Deficits In Social Motivation Research Articles

The Relevance of Animal Models of Social Isolation and Social Motivation for Understanding Schizophrenia: Review and Future Directions.

Social dysfunction in schizophrenia includes symptoms of withdrawal and deficits in social skills, social cognition, and social motivation. Based on the course of illness, with social withdrawal occurring prior to psychosis onset, it is likely that the severity of social withdrawal/isolation contributes to schizophrenia neuropathology. We review the current literature on social isolation in rodent models and provide a conceptual framework for its relationship to social withdrawal and neural circuit dysfunction in schizophrenia. We next review preclinical tasks of social behavior used in schizophrenia-relevant models and discuss strengths and limitations of existing approaches. Lastly, we consider new effort-based tasks of social motivation and their potential for translational studies in schizophrenia. Social isolation rearing in rats produces profound differences in behavior, pharmacologic sensitivity, and neurochemistry compared to socially reared rats. Rodent models relevant to schizophrenia exhibit deficits in social behavior as measured by social interaction and social preference tests. Newer tasks of effort-based social motivation are being developed in rodents to better model social motivation deficits in neuropsychiatric disorders. While experimenter-imposed social isolation provides a viable experimental model for understanding some biological mechanisms linking social dysfunction to clinical and neural pathology in schizophrenia, it bypasses critical antecedents to social isolation in schizophrenia, notably deficits in social reward and social motivation. Recent efforts at modeling social motivation using effort-based tasks in rodents have the potential to quantify these antecedents, identify models (eg, developmental, genetic) that produce deficits, and advance pharmacological treatments for social motivation.

Associations between resting-state neural connectivity and positive affect in social anxiety disorder.

Social anxiety disorder (SAD) has been characterized by deficits in social motivation and lack of reactivity to pleasurable stimuli (i.e., positive affect; [PA]). Recent neuroimaging work has shifted toward examining positively valenced motivational systems in SAD focused on reward responses. However, little is known about the associations of reward connectivity and PA in individuals with SAD. As such, the purpose of the current study was to determine whether connectivity among key units of reward neurocircuitry meaningfully relate to PA and whether these key units are more heterogeneous in SAD as compared to controls. Thirty-one participants who met diagnostic criteria for SAD and 33 control participants were included (Mage = 24.8, SD = 6.9; 55% cisgender man). Seed-based timeseries correlations were conducted in NiTime to extract region of interest (ROI) coupling correlation strength values. ANOVAs were carried out to assess whether individuals with SAD differed in ROI-to-ROI connectivity strength as compared to controls. Correlations and variance analyses were also conducted to examine the relationship between ROI-to-ROI connectivity strength and PA, as well as heterogeneity in connectivity strength and PA expression. Weaker connectivity between the left and right orbital frontal cortex was observed when comparing the SAD to the control group. Within the SAD group, PA was associated with several reward-related ROI couplings; however, these links were not observed among controls. Results further demonstrated that individuals with SAD had significantly more variability in reward connectivity strength as compared to controls. Overall, these results provide emergent evidence for the association between reward regions and PA in individuals with SAD. Additionally, these findings show that individuals with SAD demonstrate greater heterogeneity in reward connectivity.

Social motivation in infancy is associated with familial recurrence of ASD.

Pre-diagnostic deficits in social motivation are hypothesized to contribute to autism spectrum disorder (ASD), a heritable neurodevelopmental condition. We evaluated psychometric properties of a social motivation index (SMI) using parent-report item-level data from 597 participants in a prospective cohort of infant siblings at high and low familial risk for ASD. We tested whether lower SMI scores at 6, 12, and 24 months were associated with a 24-month ASD diagnosis and whether social motivation's course differed relative to familial ASD liability. The SMI displayed good internal consistency and temporal stability. Children diagnosed with ASD displayed lower mean SMI T-scores at all ages and a decrease in mean T-scores across age. Lower group-level 6-month scores corresponded with higher familial ASD liability. Among high-risk infants, strong decline in SMI T-scores was associated with 10-fold odds of diagnosis. Infant social motivation is quantifiable by parental report, differentiates children with versus without later ASD by age 6 months, and tracks with familial ASD liability, consistent with a diagnostic and susceptibility marker of ASD. Early decrements and decline in social motivation indicate increased likelihood of ASD, highlighting social motivation's importance to risk assessment and clarification of the ontogeny of ASD.

