Fig. 2.
A subset of interneurons in SO are excited by two kinetically distinct nicotinic responses. A1,Left, Cell membrane responses to hyperpolarizing and depolarizing current injection (120 pA). Right, Slow membrane depolarization and action potentials of a cell in response to brief pressure application of ACh (arrow) onto the soma. The cell was treated with atropine (1 μm) to block muscarinic receptors and 100 nm α-BgTx to block the fast α7 nAChRs. A2, Left, In another SO interneuron, pressure application of ACh to the cell soma induced a fast and a slow inward current response voltage-clamped at −70 mV. The α7 antagonist a-BgTx (100 nm) completely blocked the fast inward current but did not affect the slow inward current.A3, The α3β2 nAChR antagonist α-CTX MII (200 nm) did not affect the slow nicotinic current in another SO interneuron. A4, The nonselective nicotinic antagonist MEC (1 μm) reversibly inhibited the slow nicotinic current in another SO interneuron.A5, The nonselective nicotinic antagonist DHβE inhibited the slow nicotinic current in another SO interneuron.A6, Left, A plot of the peak inward current of a slow nicotinic response and its inhibition by MEC over time. Data from the same cell in A4.Right, A plot of the peak inward current of the slow nicotinic response and its concentration-dependent inhibition by DHβE from the cell in A5. B, Summary plot of the effects of different antagonists on the slow nicotinic current expressed as a percentage of control amplitude.C, Left, Raw data traces of the slow nicotinic current response held at varying membrane potentials.Right, The peak amplitudes of the nicotinic currents plotted against the membrane potentials at which they were recorded. Calibration: A1, Vertical, 20 mV,horizontal, left, 200 msec,right, 1 sec; A2,vertical, 100 pA, horizontal, 1 sec;A3, vertical, 20 pA,horizontal, 1 sec; A4,5,vertical, 20 pA, horizontal, 1 sec;C, vertical, 100 pA,horizontal, 1 sec.