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. 2004 May 26;24(21):5054–5062. doi: 10.1523/JNEUROSCI.5671-03.2004

Figure 3.

Figure 3.

Involvement of the cAMP-PKA pathway, but not of tyrosine kinases, in the nonphysiological target-dependent inhibition of neurotransmitter release. A, Effects of application of the cAMP-PKA activators Sp-cAMPS and forskolin (Forsk) and of the PKA kinase inhibitor Rp-cAMPS on the evoked depolarization of the sniffer B2 after C1 stimulation in C1C3 cocultures incubated in the presence or absence of anisomycin (AM). The depolarization recorded in the B2 sniffer after the stimulation of the isolated, untreated C1 neuron is shown for comparison (open bar). Statistical analysis indicates a significant increase in neurotransmitter release after treatment with AM, Sp-cAMPS, or forskolin (ANOVA: F(6,99) = 23.08, p < 0.001; Newman-Keuls multiple comparison test: p < 0.05). B, C1C3 cocultures incubated in the absence or presence of anisomycin were treated with the tyrosine kinase inhibitors genistein (Gen) or lavendustin (Lav) before recording the C1 stimulation-induced depolarization in the sniffer B2. The data in the plot indicate that tyrosine kinase inhibition does not affect either the decrease of neurotransmitter release induced by the nonphysiological target or the rescuing effect of anisomycin (ANOVA: F(6,42) = 16.15, p < 0.001; Newman-Keuls multiple comparison test: p < 0.05) between the untreated C1C3 and C1C3 treated with AM, AM plus genistein or AM plus lavendustin.