Social motivation deficits in individuals with autism spectrum disorders

<p id=p00005>Autism spectrum disorder (ASD) is a neurodevelopmental disorder that originated from childhood, social deficits are core symptoms of ASD. Previous studies, from a information processing perspective, proposed that a deficit in social cognitive is the cause of social impairment. However, research showed that the lack of cognitive ability was not the only reason for the social deficits of individuals with ASD, but also closely related to the social motivation deficits. Social motivation theory suggests that social motivation deficits exist in the early life of individuals with ASD and affect their subsequent development. Studying the social motivation of individuals with ASD is of great value to explain the causes of their social deficits and find the direction of intervention in the future. Therefore, this study summarizes the specific behaviors and internal and external influencing factors of social motivation deficits in individuals with ASD. In the future, it is important to comprehensively consider these factors, to strengthen the integrated research on the social motivation theory of individuals with ASD, so as to accurately understand the social motivation deficits of individuals with ASD. <br/>Social motivation theory suggests that social motivation is a powerful driving force to guide individual’s social behavior. The theory also highlights that social behavior is mainly manifested in social orientation, social reward and social maintenance, so this paper firstly summarizes the related researches on the behavioral level of social motivation deficits in individuals with ASD, which are mainly reflected in the following three aspects: (1) The results of social orientation research show that individuals with ASD often show impaired attention to social stimuli, reduced direct gaze on the face, reduced gaze on the eyes, etc. On the one hand, this deficit is related to their abnormal face processing strategies; on the other hand, they may have difficulties in representing the intrinsic reward value of social stimuli; (2) The results of social reward research show that social reward stimulation has no significant incentive effect on individuals with ASD. They lack the ability to experience the happiness of social interaction, cant get happiness from interaction and lack the desire to help others, which is related to the abnormality of reward processing system (amygdala, ventral striatum, prefrontal cortex and other brain regions). (3) The results of social maintenance research show that individuals with ASD have few social maintenance strategies, they are not good at maintaining social relationships with others, do not actively show their own advantages, do not actively imitate others, and lack the desire and motivation to establish and maintain good relationships with others. <br/>Finally, because the research conclusions of social motivation deficits in individual with ASD are not completely consistent, this paper comprehensively and systematically analyzes the influencing factors of social motivation deficits, and finds that it includes internal factors and external factors. The internal factors are mainly reflected in individuals age, gender and physiological mechanism, while the external factors are mainly reflected in social communication environment, experimental stimulus materials, difficulty and nature of experimental tasks. In order to improve the credibility and effectiveness of the research on the social motivation of individuals with ASD, and fully and accurately grasp the characteristics of social motivation in individuals with ASD, in the future, it is important to study the social motivation deficits of individuals with ASD of different ages and genders, to optimize the experimental tasks, broaden the types of materials, further improve the experimental design, and to strengthen the integrated research on the social motivation theory of individuals with ASD, deeply explore the relationship among the behavioral, biological and evolutionary levels under this theory, and further analyze the relationship among the three behaviors of social motivation(social orientation, social reward and social maintenance).

Potential early identification markers for children with autism spectrum disorder: Unusual vocalizations and theoretical explanations

