Oxytocin-induced antinociception in the spinal cord is mediated by a subpopulation of glutamatergic neurons in lamina I-II which amplify GABAergic inhibition-5

GABAA-R sIPSCs) were identified as outward currents (left panel) at a holding potential of 0 mV. These sIPSCs were reversibly blocked in the presence of 10 μM bicuculline, a selective antagonist of GABAA-Rs. Panel on the right illustrates an averaged current obtained from 46 individual traces. GABAA-R sIPSCs were best described by a monoexponential decay time constant in both the activation phase (τ= 1.3 ms) and deactivation phase (τ= 45.2 ms). : At a holding potential of -60 mV (i.e. at the equilibrium potential for Clions), only fast inward currents were detected (left panel). These events were AMPA-type glutamate-receptor-mediated sEPSCs (AMPA-R sEPSCs) since they were reversibly inhibited in the presence of CNQX (10 μM) a specific blocker of AMPA subtype glutamate receptor. The trace on the right was obtained by averaging 168 individual AMPA-R sEPSCs. These sEPSCs were characterized by a τof 0.9 ms and τof 4.1 ms).<p><b>Copyright information:</b></p><p>Taken from "Oxytocin-induced antinociception in the spinal cord is mediated by a subpopulation of glutamatergic neurons in lamina I-II which amplify GABAergic inhibition"</p><p>http://www.molecularpain.com/content/4/1/19</p><p>Molecular Pain 2008;4():19-19.</p><p>Published online 29 May 2008</p><p>PMCID:PMC2430948.</p><p>