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Adenosine A1 receptor antagonism prevents DSI in hippocampal CA1 pyramidal cells
J. Freire1,2,, , D.M. Rombo1,2, A.M. Sebastião1,2
1 Instituto de Farmacologia e Neurociências, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal
2 Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal

Aim: How adenosine interfere with a short-term form of neuronal plasticity dependent on endocannabinoid, the depolarization-induced suppression of inhibition (DSI).

Introduction: The widely consumed psychoactive drug cannabis, containing cannabinoid compounds, and/or caffeine, with adenosinergic antagonizing proprieties, exert their central actions by affecting cognitive operations such as learning and memory. Indeed, endogenous adenosine and endocannabinoids (eCB) are known to interfere with physiological synaptic plasticity phenomena that represent the neuronal substrate of memory formation.

Methods: Whole-cell voltage-clamp recordings (Vh=−70mV) were performed on hippocampal CA1 pyramidal cells of 3 to 5 weeks-old C57BL/6 mice. Slices (350μm thick) were perfused with artificial cerebrospinal fluid (aCSF) supplemented with glutamate receptor antagonists (CNQX, 25μM and DL-APV, 50μM) to block glutamatergic transmission and isolate GABA-mediated responses. Inhibitory postsynaptic currents (IPSCs) were evoked every 3s through a stimulation electrode placed in stratum radiatum. The recording electrode was filled with a CsCl-based intracellular solution and DSI was evoked through a 5s voltage step of +80mV. The magnitude of DSI was measured 9s after the depolarizing step and DSI recovery was evaluated between 30 and 60s after depolarization.

Results: When recording eCB-mediated DSI we observed a decrease in electrical-evoked IPSC amplitudes to 81.0±5.4% of baseline (p<0.01, n=14) that fully recovered to 90.2±5.4% after 30–60s. The adenosine A1 receptor antagonist, DPCPX (100nM), prevented DSI, recordings showing a non-significant change in IPSCs amplitude to 95.1±12.0% of baseline (p=0.3473, n=10) that was maintained throughout the recovery period (87.1±12.0%).

Conclusion: These results suggest that tonic adenosine A1 receptor activation is necessary for the occurrence of DSI. The mechanisms involved in this process remain unclear and need further investigation.1–4

V. Chevaleyre
V. Chevaleyre
A.M. Sebastião
D.M. Rombo
Cereb Cortex, 26 (2016), pp. 1081-1095 http://dx.doi.org/10.1093/cercor/bhu288

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