<p id=C10>Early identification and intervention of children with autism spectrum disorder (ASD) are critical to their developmental outcomes. Vocalizations are sounds produced by children before they learn to talk. These can be divided into two categories: nonspeech-like and speech-like. Speech-like vocalizations include consonant and vowel sounds. Nonspeech-like vocalizations are natural, vegetative sounds that do not resemble speech. The common analysis indicators of nonspeech-like vocalizations in children with ASD are fundamental frequency, pause length, and duration of crying. Commonly used analytical indicators for speech-like vocalizations are vocal complexity and vocal communication. <p id=C11>Compared with typically developing children, those with ASD display a higher fundamental frequency of crying, yet shorter pauses in its length and duration. Atypical crying may represent an early biomarker for children with ASD that aids in early detection. The complexity of speech-like vocalizations in children with ASD is unusual and manifests as a lower or higher vocal complexity than those with typical development. Unusual vocal complexity appears to be a potentially useful indicator of emergent ASD, especially high vocal complexity, which may be an early identification marker for regression in children with ASD. When compared to typically developing children, children with ASD display low rates of vocal communication production, which may also be a useful early identification marker for the presence of ASD. <p id=C12>The theoretical explanations for unusual vocalizations mainly include: motivation orientation theories, neuromotor orientation theories, perceptual orientation theory, and social feedback orientation theory. In motivation orientation theories, potential sources of variation in vocal complexity are strong intrinsic motivation of special interests and social motivation deficits. The social motivation deficits may also lead to less communicative vocalizations in children with ASD. According to neuromotor orientation theories, the immaturity or disorder of nerves leads to atypical vocal complexity in children with ASD. The delay in the development of sitting posture limits the acquisition of speech-like vocalizations in children with ASD. Damage to the vagal cranial nerve complex leads to higher fundamental frequency, shorter pauses between cry episodes of crying, and shorter crying episodes in children with ASD. The perceptual orientation theory suggests that atypical auditory processing of speech sound stimuli in children with ASD makes them unable to learn speech-like vocalizations, affecting the development of vocal complexity. Social feedback orientation theory proposes that the effectiveness of the social feedback loop of children with ASD is reduced. Thus, if the number of iterations of the social feedback loop decreases, their speech-like vocalizations are further reduced. <p id=C13>Future research may consider in (1) exploring the possibility of unusual vocalizations as unique early identification markers for children with ASD, (2) strengthening the study of crying in early screening of children with ASD, (3) constructing an automatic learning classification model based on the strongest predictive acoustic parameters, (4) analyzing the influence of intrinsic and social motivation on speech-like vocalizations in children with ASD, and (5) investigating the neural mechanisms of unusual speech-like vocalizations. These evidence may be helpful for early identification and intervention of children with ASD.

Mu-opioid receptor agonism differentially alters social behaviour and immediate early gene expression in male adolescent rats prenatally exposed to valproic acid versus controls

Mu-opioid receptors (MOPs) mediate and modulate social reward and social interaction. However, few studies have examined the functionality of this system in rodent models of social impairment. Deficits in social motivation and cognition are observed in rodents following pre-natal exposure to the anti-epileptic valproic acid (VPA), however it is not known whether MOP functionality is altered in these animals. The present study examined the effects of acute administration of the prototypical MOP agonist morphine (1 mg/kg) on social behavioural responding in the 3-chamber test and immediate early gene expression in adolescent rats (postnatal day 28–43) prenatally exposed to VPA vs saline-exposed controls. Pharmacokinetic analysis of morphine concentration, MOP binding and expression were also examined. The data revealed that sociability and social novelty preference in the 3-chamber test were reduced in rats prenatally exposed to VPA compared to saline-exposed control counterparts. Morphine reduced both sociability and social novelty preference behaviour in saline-, but not VPA-, exposed rats. Analysis of immediate early gene expression revealed that morphine reduced the expression of cfos in the prefrontal cortex of both saline- and VPA-exposed rats and reduced expression of cfos and junb in the hippocampus of VPA-exposed rats only. Pharmacokinetic analysis revealed similar concentrations of morphine in the plasma and brain of both saline- and VPA-exposed rats and similar thalamic MOP occupancy levels. Gene and protein expression of MOP in prefrontal cortex and hippocampus did not differ between saline and VPA-exposed rats. These data indicate differential effects of morphine on social responding and immediate early gene expression in the hippocampus of VPA-exposed rats compared with saline-exposed controls. This study provides support for altered MOP functionality in rats prenatally exposed to VPA, which may underlie the social deficits observed in the model.

Contribution of growth hormone secretagogue receptor (GHSR) signaling in the ventral tegmental area (VTA) to the regulation of social motivation in male mice

