Effects of oxytocin on serotonin 1B agonist-induced autism-like behavior in mice
| Autor: | Andrew C. Gray, Sarah K. Lawson, Nancy S. Woehrle |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
Male
0301 basic medicine Agonist Serotonin medicine.drug_class Perseveration Oxytocin Developmental psychology 03 medical and health sciences Behavioral Neuroscience 0302 clinical medicine medicine Animals Autistic Disorder Social Behavior Prepulse inhibition Behavior Animal Novelty Serotonin 5-HT1 Receptor Agonists medicine.disease Mice Inbred C57BL Disease Models Animal 030104 developmental biology Autism spectrum disorder Exploratory Behavior Receptor Serotonin 5-HT1B Autism medicine.symptom Psychology Neuroscience 030217 neurology & neurosurgery Social behavior medicine.drug |
| Zdroj: | Behavioural Brain Research. 314:52-64 |
| ISSN: | 0166-4328 |
| DOI: | 10.1016/j.bbr.2016.07.027 |
| Popis: | Social impairments in autism remain poorly understood and without approved pharmacotherapies. Novel animals models are needed to elucidate mechanisms and evaluate novel treatments for the social deficits in autism. Recently, serotonin 1B receptor (5-HT1B) agonist challenge in mice was shown to induce autism-like behaviors including perseveration, reduced prepulse inhibition, and delayed alternation deficits. However, the effects of 5-HT1B agonists on autism-related social behaviors in mice remain unknown. Here, we examine the effects of 5-HT1B agonist challenge on sociability and preference for social novelty in mice. We also examine the effects of 5-HT1B agonist treatment on average rearing duration, a putative rodent measure of non-selective attention. Non-selective attention is an associated feature of autism that is also not well understood. We show that 5-HT1B receptor activation reduces sociability, preference for social novelty, and rearing in mice. In addition, we examine the ability of oxytocin, an off-label treatment for the social impairments in autism, to reverse 5-HT1B agonist-induced social and attention deficits in mice. We show that oxytocin restores social novelty preference in mice treated with a 5-HT1B agonist. We also show that oxytocin attenuates 5-HT1B agonist-induced sociability and rearing deficits in mice. Our results suggest that 5-HT1B agonist challenge provides a useful pharmacological mouse model for aspects of autism, and implicate 5-HT1B in autism social and attention deficits. Moreover, our findings suggest that oxytocin may treat the social deficits in autism through a mechanism involving 5-HT1B. |
| Databáze: | OpenAIRE |
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