Search

Thyrotropin Releasing Hormone (TRH) is a tripeptide that induces the release of Thyroid Stimulating Hormone (TSH) in the blood. Besides its role in the thyroid system, TRH has been shown to regulate several neuronal systems in the brain however its role in hippocampus remains controversial. Using electrophysiological recordings in acute mouse brain slices, we show that TRH depresses glutamate responses at the CA3-CA1 synapse through an action on NMDA receptors, which, as a consequence, decreases the ability of the synapse to establish a long term potentiation (LTP). TRH also induces a late increase in AMPA/kainate responses. Together, these results suggest that TRH plays an important role in the modulation of hippocampal neuronal activities, and they contribute to a better understanding of the mechanisms by which TRH impacts synaptic function underlying emotional states, learning and memory processes.

We are interested in elucidating how the brain controls the immune system. To this aim, we have established an environmental enriched (EE) paradigm in which C57BL/6 mice experience higher levels of sensory, motor, social, and cognitive stimuli, compared to animals housed in a standard environment (EE). In agreement with previous studies, EE mice exhibited increased hippocampal neurogenesis and synaptogenesis, and decreased anxiety, and increased exploratory activity. EE housing did not result in gross alterations in the frequency of neutrophils, dendritic cells (DC), macrophages, CD4+ and CD8+ T cells and B lymphocytes in the lymphoid organs of immunologically naive animals. However, spleen DCs expressed a more mature phenotype in EE animals compared to SE mice. Furthermore, EE mice exhibited both a Th2-biaised T response upon immunization with OVA and a more robust memory T cell response. To elucidate the mechanisms that were responsible for these latter phenomena, we compared the levels of various metabolites in the serum of EE and SE mice. EE animals exhibited increased levels of adiponectin, a cytokine that is mainly secreted by adipose tissue and that modulates a number of metabolic processes, including glucose regulation and fatty acid oxidation. Most importantly, adiponectin-deficient mice housed in EE did not exhibit the Th2-biaised immune response that was observed in wild-type mice therefore suggesting a critical role of this cytokine in EE-induced immune alterations.