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. Author manuscript; available in PMC: 2009 Dec 1.
Published in final edited form as: Neuropsychopharmacology. 2009 Feb 4;34(7):1829–1842. doi: 10.1038/npp.2009.5

Figure 2. NO-cGMP signaling requires PKG to enhance GABAergic IPSCs.

Figure 2

(a) A cGMP analogue, pCPT-cGMP (100 μM), potentiates IPSCs (146 ± 9% of pre-drug values, n=4). Inset: averaged IPSCs recorded during a single such experiment before (black) and after 15 minutes in pCPT-cGMP (red). Calibration for all insets: 10ms, 100 pA.

(b) The PKG inhibitor, KT5823 (500 nM), blocks the enhancement of IPSCs by 200 μM SNAP (101 ± 6% of pre-SNAP values, n=4). KT5823 was applied at least 15 minutes prior to the addition of SNAP. Inset: averaged IPSCs recorded during single experiment in KT5823 (black) and after 15 minutes in SNAP (red).

(c) KT5823 (500 nM) also prevents the potentiation of IPSCs by 100 μM pCPT-cGMP (104 ± 6% of pre-SNAP values, n=6). KT5823 was applied at least 15 minutes prior to the addition of pCPT-cGMP. Inset: averaged IPSCs recorded during single experiment in KT5823 (black) and after 15 minutes in pCPT-cGMP (red).

(d) KT5823 (500 nM) has no effect on basal GABAergic transmission (113 ± 6% of pre-drug values, n=5). Inset: averaged IPSCs recorded during single experiment before (black) and after 10 minutes in KT5823 (red).