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Adenosine A1 receptor antagonism prevents DSI in hippocampal CA1 pyramidal cells
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"apellidos" => "Freire" "email" => array:1 [ 0 => "joanamorimf@gmail.com" ] "referencia" => array:3 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">1</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">2</span>" "identificador" => "aff0010" ] 2 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "D.M." "apellidos" => "Rombo" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">1</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">2</span>" "identificador" => "aff0010" ] ] ] 2 => array:3 [ "nombre" => "A.M." "apellidos" => "Sebastião" "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">1</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">2</span>" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Instituto de Farmacologia e Neurociências, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal" "etiqueta" => "1" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal" "etiqueta" => "2" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Aim:</span> How adenosine interfere with a short-term form of neuronal plasticity dependent on endocannabinoid, the depolarization-induced suppression of inhibition (DSI).</p><p id="par0010" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Introduction:</span> 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.</p><p id="par0015" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Methods:</span> Whole-cell voltage-clamp recordings (Vh<span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span>−70<span class="elsevierStyleHsp" style=""></span>mV) were performed on hippocampal CA1 pyramidal cells of 3 to 5 weeks-old C57BL/6 mice. Slices (350<span class="elsevierStyleHsp" style=""></span>μm thick) were perfused with artificial cerebrospinal fluid (aCSF) supplemented with glutamate receptor antagonists (CNQX, 25<span class="elsevierStyleHsp" style=""></span>μM and DL-APV, 50<span class="elsevierStyleHsp" style=""></span>μM) to block glutamatergic transmission and isolate GABA-mediated responses. Inhibitory postsynaptic currents (IPSCs) were evoked every 3<span class="elsevierStyleHsp" style=""></span>s 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 5<span class="elsevierStyleHsp" style=""></span>s voltage step of +80<span class="elsevierStyleHsp" style=""></span>mV. The magnitude of DSI was measured 9<span class="elsevierStyleHsp" style=""></span>s after the depolarizing step and DSI recovery was evaluated between 30 and 60<span class="elsevierStyleHsp" style=""></span>s after depolarization.</p><p id="par0020" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Results:</span> When recording eCB-mediated DSI we observed a decrease in electrical-evoked IPSC amplitudes to 81.0<span class="elsevierStyleHsp" style=""></span>±<span class="elsevierStyleHsp" style=""></span>5.4% of baseline (<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span><<span class="elsevierStyleHsp" style=""></span>0.01, <span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span>14) that fully recovered to 90.2<span class="elsevierStyleHsp" style=""></span>±<span class="elsevierStyleHsp" style=""></span>5.4% after 30–60<span class="elsevierStyleHsp" style=""></span>s. The adenosine A1 receptor antagonist, DPCPX (100<span class="elsevierStyleHsp" style=""></span>nM), prevented DSI, recordings showing a non-significant change in IPSCs amplitude to 95.1<span class="elsevierStyleHsp" style=""></span>±<span class="elsevierStyleHsp" style=""></span>12.0% of baseline (<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span>0.3473, <span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span>10) that was maintained throughout the recovery period (87.1<span class="elsevierStyleHsp" style=""></span>±<span class="elsevierStyleHsp" style=""></span>12.0%).</p><p id="par0025" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Conclusion:</span> These results suggest that tonic adenosine A1 receptor activation is necessary for the occurrence of DSI. 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