Intraamygdaloid oxytocin reduces anxiety in valproate-induced autism model
01/30/2020
László Kristóf1, 2, Géczi Fanni1, 2, Ollmann Tamás1, 2, Kovács Anita1, 2, Péczely László1, 2, László Bettina1, 2, Kállai Veronika1, 2, Kertes Erika1, 2, Berta Beáta1, 2, Karádi Zoltán1, 2, 3, Lénárd László1, 2, 3
1 Institute of Physiology, University of Pécs, Medical School, Pécs, Hungary;
2 Centre for Neuroscience, Szentágothai Research Centre, University of Pécs, Pécs, Hungary;
3 Molecular Neuroendocrinology and Neurophysiology Research Group, Szentágothai Research Centre, University of Pécs, Pécs, Hungary
In autism research, the valproate model is a widely accepted animal model. Studies indicate that a single prenatal exposure to valproate in rodents results in lifelong behavioral impairments that represent the core signs of autism. The essence of the valproate rat model is that female rats receive 500 mg/bwkg i.p. valproate on the 12.5th day of gestation and consequently the offspring show autistic-like behavior. In our experiments, these offspring are examined. Our previous findings indicated that in the rat central nucleus of amygdala (CeA) oxytocin (OT) has a dose dependent anxiolytic effect. The aim of our present study was to examine in the rat CeA the possible effects of OT on anxiety in valproate-induced autism model.Male wistar rats, prenatally treated with valproate, were microinjected bilaterally with 10 ng OT (Sigma: O6379, injected in volume of 0.4 μl) or vehicle and intact control animals received vehicle solution as well. Valproate treated rats receiving 10 ng OT spent significantly longer time on the open arms in elevated plus maze test than the valproate treated control animals. Valproate treated control animals spent significantly less time on the open arms than the intact controls but there was no significant difference between 10 ng OT microinjected valproate treated rats and intact controls. Our results show that in the rat CeA OT reduces anxiety in valproate-induced autism model. The project has been supported by the European Union, co-financed by the European Social Fund (EFOP-3.6.1.-16-2016-00004) Supported by the ÚNKP-19-4-PTE-86 New National Excellence Program of the Ministry for Innovation and Technology.