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The Lab For neurobiology of social behavior

We have developed novel experimental setups and methodologies aimed to allow automated analysis of social behavior in rat and mouse models of ASD. Currently we are combining these setups and methodologies into one system enabling deep phenotyping of deficits in social behavior exhibited by these models. The system will analyze multiple parameters of social behavior, including physical interactions and vocal communication, as well as multiple physiological parameters such as sniffing, heart rate, body temperature and brain activity. Using these data, we obtain new insights into the mechanisms underlying the impaired social behavior displayed by animal models of ASD.

We explore how social information is turned into memory of specific individuals, which is the basis for all our long-term social relationships. This type of memory is termed “social recognition memory” and is known to be dependent on a dedicated network of brain regions, as well as on the brain activity of multiple neuropeptides. In the lab we investigate the neuronal and molecular mechanisms underlying this memory, and especially the role of two hypothalamic neuropeptides, oxytocin and vasopressin.

Social species are defined by forming and relying on social structures that are greater and more meaningful than the individual. Being amongst the most social species on earth, social relationships are a crucial part of human lives, and have a significant impact on our health. While positive social relationships are protective for health, accumulating evidence suggest that weak social relationships are associated with a wide variety of adverse health outcomes. In the past few decades, social isolation has been recognized as a risk factor for broad-based morbidity and mortality. Interestingly, social isolation was shown to be a stronger risk factor than smoking, obesity, sedentary lifestyle, and high blood pressure (House et al. 1988). Others and we have found that long-term social recognition memory of rodents is abolished by acute social isolation. We use in vivo electrophysiology, molecular methodologies and next-generation sequencing in order to reveal the mechanisms underlying the impairing effect of social isolation on social recognition memory of rats and mice. We believe that these experiments will pave the way for the development of efficient interventions that will alleviate the destructive influence of social isolation on Human health.

We explored neuronal mechanisms involved in autism spectrum disorder (ASD), the prevalence of which has sharply increased over the past 30 years, with a current occurrence of about 1% of the population. We collaborate with Dr. Joseph Buxbaum of Mount Sinai Medical School in New York in the analysis of a new animal model of ASD developed by him, the Shank3-defficient rats. The Shank3 deficiency is one of the most established models of syndromic ASD hence we find great interest in exploring the neuronal mechanisms underlying its symptoms. We also explore several other rat and mice models of autism, hoping to reveal the modified brain activity, which is associated with the deficits in social behavior displayed by these animals.

We are using chronically implanted electrode microarrays for in vivo electrophysiological recordings from rats and mice during social behavior. These arrays are custom-made and were designed by us to allow recordings from many areas of the social brain. Using these arrays, we probe the spatial and temporal distribution of brain activity induced in the social brain by various types of social stimuli. The unique design of our arrays enable us to combine these recordings with optogenetic and pharmacogenetic stimulation protocols and to explore their effect on social information processing.