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.
Keywords: 2-Amino-5-Phosphonopentanoic acid (DL-APV, PubCem CID 1216); 6-Cyano-7-Nitroquinoxaline-2,3-Dione (CNQX, PubCem CID 3721046); AMPA/kainate receptors; Bicuculline (PubCem CID 10237); CGP55845A (PubCem CID 123885); Glutamatergic transmission; Glycine (PubCem CID 750); Hippocampus; Long-Term Potentiation (LTP); Mice; N-Methyl d-Aspartate (NMDA, PubCem CID 22880); NMDA receptors; QX314 (PubCem CID 3925); Thyrotropin-Releasing Hormone (TRH); Thyrotropin-releasing hormone (TRH, PubCem CID 32281).
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