Most psychiatric disorders are characterized by deficits in the ability to interact socially with others. Ghrelin, a hormone normally associated with the regulation of glucose utilization and appetite, is also implicated in the modulation of motivated behaviors including those associated with food and sex rewards. Here we hypothesized that deficits in ghrelin receptor (growth hormone secretagogue receptor; GHSR) signaling are also associated with deficits in social motivation in male mice. To test this hypothesis, we compared social motivation in male mice lacking GHSR or mice treated with the GHSR antagonist JMV2959 with that of WT or vehicle-treated mice. GHSR signaling in dopamine cells of the ventral tegmental area (VTA) has been implicated in the control of sexual behavior, thus we further hypothesized that GHSR signaling in the VTA is important for social motivation. Thus, we conducted studies where we delivered JMV2959 to block GHSR in the VTA of mice, and studies where we rescued the expression of GHSR in the VTA of GHSR knockout (KO) mice. Mice lacking GHSR or injected with JMV2959 peripherally for 3 consecutive days displayed lower social motivation as reflected by a longer latency to approach a novel conspecific and shorter interaction time compared to WT or vehicle-treated controls. Furthermore, intra-VTA infusion of JMV2959 resulted in longer latencies to approach a novel conspecific, whereas GHSR KO mice with partial rescue of the GHSR showed decreased latencies to begin a novel social interaction. Together, these data suggest that GHSR in the VTA facilitate social approach in male mice, and GHSR-signaling deficits within the VTA result in reduced motivation to interact socially.

Sex-dependent and ontogenetic effects of low dose ethanol on social behavioral deficits induced by mouse maternal separation

Early life stress can induce lifelong emotional and social behavioral deficits that may in some cases be alleviated by drugs or alcohol. A model for early life stress, rodent maternal separation, recapitulates these behavioral sequelae, which are not limited to potentiated anxiety-like behavior, attenuated social motivation, and altered reward-seeking. Here we employed mouse maternal separation with early weaning (MSEW), consisting of pup-dam separation lasting 4–8 hours on postnatal days (PD) 2–16, with early weaning on PD 17. Prior MSEW studies have limited subjects by age or sex, so we more comprehensively investigated MSEW effects in both sexes, during adolescence and adulthood. We found universal effects of MSEW to include lifelong enhancement of anxiety-like and despair behavior, as well as deficits in social motivation. We also observed some sex-dependent effects of MSEW, namely that female MSEW mice exhibited social habituation to a greater degree than their male counterparts. Low dose ethanol administration had no major effects on the social behavior of non-stressed mice. But interestingly, MSEW-induced social habituation was counteracted by low dose ethanol in adolescent female mice, and potentiated in adolescent male mice. These effects were absent in adult animals, suggesting that ethanol may exert differential effects on the developing brain in such a manner to produce age-, sex-, and stress-dependent effects upon social behavior. Together, results indicate that MSEW reliably produces long-lasting impairments in emotional and social behaviors in both sexes and across the lifespan, but may exert more salient social behavioral effects on female animals.

People with schizophrenia do not show the normal benefits of social versus nonsocial attentional cues.

Schizophrenia is associated with impairments in social motivation. Social attention has been proposed as an underlying mechanism for social motivation. However, studies in schizophrenia have rarely examined social attention, and none of these studies examined the effects with rapidly presented stimuli. The current study examined whether individuals with schizophrenia have reduced social attention and whether reduced social attention was related to social motivation deficits (measured with the Clinical Assessment Interview for Negative Symptoms) and decreased social functioning (Role Functioning Scale). Thirty-seven outpatients with schizophrenia and 29 healthy participants completed a gaze cueing task with directional social cues (eye gaze) and nonsocial cues (arrows) at varying stimulus onset asynchronies. As predicted, schizophrenia participants had reduced social attention relative to nonsocial attention, compared with healthy participants. Healthy participants were quicker to respond to social cues than nonsocial cues, but schizophrenia participants did not exhibit this same pattern. Schizophrenia participants showed higher accuracy when targets appeared in the same location as a directional cue (i.e., congruency) for nonsocial, but not social, cues. Contrary to expectations, reduced social attention was not significantly correlated with clinically rated social motivation deficits or decreased social functioning in the schizophrenia group. These findings provide evidence for social attention deficits in schizophrenia, but without a clear mapping of its influence on social motivation. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Learning the Affective Value of Others in Schizophrenia: Examining the Role of Negative Symptoms and Cognitive Deficits

