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. 2019 Jun 19;39(25):4909–4930. doi: 10.1523/JNEUROSCI.2226-18.2019

Figure 11.

Figure 11.

Loss of GABAB tone unmasks a Ca2+-dependent IsAHP. A, I–V relationship of the rebound outward current enhanced by Y2R activation. We isolated this with a series of brief (30 ms) hyperpolarizing voltage steps applied during its peak (insets), both in control and in [ahx5–24]NPY (1 μm; not illustrated; n = 3 cells, 3 rats). Net rebound current was measured as the difference between resting current before initiation of the voltage protocol and at the arrow placed immediately before the end of the hyperpolarizing steps, below the expanded trace in the inset. B, In [ahx5–24]NPY (1 μm), Cd2+ (100–200 μm) significantly decreased the rebound outward current (Irebound) from 73.3 ± 23.2 pA to 30.3 ± 15.5 pA (t(9) = 4.698; p = 0.0011; n = 10 cells, 8 rats; Student's paired t test). Seven PNs received 100 μm Cd2+; 3 received 200 μm Cd2+. As both doses had similar effects, we pooled these data. C, A representative outward rebound current following [ahx5–24]NPY (1 μm; blue), as in A. Treatment with UCL 2077 (10 μm; gray) substantially decreased this outward current. D, UCL 2077 (10 μm) treatment significantly decreased Irebound from 122.2 ± 38.3 pA to 49.6 ± 8.2 pA (p = 0.0260; n = 6 cells, 4 rats; Mann–Whitney U test). *p < 0.05, **p < 0.01.