Corticosterone modulates Acid sensing ion channels type 1a (ASIC-1a) dependent long-term potentiation at the mouse anterior cingulate cortex

MARÍA NATALIA GOBETTO; OSVALDO D. UCHITEL; CARLOTA GONZÁLEZ-INCHAUSPE; ADRIANA ALBANESE

Buenos Aires

Congreso; XXXV Reunión Anual SAN 2020; 2020

SAN; SOCIEDAD ARGENTINA DE INVESTIGACIÓN EN NEUROCIENCIAS

Acid-sensing ion channels (ASIC) are involved in synaptic plasticity, activity-dependent longtermpotentiation (LTP) is an example. Neurons in the anterior cingulate cortex (ACC)express ASIC-1a. Its postsynaptic activation generates synaptic currents (ASIC1a-SCs) thatadd to the glutamatergic excitatory postsynaptic currents (EPSCs). Corticosterone (CS) hasbeen shown to modulate ASIC-SCs. In wild type (WT) and ASIC-/- C57BL/6 mice, agedP30-60, we performed whole-cell patch-clamp recordings from pyramidal neurons in layerII/III of the ACC to evoke glutamatergic AMPA receptor-mediated EPSCs. After blockingAMPA, NMDA, GABA and glycine receptors (r), we detected ASIC-SCs sensitive to ASIC-1a inhibitor psalmotoxin-1 (PcTx1). CS added to the aCSF increased ASIC1a-SC amplitude.PcTx1 reduced the amplitude of ASIC1a-SCs treated with CS. Under control conditions, asingle theta-burst stimulation (TBS) did not cause LTP of glutamatergic EPSCs. Afterincubation with CS, one TBS induced significant LTP of EPSC amplitudes in WT. Themagnitude of LTP when CS was applied together with an NMDAr inhibitor was notsignificantly different to that with CS alone. In the presence of CS, LTP was abolished whenASIC-1a was blocked by PcTx1, and impaired in ASIC-/-. Pre-treatment with CS at 35ºCshowed enhanced EPSCs. We have demonstrated that CS, acting through ASIC-1a,reduces the threshold for LTP induction of glutamatergic ESPCs. The effect of CS is alsoenhanced by temperature.