Prior research has examined the hypothesis that negative symptoms, such as anhedonia and lack of motivation, are caused by impaired memory for positive or rewarding experiences. Results have been inconsistent and less work has examined memory for socially-relevant information. The current study employed a repeated measures design to assess immediate and delayed recall of valenced material among 50 individuals with schizophrenia or schizoaffective disorder and 25 demographically-matched controls. We examined the contribution of negative symptoms and cognitive deficits to the recall of positive material on two different tasks: 1) recall for valenced words and 2) the associative learning of valenced social acts paired with facial stimuli. Results indicated that for the word list recall task, individuals with schizophrenia recalled fewer negative words during the immediate recall phase than controls. On the social affective learning task, individuals with schizophrenia, compared to controls, demonstrated poorer learning of positive social behavior associations. Within individuals with schizophrenia, cognitive impairment, but not symptoms, was related to poorer performance on both tasks. In controls, symptoms reflecting deficits in social motivation and pleasure (but not cognitive functioning) were associated with poorer performance in learning associations with positive social behaviors on the affective learning task. Findings suggest that poor learning and recall of positive information in schizophrenia is particularly salient for social stimuli and that reduced recall of social information in schizophrenia is related to general cognitive ability but not negative symptoms. Implications for findings and future directions are discussed.

Grant Report on Social Reward Learning in Schizophrenia †.

We report on the ongoing R21 project “Social Reward Learning in Schizophrenia”. Impairments in social cognition are a hallmark of schizophrenia. However, little work has been done on social reward learning deficits in schizophrenia. The overall goal of the project is to assess social reward learning in schizophrenia. A probabilistic reward learning (PRL) task is being used in the MRI scanner to evaluate reward learning to negative and positive social feedback. Monetary reward learning is used as a comparison to assess specificity. Behavioral outcomes and brain areas, included those involved in reward, are assessed in patients with schizophrenia or schizoaffective disorder and controls. It is also critical to determine whether decreased expected value (EV) of social stimuli and/or reward prediction error (RPE) learning underlie social reward learning deficits to inform potential treatment pathways. Our central hypothesis is that the pattern of social learning deficits is an extension of a more general reward learning impairment in schizophrenia and that social reward learning deficits critically contribute to deficits in social motivation and pleasure. We hypothesize that people with schizophrenia will show impaired behavioral social reward learning compared to controls, as well as decreased ventromedial prefrontal cortex (vmPFC) EV signaling at time of choice and decreased striatal RPE signaling at time of outcome, with potentially greater impairment to positive than negative feedback. The grant is in its second year. It is hoped that this innovative approach may lead to novel and more targeted treatment approaches for social cognitive impairments, using cognitive remediation and/or brain stimulation.

Dynamic functional connectivity analysis reveals decreased variability of the default-mode network in developing autistic brain.

Accumulating neuroimaging evidence suggests that abnormal functional connectivity of the default mode network (DMN) contributes to the social-cognitive deficits of autism spectrum disorder (ASD). Although most previous studies relied on conventional functional connectivity methods, which assume that connectivity patterns remain constant over time, understanding the temporal dynamics of functional connectivity during rest may provide new insights into the dysfunction of the DMN in ASD. In this work, dynamic functional connectivity analysis based on sliding time window correlation was applied to the resting-state functional magnetic resonance imaging data of 28 young children with ASD (age range: 3-7 years) and 29 matched typically developing controls (TD group). In addition, k-means cluster analysis was performed to identify distinct temporal states based on the spatial similarity of each functional connectivity pattern. Compared with the TD group, young children with ASD showed decreased dynamic functional connectivity variance between the posterior cingulate cortex (PCC) and the right precentral gyrus, which is negatively correlated with social motivation and social relating. Cluster analysis revealed significant differences in functional connectivity patterns between the ASD and TD groups in discrete temporal states. Our findings reveal that atypical dynamic interactions between the PCC and sensorimotor cortex are associated with social deficits in ASD. Results also highlight the critical role of PCC in the social-cognitive deficits of ASD and support the concept that understanding the dynamic neural interactions among brain regions can provide insights into functional abnormalities in ASD. Autism Research 2018, 11: 1479-1493. © 2018 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: Social cognitive dysfunction in autism spectrum disorder (ASD) is associated with dysfunction of the default mode network (DMN), a set of brain areas involved in various domains of social processing. We found that decreases in the dynamic functional connectivity variance between the posterior cingulate cortex and the sensorimotor cortex are associated with deficits in social motivation and social relating in young children with ASD. This result suggests that aberrations in the DMN and its dynamic interactions with other networks contribute to atypical integration of information with respect to self and others.

