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. Author manuscript; available in PMC: 2012 Jun 26.
Published in final edited form as: Nat Med. 1999 Aug;5(8):888–894. doi: 10.1038/11330

Fig. 4.

Fig. 4

The effects of protein kinase blockers on the enhanced amplitude of the evoked IPSCs in CA1 pyramidal cells after hyperthermia-induced seizures. a, Staurosporin (0.5 μM; 2 h of incubation) abolished the difference between the evoked IPSC amplitudes in CA1 cells from control and experimental (HT) rats (1 week after seizures). The amplitude of the evoked IPSCs without staurosporin from the same HT rats was increased (as expected from Fig. 2). Control with staurosporin (○), n = 7 cells; control without staurosporin (●), n = 6 cells; HT with staurosporin (△), n = 8 cells; HT without staurosporin (▲), n = 7 cells. *, P < 0.05. The ability of staurosporin to abolish the difference between control and HT rats indicates the involvement of a protein kinase in the presynaptic potentiation of the GABAA responses in CA1 cells after hyperthermia-induced seizures. b, The PKA-specific inhibitor Rp-cAMPS (100 μM) also abolished the enhanced evoked IPSC amplitude recorded from CA1 pyramidal cells of HT rats 1 week after hyperthermia-induced seizures. Control with Rp-cAMPS (○), n = 7 cells; control without Rp-cAMPS (●), n = 7 cells; HT with Rp-cAMPS (△), n = 7 cells; HT without Rp-cAMPS (▲), n = 8 cells; the brain slices were incubated in Rp-cAMPS for 2 hours. *, P < 0.05. c, Incubation of the brain slices with the specific PKC inhibitor calphostin C (1 μM, 2 h of incubation) did not have any effect on the increased amplitude of the monosynaptically evoked IPSCs in CA1 pyramidal cells from HT or control rats 1 week after hyperthermia-induced seizures. Control with calphostin-C (○), n = 6 cells; control without calphostin-C (●), n = 6 cells; HT with calphostin-C (△), n = 9 cells; HT without calphostin-C (▲), n = 6 cells. In contrast, the same concentration of calphostin was able to block the PDBU-induced increase in the evoked IPSC amplitude, indicating that the PKC antagonist was effectively blocking PKC activity in these experiments. d, Forskolin (10 μM) enhanced the amplitude of the evoked IPSCs in CA1 cells from HT rats to a significantly greater degree than in control rats. Evoked IPSC after forskolin with respect to the amplitude of the evoked IPSC before forskolin: control, 155.0 ± 20%; HT, 381.0 ± 81%; n = 5 for both groups. *, P < 0.05. Thus PKA, but not PKC, is involved in the presynaptic enhancement of the inhibitory neurotransmission after HT-induced seizures.