Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

OBJECTIVE: Prenatal exposure to valproic acid (VPA) enhances the risk for later development of autism spectrum disorders (ASD). An altered gamma-aminobutyric acid (GABA) system may be a key factor in ASD. Here we investigated possible changes in the GABA system in rats exposed to a low dose of prenatal VPA. METHOD: We performed autoradiography with [3H]muscimol, (a GABAA receptor agonist), and [11C]Ro15-4513 (a partial agonist of the GABAA α1+5 receptor subtypes), in brain sections containing amygdala, thalamus and hippocampus of rats treated prenatally with 20 mg/kg VPA or saline from the 12th day of gestation. Result Prenatal VPA significantly increased [11C]Ro15-4513 binding in the left amygdala compared with controls (p<0.05). This difference was not observed in the hippocampus, thalamus or right amygdala. No differences were observed in [3H]muscimol binding. CONCLUSION: We observed an asymmetric increase in GABAA receptor binding. Disturbances in the GABAA receptor system have also been detected in human autism with [11C]Ro15-4513.

Original publication

DOI

10.1017/neu.2016.59

Type

Journal article

Journal

Acta Neuropsychiatr

Publication Date

10/2017

Volume

29

Pages

309 - 314

Keywords

GABA, [11C]Ro-154513, autism spectrum disorders, autoradiography, valproic acid, Amygdala, Animals, Autism Spectrum Disorder, Autoradiography, Azides, Benzodiazepines, Carbon Radioisotopes, Disease Models, Animal, Female, GABA Agents, GABA-A Receptor Agonists, Male, Muscimol, Pregnancy, Prenatal Exposure Delayed Effects, Rats, Receptors, GABA-A, Valproic Acid