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Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior.

ABSTRACT: Williams syndrome (WS) is a condition caused by a deletion of ?26-28 genes on chromosome 7q11.23 often characterized by abnormal social behavior and disrupted oxytocin (OT) and vasopressin (AVP) functioning. The observation that individuals with WS exhibit OT and AVP dysregulation is compelling. There is currently a lack of evidence that any of the genes typically deleted in WS have any direct effect on either OT or AVP. In this perspective article, we present a novel epigenetic model describing how DNA methylation may impact the expression of key genes within the OT and AVP systems, which may ultimately influence the social behavior observed in WS. We draw support from data pooled from a prior empirical research study (Henrichsen et al., 2011), demonstrating that OXTR is overexpressed in WS. These preliminary findings may create new opportunities to target the OT and AVP systems with the specific goal of improving outcomes in WS and other psychiatric conditions.

SUBMITTER: Haas BW

PROVIDER: S-EPMC4330921 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior.

Haas Brian W BW Smith Alicia K AK

Frontiers in genetics 20150217

Williams syndrome (WS) is a condition caused by a deletion of ∼26-28 genes on chromosome 7q11.23 often characterized by abnormal social behavior and disrupted oxytocin (OT) and vasopressin (AVP) functioning. The observation that individuals with WS exhibit OT and AVP dysregulation is compelling. There is currently a lack of evidence that any of the genes typically deleted in WS have any direct effect on either OT or AVP. In this perspective article, we present a novel epigenetic model describing ...[more]

PMID: 25741359

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Project description:Recent studies support the hypothesis that the adverse effects of early-life adversity and transgenerational stress on neural plasticity and behavior are mediated by inflammation. The objective of the present study was to investigate the immune and behavioral programing effects of intranasal (IN) vasopressin (AVP) and oxytocin (OXT) treatment of chronic social stress (CSS)-exposed F1 dams on F2 juvenile female offspring. It was hypothesized that maternal AVP and OXT treatment would have preventative effects on social stress-induced deficits in offspring anxiety and social behavior and that these effects would be associated with changes in interferon-? (IFN?). Control and CSS-exposed F1 dams were administered IN saline, AVP, or OXT during lactation and the F2 juvenile female offspring were assessed for basal plasma IFN? and perseverative, anxiety, and social behavior. CSS F2 female juvenile offspring had elevated IFN? levels and exhibited increased repetitive/perseverative and anxiety behaviors and deficits in social behavior. These effects were modulated by AVP and OXT in a context- and behavior-dependent manner, with OXT exhibiting preventative effects on repetitive and anxiety behaviors and AVP possessing preventative effects on social behavior deficits and anxiety. Basal IFN? levels were elevated in the F2 offspring of OXT-treated F1 dams, but IFN? was not correlated with the behavioral effects. These results support the hypothesis that maternal AVP and OXT treatment have context- and behavior-specific effects on peripheral IFN? levels and perseverative, anxiety, and social behaviors in the female offspring of early-life social stress-exposed dams. Both maternal AVP and OXT are effective at preventing social stress-induced increases in self-directed measures of anxiety, and AVP is particularly effective at preventing impairments in overall social contact. OXT is specifically effective at preventing repetitive/perseverative behaviors, yet is ineffective at preventing deficits in overall social behavior.

Project description:We recently demonstrated that vasopressin (AVP) in the lateral septum modulates social play behavior differently in male and female juvenile rats. However, the extent to which different social contexts (i.e., exposure to an unfamiliar play partner in different environments) affect the regulation of social play remains largely unknown. Given that AVP and the closely related neuropeptide oxytocin (OXT) modulate social behavior as well as anxiety-like behavior, we hypothesized that these neuropeptides may regulate social play behavior differently in novel (novel cage) as opposed to familiar (home cage) social environments. Administration of the specific AVP V1a receptor (V1aR) antagonist (CH2)5Tyr(Me(2))AVP into the lateral septum enhanced home cage social play behavior in males but reduced it in females, confirming our previous findings. These effects were context-specific because V1aR blockade did not alter novel cage social play behavior in either sex. Furthermore, social play in females was reduced by AVP in the novel cage and by OXT in the home cage. Additionally, females administered the specific OXT receptor antagonist desGly-NH2,d(CH2)5-[Tyr(Me)(2),Thr(4)]OVT showed less social play in the novel as compared to the home cage. AVP enhanced anxiety-related behavior in males (tested on the elevated plus-maze), but failed to do so in females, suggesting that exogenous AVP alters social play and anxiety-related behavior via distinct and sex-specific mechanisms. Moreover, none of the other drug treatments that altered social play had an effect on anxiety, suggesting that these drug-induced behavioral alterations are relatively specific to social behavior. Overall, we showed that AVP and OXT systems in the lateral septum modulate social play in juvenile rats in neuropeptide-, sex- and social context-specific ways. These findings underscore the importance of considering not only sex, but also social context, in how AVP and OXT modulate social behavior.

Dataset Information

Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior.

Publications

Oxytocin, vasopressin, and Williams syndrome: epigenetic effects on abnormal social behavior.

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