OXYTOCIN RECEPTOR-MEDIATED MOLECULAR REGULATION OF TACTILE CORTICAL PLASTICITY DURING MOTHERHOOD

Oxytocin is widely recognized for its role in modulating social behaviors, such as mother–infant bonding. During the transition to motherhood, oxytocin regulates physiological changes in the female body and brain and enhances cortical plasticity, enabling mothers to adequately respond to infant needs. Mother–infant bonding relies heavily on mutual tactile stimulation, and consistent responsiveness to tactile cues from pups is crucial for maternal care.Using large-scale recordings, we found that this responsiveness is associated with oxytocin receptor (OTR)–mediated neuronal plasticity within the primary somatosensory cortex (S1) of rat mothers in early stages of maternity. Previous studies suggest that cortical plasticity can be associated with changes of interneuronal parvalbumin (PV)-expression. PV-neuron-driven plasticity is associated with structural remodeling of extracellular matrix proteins, called "perineuronal nets" (PNNs), which are in turn regulated by microglia. Molecularly, we therefore quantified PV interneurons, PNNs, and microglia under conditions of impaired OTR expression in S1, achieved through a local OTR knock-out (OTR-KO). Our results indicate that local OTR-KO in S1 leads to an increased density of PV interneurons and PNNs, accompanied by increased distances between PNNs and microglia. These alterations suggest an alteration of the excitation - inhibition balance within cortical circuits driven by PV interneurons. Consistent with this observation, we hypothesize that such imbalance may result from GABA insufficiency in OTR-expressing PV neurons, leading to network hyperexcitability and reduced precision in tactile stimulus processing in mothers with impaired OTR expression. We expect these network perturbations to be reflected in in vivo electrophysiological recordings.