Prolactin enhances hippocampal synaptic plasticity in female mice of reproductive age

Dynamic signaling between the endocrine system (ES) and the nervous system (NS) is essential for brain and body homeostasis. In particular, reciprocal interaction occurs during pregnancy and motherhood that may involve changes in some brain plasticity processes. Prolactin (PRL), a hormone with pleiotropic effects on the NS, promotes maternal behavior and has been linked to modifications in brain circuits during motherhood; however, it is unclear whether PRL may regulate synaptic plasticity. Therefore, the main aim of the present work was to determine the cellular and molecular mechanisms triggered by PRL that regulate synaptic plasticity in the hippocampus. By analyzing extracellular recordings in CA3-CA1 synapses of hippocampal slices, we report that PRL modifies short and long-term synaptic plasticity in female mice of reproductive age, but not in sexually immature females or adult males. This effect is carried out through mechanisms that include participation of GABA(A) receptors and activation of the JAK2-mediated signaling pathway. These findings show for the first time how PRL enhances the synaptic strength in hippocampal circuits and that this effect is sexually dimorphic, which would influence complex brain processes in physiological conditions like pregnancy and lactation.

Automated summary

The study demonstrates that prolactin enhances short and long-term synaptic plasticity in hippocampal circuits of female mice of reproductive age, but not in sexually immature females or adult males. This effect is mediated through mechanisms involving GABA(A) receptors and JAK2 signaling pathway.