Lack of Privileged Access to Awareness for Rewarding Social Scenes in Autism Spectrum Disorder

Reduced social motivation is hypothesised to underlie social behavioural symptoms of Autism Spectrum Disorder (ASD). The extent to which rewarding social stimuli are granted privileged access to awareness in ASD is currently unknown. We use continuous flash suppression to investigate whether individuals with and without ASD show privileged access to awareness for social over nonsocial rewarding scenes that are closely matched for stimulus features. Strong evidence for a privileged access to awareness for rewarding social over nonsocial scenes was observed in neurotypical adults. No such privileged access was seen in ASD individuals, and moderate support for the null model was noted. These results suggest that the purported deficits in social motivation in ASD may extend to early processing mechanisms.

Social motivation in patients with schizophrenia spectrum disorders: how it is recognized in the rehabilitation process

The practice of psychosocial intervention for schizophrenia patients is dominated by cognitive–behavioural techniques. There is good justification for this on the basis of the empirical evidence, which speaks in favour of the efficacy of these approaches. Deficits in neurocognition and poor social skills in patients are considered the main targets of psychiatric rehabilitation programmes. However, there are research findings that suggest that distorted social motivation in the form of social anhedonia affects social cognition in schizophrenia patients. The authors describe a compound model of social cognition that includes its motivational component. The model rests on methodological assumptions of the Vygotskian Cultural-Historical Theory of Development, including that of the unity of intellectual and affective processes. The authors review the history of research into cognitive deficits in schizophrenia based on this assumption, and also the most recent empirical evidence confirming that social anhedonia contributes significantly to the impaired social cognition in schizophrenia. The authors conclude that rehabilitation programmes for schizophrenia patients must include psychosocial interventions focused on the remediation of social cognition impairment by means of techniques targeting the remediation of social motivation deficits.

Sustained opioid antagonism modulates striatal sensitivity to baby schema in opioid use disorder

BackgroundChronic opioid misuse is associated with reduced sensitivity to natural rewards and social motivation deficits that include impaired caregiving. The neurobiological mechanisms underlying these deficits and their response to treatment are not well understood. Baby schema (Kindchenschema) is a set of juvenile physical features, which is perceived as “cute” and triggers motivation for caregiving. Recent studies suggest that the “baby schema effect” is mediated by the brain “reward” network. We studied the impact of opioid antagonist treatment on the baby schema response in patients with opioid use disorder. MethodsForty-seven (24 F) recently detoxified patients with opioid use disorder underwent functional magnetic resonance imaging (fMRI) while viewing infant portraits that were parametrically manipulated for baby schema content and rating them for cuteness, at baseline and during treatment with the injectable extended release opioid antagonist naltrexone (XRNTX). The study was not placebo-controlled. ResultsThe behavioral effect of baby schema, indexed by “cuteness” ratings, was present and unaffected by XRNTX. The brain response to baby schema was absent at baseline, but present in the bilateral ventral striatum after two weeks of XRNTX treatment. The decline in self-reported craving for opioids was positively correlated with the brain fMRI response to baby schema in the bilateral ventral striatum. ConclusionsOpioid antagonist treatment modulated the brain reward system response to a marker of caregiving motivation in patients with opioid use disorder. Neural response to baby schema may offer a novel probe of social motivation and affiliative behaviors in this population.

Social motivation and implicit theory of mind in children with autism spectrum disorder.

The goal of the present study was to examine the link between poor attention to social information and mindreading abilities in children with autism spectrum disorder (ASD). Results demonstrated that children with ASD tended to perform worse than neurotypical children on both social orienting and theory of mind tasks. Preference for human faces and motion tended to be related but only for the neurotypical children. These findings provide partial support for the social motivation theory.

