3) and impaired anticipatory choice behavior (Experiment 4). None of these dorsal hippocampal manipulations affected consummatory responses in animals experiencing sucrose downshifts. Accordingly, we found no evidence of increased neural activation in either the dorsal or ventral HC, as measured by c-Fos expression, after a sucrose downshift task involving consummatory suppression (Experiment 6). The results highlight the HC's pivotal role in adaptively modulating anticipatory behavior in response to a variety of situations involving frustrative nonreward, while having no effect on adjustments on consummatory behavior. The data supporting this conclusion were obtained under heterogeneous experimental conditions derived from a multi-laboratory collaboration, ensuring the robustness and high reproducibility of our findings. Spatial orientation, memory update, choice of reward signals of different values, and anticipatory versus consummatory adjustments to reward downshift are discussed as potential mechanisms that could account for the specific effects observed from HC manipulations.Ítem Frustrative nonreward: Detailed c-Fos expression patterns in the amygdala after consummatory successive negative contrast(Academic Press Inc, 2024-05-28) Arjol, David; Agüera, Antonio; Hagen, Christopher; Papini, Mauricio R.The amygdala has been implicated in frustrative nonreward induced by unexpected reward downshifts, using paradigms like consummatory successive negative contrast (cSNC). However, existing evidence comes from experiments involving the central and basolateral nuclei on a broad level. Moreover, whether the amygdala’s involvement in reward downshift requires a cSNC effect (i.e., greater suppression in downshifted animals than in unshifted controls) or just consummatory suppression without a cSNC effect, remains unclear. Three groups were exposed to (1) a large reward disparity leading to a cSNC effect (32-to-2% sucrose), (2) a small reward disparity involving consummatory suppression in the absence of a cSNC effect (8-to-2% sucrose), and (3) an unshifted control (2% sucrose). Brains obtained after the first reward downshift session were processed for c-Fos expression, a protein often used as a marker for neural activation. c-Fos-positive cells were counted in the anterior, medial, and posterior portions (A/P axis) of ten regions of the rat basolateral, central, and medial amygdala. c-Fos expression was higher in 32-to-2% sucrose downshift animals than in the other two groups in four regions: the anterior and the medial lateral basal amygdala, the medial capsular central amygdala, and the anterior anterio-ventral medial amygdala. None of the areas exhibited differential c-Fos expression between the 8-to-2% sucrose downshift and the unshifted conditions. Thus, amygdala activation requires exposure to a substantial reward disparity. This approach has identified, for the first time, specific amygdala areas relevant to understand the cSNC effect, suggesting follow-up experiments aimed at testing the function of these regions in reward downshift.Ítem Ketamine retards recovery from reward downshift and supports conditioned taste aversion(Elsevier Inc., 2023-12-01) Agüera, Antonio ; Cándido, Clara; Donaire, Rocío; Papini, Mauricio R.; Torres-Bares, CarmenKetamine is a noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonist with antidepressant, anxiolytic, and memory effects in clinical and preclinical studies. The present studies investigated the behavioral effects of ketamine in animals exposed to a consummatory successive negative contrast (cSNC) task involving unexpected reward downshift, negative emotion (frustration), and aversive memory. Food-restricted male rats had 5-min access to 32 % sucrose in each of 10 preshift sessions followed by 4 % sucrose in 4 postshift sessions. Unshifted controls had access to 4 % sucrose during all 14 sessions. Ketamine (10 mg/kg, ip) was injected 30 min before sessions 11 and 12 (Experiment 1) or immediately after session 11 (Experiment 3). The results showed that both pre- and postdownshift session injection of ketamine increased consummatory suppression, as Group 32-4/Ket exhibited lower sucrose intake than Groups 32-4/Sal, 4-4/Ket, and 4-4/Sal. These effects extended beyond the day(s) of injection. Experiments 2 and 4 showed that the same dose, route of administration, and time of injection induced significant conditioned taste aversion to 4 % sucrose, in the absence of reward downshift. These data suggest that ketamine induces an aversive state that may summate with frustration induced by reward downshift in the cSNC task and also support a conditioned taste aversion to 4 % sucrose in the absence of reward downshift. Implications for these and other experiments involving pre- and postsession administration of ketamine are discussed.Ítem Surprising reward downshift activates the lateral habenula, but not the medial habenula, as measured in terms of c-fos expression(Elsevier Inc., 2023-10-01) Agüera, Antonio; Navarro-Expósito, Alejandro; Zafra, David; Sabariego, Marta; Papini, Mauricio R.; Torres-Bares, CarmenConvergent results suggest that lateral habenula (LHb) activity reduces reward value and enhances aversive learning. Electrical stimulation of LHb neurons reduces sucrose intake and cocaine/morphine seeking, whereas LHb lesions attenuate taste aversion learning and avoidance of predator odor, retard appetitive extinction, and interfere with appetitive conditioned inhibition training. However, the role of the LHb in consummatory successive negative contrast (cSNC), an animal model of acute anxiety/frustration induced by reward loss, remains unknown. We hypothesized that a surprising reward downshift would enhance activity in the LHb. Three groups of rats received access to sucrose during eleven 5-min sessions. Group 32-2 had access to 32% sucrose for 10 sessions followed by a downshift to 2% sucrose on session 11. Groups 2-2 and 32-32 (unshifted controls) had access to 2% and 32% sucrose, respectively, in each of 11 sessions. After session 11, all animals were perfused and brains were prepared for immunohistochemistry of c-Fos expression, a marker of neuronal depolarization. There was less sucrose consumption on session 11 in Group 32-2 than in Groups 2-2 and 32-32—the cSNC effect (p<0.04). Cell density was elevated in the lateral and medial sections of the LHb in Group 32-2, relative to unshifted groups (ps<0.02). No group differences were observed in the medial habenula (p>0.60). These results suggest that the LHb is involved in the cSNC effect, but its precise function remains to be determined, whether it affects cSNC by detecting the mismatch between obtained and expected rewards (reward relativity) or triggers negative emotion (frustrative nonreward) elicited by the reward loss event. Further studies involving integrated assessment of c-Fos in a wide range of brain regions, including the LHb, may clarify the fit of the LHb activity in the connectome underlying the response to reward downshift.