Plasticidad sináptica en el hipocampo regulada por factores endocrinosPapel de la prolactina

Zusammenfassung

Cells of nervous tissue can modify their structural and functional organization through a property called neuronal plasticity. This enables the nervous system (NS) to perform continuous morphological and synaptic adjustments to create new connections and generate new circuits. Moreover, the endocrine system (ES) and NS are both essential to the communication throughout the body and the maintenance of homeostasis. In most cases, they work in different ways and have different means of transmitting their signals from one place to another but the two systems also overlap and work together in important respects. It is well stablished that ES modulates brain plasticity but it is not clear yet whether hormones, such as prolactin, may regulate functional synaptic plasticity. Therefore, the main aim of the present work was to determine the cellular and molecular mechanisms mediated by prolactin which regulate different forms of synaptic plasticity such as long-term potentiation (LTP) in the hippocampus. Using extracellular and patch-clamp electrophysiological techniques in brain slices of mice as well as extracellular in vivo recordings of urethane anesthetized mice, we have determined that PRL can modify the short and long term synaptic plasticity in hippocampus. These changes are carried out through mechanisms that include GABAergic and dopaminergic receptors regulation, changes in the probability of neurotransmitter release and activation the JAK2-mediated signalling pathway. In addition, we demonstrate that a synergistic action between PRL and β-estradiol can improve the synaptic strength of the CA1 region in the hippocampus under suppression of ovarian function. These findings will enhance our understanding of the mechanisms by which the NS processes, stores and recalls information, thereby facilitating complex processes such as learning in general and particular physiological situation. Furthermore, this knowledge will provide new insight into NS pathologies that involve a deficit in the different forms of learning and memory as well as synaptic and circuital changes that occur in different diseases of NS.