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Anxiolytic Treatment Impairs Helping Behavior in Rats.

ABSTRACT: Despite decades of research with humans, the biological mechanisms that motivate an individual to help others remain poorly understood. In order to investigate the roots of pro-sociality in mammals, we established the helping behavior test, a paradigm in which rats are faced with a conspecific trapped in a restrainer that can only be opened from the outside. Over the course of repeated test sessions, rats exposed to a trapped cagemate learn to open the door to the restrainer, thereby helping the trapped rat to escape (Ben-Ami Bartal et al., 2011). The discovery of this natural behavior provides a unique opportunity to probe the motivation of rodent helping behavior, leading to a deeper understanding of biological influences on human pro-sociality. To determine if an affective response motivates door-opening, rats receiving midazolam, a benzodiazepine anxiolytic, were tested in the helping behavior test. Midazolam-treated rats showed less helping behavior than saline-treated rats or rats receiving no injection. Yet, midazolam-treated rats opened a restrainer containing chocolate, highlighting the socially specific effects of the anxiolytic. To determine if midazolam interferes with helping through a sympatholytic effect, the peripherally restricted beta-adrenergic receptor antagonist nadolol was administered; nadolol did not interfere with helping. The corticosterone response of rats exposed to a trapped cagemate was measured and compared to the rats' subsequent helping behavior. Rats with the greatest corticosterone responses showed the least helping behavior and those with the smallest responses showed the most consistent helping at the shortest latency. These results are discussed in terms of their implications for the interaction between stress and pro-social behavior. Finally, we observed that door-opening appeared to be reinforcing. A novel analytical tool was designed to interrogate the pattern of door-opening for signs that a rat's behavior on one session influenced his behavior on the next session. Results suggest that helping a trapped rat has a greater motivational value than does chocolate. In sum, this series of experiments clearly demonstrates the fundamental role of affect in motivating pro-social behavior in rodents and the need for a helper to resonate with the affect of a victim.

SUBMITTER: Ben-Ami Bartal I

PROVIDER: S-EPMC4896909 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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Anxiolytic Treatment Impairs Helping Behavior in Rats.

Ben-Ami Bartal Inbal I Shan Haozhe H Molasky Nora M R NM Murray Teresa M TM Williams Jasper Z JZ Decety Jean J Mason Peggy P

Frontiers in psychology 20160608

Despite decades of research with humans, the biological mechanisms that motivate an individual to help others remain poorly understood. In order to investigate the roots of pro-sociality in mammals, we established the helping behavior test, a paradigm in which rats are faced with a conspecific trapped in a restrainer that can only be opened from the outside. Over the course of repeated test sessions, rats exposed to a trapped cagemate learn to open the door to the restrainer, thereby helping the ...[more]

PMID: 27375528

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Project description:Empathy is the ability to (a) be affected by and share the emotional state of another; (b) assess the reasons for the other's state; and (c) identify with the other, adopting their perspective. This phenomenon has been shown to exist in several species and is proposed as a motivator for prosocial behavior. The experimental study of this feature in laboratory rodents is a more viable alternative in comparison to wild animals. A recent report showed that rats opened a door to free their cage mate from a restraint box. Although this behavior has been suggested to be motivated by empathy, this fact has been questioned by several studies that proposed other motivators for the releasing behavior. In the present study, we use an adaptation of the protocol of releasing behavior to investigate aspects of empathy and pro-sociality such as familiarity and reciprocity. In addition, we addressed some potential motivational factors that could influence this behavior. The main results showed that (1) rats opened the restraint box to free conspecifics most of the time; (2) direct reciprocity or past restriction experience did not improve releasing performance, probably due to a ceiling effect; (3) after a series of trials in the presence of a restricted conspecific, the free rat continues to open the restraint box even if it is empty; (4) in general, the opening performance improves across trials and phases, resembling learning curves; (5) if the first series of trials occurs with the empty box, the opening behavior does not occur and is modest in subsequent trials with a trapped animal; (6) the exploratory drive toward the restraint box and desire for social contact do not seem to function as key motivators for releasing behavior. In conclusion, our findings do not support that the opening behavior is exclusively related to empathic motivation. While multiple factors might be involved, our study suggests that task learning triggered (and possibly reinforced) by the presence of the restricted rat can function as a motivator. Further investigations are required to fully understand the mechanisms and motivation factors guiding the releasing behavior.

Project description:Anxiety is evoked by a threatening situation and display adaptive or defensive behaviors, found similarly in animals and humans. Neuropeptide Y (NPY) Y1 receptor (NPYY1R) and Galanin (GAL) receptor 2 (GALR2) interact in several regions of the limbic system, including the amygdala. In a previous study, GALR2 enhanced NPYY1R mediated anxiolytic actions on spatiotemporal parameters in the open field and elevated plus maze, involving the formation of GALR2/NPYY1R heteroreceptor complexes in the amygdala. Moreover, the inclusion of complementary ethological parameters provides a more comprehensive profile on the anxiolytic effects of a treatment. The purpose of the current study is to evaluate the anxiolytic effects and circuit activity modifications caused by coactivation of GALR2 and NPYY1R. Ethological measurements were performed in the open field, the elevated plus-maze and the light-dark box, together with immediate early gene expression analysis within the amygdala-hypothalamus-periaqueductal gray (PAG) axis, as well as in situ proximity ligation assay (PLA) to demonstrate the formation of GALR2/NPYY1R heteroreceptor complexes. GALR2 and NPYY1R coactivation resulted in anxiolytic behaviors such as increased rearing and head-dipping, reduced stretch attend postures and freezing compared to single agonist or aCSF injection. Neuronal activity indicated by cFos expression was decreased in the dorsolateral paracapsular intercalated (ITCp-dl) subregion of the amygdala, ventromedial hypothalamic (VMH) nucleus and ventrolateral part of the periaqueductal gray (vlPAG), while increased in the perifornical nucleus of the hypothalamus (PFX) following coactivation of GALR2 and NPYY1R. Moreover, an increased density of GALR2/NPYY1R heteroreceptor complexes was explicitly observed in ITCp-dl, following GALR2 and NPYY1R coactivation. Besides, knockdown of GALR2 was found to reduce the density of complexes in ITCp-dl. Taken together, these results open up the possibility that the increased anxiolytic activity demonstrated upon coactivation of NPYY1R and GALR2 receptor was related to actions on the ITCp-dl. GALR2-NPYY1R heteroreceptor complexes may inhibit neuronal activity, by also modifying the neuronal networks of the hypothalamus and the PAG. These results indicate that GALR2/NPYY1R interactions in medial paracapsular intercalated amygdala can provide a novel integrative mechanism in anxiolytic behavior and the basis for the development of heterobivalent agonist drugs targeting GALR2/NPYY1R heteromers, especially in the ITCp-dl of the amygdala for the treatment of anxiety.

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Anxiolytic Treatment Impairs Helping Behavior in Rats.

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Anxiolytic Treatment Impairs Helping Behavior in Rats.

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