Social deficits are common in several psychiatric disorders, including autism spectrum disorders and schizophrenia. Individuals with severe social dysfunction can experience significant difficulties with everyday functioning.
Oxytocin and vasopressin are hormones that play key roles in emotional and social behaviors and bonding. Oxytocin has been suggested as a treatment to improve social behavior in individuals with autism, and initial studies in humans appear promising.
Now, scientists have further characterized a mouse model that provides some insights into biological factors related to social deficits, by comparing mice that had their oxytocin receptor gene made inactive, using a specialized technique called genetic knockout, with unaltered mice.
The knockout mice (OTR-/-) displayed impaired social behavior, increased aggression and reduced cognitive flexibility leading to resistance to change. These behaviors returned to normal when the OTR-/-mice were given oxytocin or vasopressin treatment.
"These findings confirm and highlight the importance of oxytocin for social behaviors. This animal model also may be useful in evaluating the effectiveness of drugs, including vasopressin agonists, that may help improve social behavior in autism, schizophrenia, and other disorders" said Dr. John Krystal, Editor of Biological Psychiatry, the journal publishing these results.
"While no animal model can be expected to replicate the full complexity of the human behavioral autistic phenotype, the OTR-/- mouse may really help to understand the co-occurrence of these symptoms as a syndrome," explained Dr. Bice Chini, author and senior researcher of CNR -- Institute of Neuroscience, Milano.
One important goal now is to fully characterize the neurodevelopmental processes modulated by oxytocin and vasopressin in order to fully understand their ability to reverse autistic symptoms.
Mariaelvina Sala, Daniela Braida, Daniela Lentini, Marta Busnelli, Elisabetta Bulgheroni, Valeria Capurro, Annamaria Finardi, Andrea Donzelli, Linda Pattini, Tiziana Rubino, Daniela Parolaro, Katsuhiko Nishimori, Marco Parenti, Bice Chini. Pharmacologic Rescue of Impaired Cognitive Flexibility, Social Deficits, Increased Aggression, and Seizure Susceptibility in Oxytocin Receptor Null Mice: A Neurobehavioral Model of Autism. Biological Psychiatry, 2011; 69 (9): 875 DOI: 10.1016/j.biopsych.2010.12.022
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Thanks and Regards,
Bhupesh Sharma
Research is the Best Part of Life
The short answer is no. Both ASD and schizophrenia are multidimensional, i.e. they do not have a single cause. In addition, it is an interplay of genes and environment (f.e. upraising). One knows that even a predisposition for schizophrenia may not lead to the disorder if the person is raised in a very supportive social environment (not anonymous big cities with stressed parents). Similar early inventions and "training" can minimise the "oddity" of ASD.
Furthermore, my approach is that ASD and schizophrenia are just "extreme tails" of the neurodiversity we humans come with. Allowing us adaption to various environments, depending on whether more creativity, more nerdiness etc are required. Given that, there are neurobiological underpinnings for this variability. Not simple ones, but by looking at one factor at a time, we can shed light on it. In this regard, the genetic studies and the neurotransmitter studies that you cite, present us parts of the puzzle. Though, we need quite sophisticated designs: knockout mice, wild type mice, rearing counterbalanced (i.e. KO -/- mice reared by WT mice and vice versa, and KO offspring reared by KO -/+ mice and vice versa), all need to be tested on a battery of tasks, and ideally one finds tasks were the KO mice outperform the WT mice (double dissociation). This is a huge task and still not complete, because the "disadvantage" of mice research is that cognitive performance and social behaviour depend on the strain of mice used, how automatic the testing is (handling influence) etc. Systematically varying all those factors is easily a program for a decade. Extrapolating from mice to humans is still far-fetched when it comes to such complex disorder as mental illness are - nevertheless I fully support this research, just would be careful with the interpretation and generalisation.
I hope can be a good response
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