Article Figures & Data
Figures
- Fig. 1.
Connectivity of the intercalated cell masses. Scheme of a coronal section through the amygdaloid complex of the guinea pig. ITC cell masses (arrows) receive glutamatergic inputs from components of the basolateral complex [namely, the lateral (LA), the basolateral (BL), and the basomedial (BM) nuclei] and contribute a GABAergic projection to the lateral and medial sectors of the central nucleus (CEL andCEM , respectively). ITC cell masses are interconnected by lateromedial connections. EC, External capsule; OT, optic tract; PU, putamen; Rh, rhinal sulcus; D, dorsal;M, medial; V, ventral; L, lateral.
- Fig. 2.
Suprathreshold depolarizations elicit ADPs in ITC cells. A, Depolarizing current pulses of gradually increasing amplitude (left to right), applied at −60 mV. B, Depolarizing current pulses adjusted to elicit approximately the same number of spikes were delivered from different Vm values.C, Spike trains elicited from depolarizedVm values lead to tonic firing. Voltage scale is the same for A–C. Time scale is the same forA and B.
- Fig. 3.
ADP does not depend on Na+ or Ca2+ influx through voltage-gated channels but is associated to an Rin increase.A, ADP response in control conditions (A1), in the presence of 0.5 μm TTX (A2), and after substitution of Ca2+with Mg2+ and the addition of BAPTA-AM (50 μm) to the Ringer's solution for 30 min (A3). Same cell in all conditions.Vm, −60 mV. Rest, −81 mV.B, Effect of Cd2+ (100 μm), La3+ (100 μm), and replacement of Ca2+ with Co2+ on the ADP. We returned to control Ringer's solution between each treatment. Cd2+ and La3+increased the amplitude of the ADP, presumably because they reduced Ca2+-dependent K+ conductances, thus increasing the input resistance. C, Voltage response to current pulses (−0.01 nA) before and after ADP induction. During the ADP, current (bottom trace) was manually injected into the cells to maintain the Vmat a constant value.
- Fig. 4.
ADP varies in a Nernstian manner with [K+]o and is reduced by TEA.A, ADP induction by depolarizing pulses to ∼0 mV from different Vm values with [K+]o of 2.5 (A1) and 21 (A2) mm. TTX (0.5 μm) was present. B1, Relationship between ADP amplitude and prepulse potential for [K+]o of 2.5 (filled circles), 13.5 (open triangles), 21 (open circles), and 30 (open diamonds) mm.B2, ADP reversal potential as a function of [K+]o (filled triangles). Continuous line, Nernst prediction.C, Response to depolarizing pulses to 0 mV in Ringer's solution (C1), with 40 mm TEA (C2), and after 30 min in control Ringer's solution (C3). TTX (0.5 μm) was present throughout. Prepulse Vm was −60 mV.
- Fig. 5.
Time and voltage dependence of the ADP.A, Effect of changes in pulse duration (A1) on ADP amplitude (A2) and duration (A3). B1, Depolarizing pulses of increasing amplitudes from −60 mV. Insets, Normalized ADP amplitude (filled triangles) versus the peakVm reached during the current pulses (n = 7). B2, Normalized ADP amplitude (filled circles) caused by depolarizing current pulses to 0 mV as a function of the prepulseVm (n = 7).Dashed line is a polynomial fit of the data.Continuous line fits the data after correction for changes in K+ driving force andRin. Inset, Changes inRin (open circles) estimated by measuring voltage responses to current pulses of ±0.01 nA in the same cells.
- Fig. 6.
Impact of ISD on ITC responsiveness. A, Changes in the degree of activation of ISD when suprathreshold current pulses are applied from −75 (A1) or −62 (A2) mV. Symbols below traces indicate the hypothesized state of the channels. B, Voltage response (top trace) to repetitive current pulses (bottom trace) applied from a Vm of −74 (B1) or −66 (B2) mV. C, Response to repetitive electrical stimuli in the basolateral complex delivered at two different frequencies before versus after a suprathreshold current pulse from −60 mV. Voltage scale is the same for A–C.
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