PKA Inhibitor H89 (N-[2-p-bromocinnamylamino-ethyl]-5-isoquinolinesulfonamide) Attenuates Synaptic Dysfunction and Neuronal Cell Death following Ischemic Injury

<div>The measurement of BDNF expression in Neuro2A cells after H/R-induced injury. The level of BDNF was evaluated by immunocytochemistry. This image shows that the expression of BDNF in the H/R group was reduced compared to the normal group. H89 pretreatment increased the expression of BDNF in N2A cells in spite of hypoxia reperfusion injury. Scale bar: 200 <i>μ</i>m, BDNF: green, 4′,6-diamidino-2-phenylindole (DAPI): blue, normal: the normal control group, H/R: 4 hr hypoxia and 18 hr reperfusion injury group, and H89: 2 hr PKA inhibitor H89 treatment group before 4 hr hypoxia and 18 hr reperfusion injury.</div>

Neural Plasticity

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Figure 6

Figure 6: PKA Inhibitor H89 (N-[2-p-bromocinnamylamino-ethyl]-5-isoquinolinesulfonamide) Attenuates Synaptic Dysfunction and Neuronal Cell Death following Ischemic Injury 

Figure 6 | PKA Inhibitor H89 (N-[2-p-bromocinnamylamino-ethyl]-5-isoquinolinesulfonamide) Attenuates Synaptic Dysfunction and Neuronal Cell Death following Ischemic Injury 