Adult forebrain NMDA receptors gate social motivation and social memory

Motivation to engage in social interaction is critical to ensure normal social behaviors, whereas dysregulation in social motivation can contribute to psychiatric diseases such as schizophrenia, autism, social anxiety disorders and post-traumatic stress disorder (PTSD). While dopamine is well known to regulate motivation, its downstream targets are poorly understood. Given the fact that the dopamine 1 (D1) receptors are often physically coupled with the NMDA receptors, we hypothesize that the NMDA receptor activity in the adult forebrain principal neurons are crucial not only for learning and memory, but also for the proper gating of social motivation. Here, we tested this hypothesis by examining sociability and social memory in inducible forebrain-specific NR1 knockout mice. These mice are ideal for exploring the role of the NR1 subunit in social behavior because the NR1 subunit can be selectively knocked out after the critical developmental period, in which NR1 is required for normal development. We found that the inducible deletion of the NMDA receptors prior to behavioral assays impaired, not only object and social recognition memory tests, but also resulted in profound deficits in social motivation. Mice with ablated NR1 subunits in the forebrain demonstrated significant decreases in sociability compared to their wild type counterparts. These results suggest that in addition to its crucial role in learning and memory, the NMDA receptors in the adult forebrain principal neurons gate social motivation, independent of neuronal development.

Brief Report: Insistence on Sameness, Anxiety, and Social Motivation in Children with Autism Spectrum Disorder.

While the function of restricted repetitive behaviors (RRBs) in autism spectrum disorder (ASD) is unclear, RRBs may function as anxiety reduction strategies (Joosten et al. J Autism Dev Disord 39(3):521-531, 2009. Moreover, anxiety in ASD is associated with low social motivation (Swain et al. J Autism Dev Disord, 2015. The present study examined social motivation as a mediator between anxiety and RRBs in a sample of 44 children (2-17years old; 80% male) with ASD. The relationship between anxiety and IS, but not other RRBs, was partially mediated by social motivation. These findings suggest anxiety is linked to social motivation deficits in children with ASD, which may increase ritualized behaviors and difficulties with changes in routine. Implications are discussed for differing functions and treatment of RRB domains.

Measuring the value of social engagement in adults with and without autism.

BackgroundDifferences in social communication are commonly reported in autism spectrum condition (ASC). A recent theory attributes this to a reduced motivation to engage with others, that is, deficits in social motivation. However, there are currently few simple, direct, behavioural ways to test this claim. This study uses a new behavioural measure of social motivation to test if preferences for direct gaze and face stimuli are linked to autistic traits or an ASC diagnosis. Our novel choose-a-movie (CAM) paradigm measures the effort participants invest to see particular stimuli. This aspect of social motivation is also known as social seeking.MethodsIn experiment 1, 80 typical adults completed the CAM task and a measure of autistic traits. In experiment 2, 30 adults with ASC and 24 age/IQ-matched typical adults completed the CAM paradigm.ResultsThe results from study one showed that typical adults prefer social stimuli over non-social, but this preference is weaker in those with higher levels of autistic traits. In study two, adults with ASC showed a significant reduction in their preference for direct gaze but little difference in their preference for faces without direct gaze.ConclusionsThese data show that social motivation can be measured in a simple, direct, behavioural paradigm. Furthermore, adults with ASC prefer direct gaze less than typical adults but may not avoid faces without direct gaze. This data advance our understanding of how social motivation may differ between those with and without autism.

Validation of operant social motivation paradigms using BTBR T+tf/J and C57BL/6J inbred mouse strains.

BackgroundAs purported causal factors are identified for autism spectrum disorder (ASD), new assays are needed to better phenotype animal models designed to explore these factors. With recent evidence suggesting that deficits in social motivation are at the core of ASD behavior, the development of quantitative measures of social motivation is particularly important. The goal of our study was to develop and validate novel assays to quantitatively measure social motivation in mice.MethodsIn order to test the validity of our paradigms, we compared the BTBR strain, with documented social deficits, to the prosocial C57BL/6J strain. Two novel conditioning paradigms were developed that allowed the test mouse to control access to a social partner. In the social motivation task, the test mice lever pressed for a social reward. The reward contingency was set on a progressive ratio of reinforcement and the number of lever presses achieved in the final trial of a testing session (breakpoint) was used as an index of social motivation. In the valence comparison task, motivation for a food reward was compared to a social reward. We also explored activity, social affiliation, and preference for social novelty through a series of tasks using an ANY-Maze video-tracking system in an open-field arena.ResultsBTBR mice had significantly lower breakpoints in the social motivation paradigm than C57BL/6J mice. However, the valence comparison task revealed that BTBR mice also made significantly fewer lever presses for a food reward.ConclusionsThe results of the conditioning paradigms suggest that the BTBR strain has an overall deficit in motivated behavior. Furthermore, the results of the open-field observations may suggest that social differences in the BTBR strain are anxiety induced.