TRH modulates glutamatergic synaptic inputs on CA1 neurons of the mouse hippocampus in a biphasic manner

• In acute mouse hippocampal slices, TRH modulates the excitatory transmission in CA1 pyramidal neurons in a complex way.
• TRH displays a biphasic effect on glutamatergic CA3-CA1 transmission, first a depression followed by a potentiation.
• Depression of excitatory CA3-CA1 transmission is prevented by the NMDA receptor antagonist DL-APV.
• TRH blocks the induction of LTP by a high frequency stimulation of the Shaffer's collaterals.
• Potentiation of the CA3-CA1 transmission is accelerated by NMDA receptor antagonism and modulated by GABA antagonists.

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.

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