Amygdala, Oxytocin, and Social Cognition in Autism Spectrum Disorders

In the past decade, the elaboration of animal models has brought significant advances in understanding the development of the limbic neural circuitry and the modulatory role of hormones and neuropeptides in complex behaviors, such as social cognition. The study of Gur et al. ( ) in this issue of Biological Psychiatry yields important and exciting results elucidating the molecular mechanism by which oxytocin (OT) enhances social recognition memory (SRM) in adult Sprague-Dawley male rats. In rodents, the acquisition of information about conspecifics is mediated by olfactory and pheromonal signals, conveyed via the main olfactory bulb and the accessory olfactory bulb (AOB), both projecting to the medial amygdala (MeA). OT receptors are known to be variably expressed in many regions of the limbic circuit devoted to social behavior, including the amygdala, and OT activity on this structure improves the organism’s ability to remember individuals that it has previously encountered. However, its specific mode of action is not well understood. The important contribution of this work consisted in revealing that part of the protein synthesis underlying long-term consolidation of SRM in rodents occurs in the AOB and the MeA pathway, and this synapse-specific process is augmented by OT. Local blockage of protein synthesis in the MeA before memory acquisition blocks the consolidation of long-term SRM in adult rats, resulting in failure to discriminate familiar from novel juveniles. Notably, no effect has been observed on short-term SRM and long-term nonsocial olfactory recognition memory.