Social Context, Stress, Neuropsychiatric Disorders, and the Vasopressin 1b Receptor

Caldwell, Heather K.; Aulino, Elizabeth A.; Rodriguez, Karla M.; Witchey, Shannah K.; Yaw, Alexandra M.

doi:10.3389/fnins.2017.00567

Cited by 34 publications

(32 citation statements)

References 96 publications

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“…Variants of the vasopressin receptor 1A gene (AVPR1A) in humans have also been associated with ASD [ 181 ] and IN vasopressin has been shown to modulate brain regions involved in processing emotional information, such as the medial prefrontal cortex–amygdala [ 182 ] and temporal-parietal junction [ 183 ]. In addition, knockout, rescue, and overexpression of AVPR1A in rodents modulates social function [ 184 ]. Curiously, both vasopressin agonists and antagonists are being studied in clinical trials.…”

Section: Drug Treatments For Improving Social Interaction In Autism Smentioning

confidence: 99%

Social Skills Deficits in Autism Spectrum Disorder: Potential Biological Origins and Progress in Developing Therapeutic Agents

Frye

2018

CNS Drugs

111

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Autism spectrum disorder is defined by two core symptoms: a deficit in social communication and the presence of repetitive behaviors and/or restricted interests. Currently, there is no US Food and Drug Administration-approved drug for these core symptoms. This article reviews the biological origins of the social function deficit associated with autism spectrum disorder and the drug therapies with the potential to treat this deficit. A review of the history of autism demonstrates that a deficit in social interaction has been the defining feature of the concept of autism from its conception. Abnormalities identified in early social skill development and an overview of the pathophysiology abnormalities associated with autism spectrum disorder are discussed as are the abnormalities in brain circuits associated with the social function deficit. Previous and ongoing clinical trials examining agents that have the potential to improve social deficits associated with autism spectrum disorder are discussed in detail. This discussion reveals that agents such as oxytocin and propranolol are particularly promising and undergoing active investigation, while other agents such as vasopressin agonists and antagonists are being activity investigated but have limited published evidence at this time. In addition, agents such as bumetanide and manipulation of the enteric microbiome using microbiota transfer therapy appear to have promising effects on core autism spectrum disorder symptoms including social function. Other pertinent issues associated with developing treatments in autism spectrum disorder, such as disease heterogeneity, high placebo response rates, trial design, and the most appropriate way of assessing effects on social skills (outcome measures), are also discussed.

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Section: Drug Treatments For Improving Social Interaction In Autism Smentioning

confidence: 99%

Social Skills Deficits in Autism Spectrum Disorder: Potential Biological Origins and Progress in Developing Therapeutic Agents

Frye

2018

CNS Drugs

111

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“…Most of the research on nonapeptide receptor impacts on social behavior has focused on V1aR and OTR, due, in part, to their wide distribution across several areas of the brain that regulate social behavior and their extensive implication in several areas of social behavior, perhaps most notably pair bonding (16,17). Although the role of V1bR is beginning to emerge as an important modulator of social memory and aggression (18), its distribution appears to be relatively restricted to the hippocampus (HPC) and pituitary, its influence on behavior is comparably nuanced, and the developmental trajectories and sensitivity to early-life experiences of V1bR have not been investigated. Furthermore, V2R is primarily associated with peripheral functions of VP.…”

Section: Introductionmentioning

confidence: 99%

Paternal deprivation impairs social behavior putatively via epigenetic modification to lateral septum vasopressin receptor

et al. 2020

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Although it is well appreciated that the early-life social environment asserts subsequent long-term consequences on offspring brain and behavior, the specific mechanisms that account for this relationship remain poorly understood. Using a novel assay that forced biparental pairs or single mothers to prioritize caring for offspring or themselves, we investigated the impact of parental variation on adult expression of nonapeptide-modulated behaviors in prairie voles. We demonstrated that single mothers compensate for the lack of a co-parent. Moreover, mothers choose to invest in offspring over themselves when faced with a tradeoff, whereas fathers choose to invest in themselves. Furthermore, our study suggests a pathway whereby variation in parental behavior (specifically paternal care) may lead to alterations in DNA methylation within the vasopressin receptor 1a gene and gene expression in the lateral septum. These differences are concomitant with changes in social approach, a behavior closely associated with septal vasopressin receptor function.

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“…The neuromodulatory actions of arginine-vasopressin (Avp) are required for the typical expression of social and stress-related behaviors in clinical populations and preclinical models (Caldwell, Aulino et al 2017, Williams Avram and Cymerblit-Sabba 2017). Avp acts in the central nervous system through its G-protein coupled receptors, Avpr1a and Avpr1b.…”

Section: Introductionmentioning

confidence: 99%

NMDA receptor in vasopressin 1b neurons is not required for short-term social memory, object memory or aggression

Avram

Fastman

Cymerblit‐Sabba

et al. 2019

Preprint

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The vasopressin 1b receptor (Avpr1b) plays an important role in social behaviors including aggression, social learning and memory. Genetic removal of Avpr1b from mouse models results in deficits in aggression and short-term social recognition in adults. Avpr1b gene expression is highly enriched in the pyramidal neurons of the hippocampal cornu ammonis 2 (CA2) region. Activity of the hippocampal CA2 has been shown to be required for normal short-term social recognition and aggressive behaviors. Vasopressin acts to enhance synaptic responses of CA2 neurons through a NMDA-receptor dependent mechanism. Genetic removal of the obligatory subunit of the NMDA receptor (Grin1) within distinct hippocampal regions impairs non-social learning and memory. However, the question of a direct role for NMDA receptor activity in Avpr1b neurons to modulate social behavior remains unclear. To answer this question, we first created a novel transgenic mouse line with Cre recombinase knocked into the Avpr1b coding region to genetically target Avpr1b neurons. We confirmed this line has dense Cre expression throughout the dorsal and ventral CA2 regions of the hippocampus, along with scattered expression within the caudate-putamen and olfactory bulb. Conditional removal of the NMDA receptor was achieved by crossing our line to an available floxed Grin1 line. The resulting mice were measured on a battery of social and memory behavioral tests. Surprisingly, we did not observe any differences between Avpr1b-Grin1 knockout mice and their wildtype siblings. We conclude that mice without typical NMDA receptor function in Avpr1b neurons can develop normal aggression as well as short-term social and object memory performance.Significance StatementActivity of neurons that express vasopressin 1b receptor are essential for aggressive and social recognition behaviors. We created a novel transgenic mouse to allow selective targeting of vasopressin 1b neurons. Our studies indicate that NMDA receptor expression in vasopressin 1b neurons (including most CA2 neurons) are not required for development of the typical expression of aggression or recognition memory. Thus, CA2 neurons may have a unique way of incorporating novel stimuli into memory that deserves further investigation.

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Social Context, Stress, Neuropsychiatric Disorders, and the Vasopressin 1b Receptor

Cited by 34 publications

References 96 publications

Social Skills Deficits in Autism Spectrum Disorder: Potential Biological Origins and Progress in Developing Therapeutic Agents

Social Skills Deficits in Autism Spectrum Disorder: Potential Biological Origins and Progress in Developing Therapeutic Agents

Paternal deprivation impairs social behavior putatively via epigenetic modification to lateral septum vasopressin receptor

NMDA receptor in vasopressin 1b neurons is not required for short-term social memory, object memory or aggression

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