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Figure 1 | Molecular Pain

Figure 1

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

Figure 1

characterization of fast spontaneous inhibitory and excitatory synaptic currents in lamina II. Glycine-receptor-mediated sIPSCs were blocked in these experiments by adding 1 μM strychnine in the general bath perfusion. A: GABAA-receptor-mediated sIPSCs (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 (τR = 1.3 ms) and deactivation phase (τD = 45.2 ms). B: At a holding potential of -60 mV (i.e. at the equilibrium potential for Cl- ions), 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 τR of 0.9 ms and τD of 4.1 ms).

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Molecular Pain

ISSN: 1744-8069

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