## 3 Results
\begin{table}
\begin{tabular}{c c c c} \hline \multirow{2}{*}{**Group**} & **Baseline at 14 DIV** & **1 Day after Hypoxia** & **7 Days after Hypoxia** \\  & **(Before Exposure to the** & **(14 DIV)** & **(21 DIV)** \\ \hline \multicolumn{4}{c}{_Average number of small network bursts/10 min_} \\ Intact (\(n=6\)) & 14.41 \(\pm\) 0.84 & 16.45 \(\pm\) 1.28 & 36.33 \(\pm\) 4.39 \# \\ Hypoxia (\(n=6\)) & 13.83 \(\pm\) 1.30 & 13.17 \(\pm\) 1.85 & 15.33\(\pm\) 2.75 \({}^{*}\) \\ Hypoxia + IKK\(\beta\) inhibitor (\(n=6\)) & 15.17 \(\pm\) 1.35 & 12.16 \(\pm\) 2.18 & 22.66 \(\pm\) 1.76 \({}^{*}\) \\ Hypoxia + SRC inhibitor (\(n=6\)) & 15.50 \(\pm\) 1.64 & 11.83 \(\pm\) 1.45 & 19.83 \(\pm\) 1.94 \({}^{*}\) \\  & _Average number of spikes in a network burst_ & & \\ Intact (\(n=6\)) & 15.67 \(\pm\) 2.07 & 16.50 \(\pm\) 1.28 & 90.33 \(\pm\) 11.63 \# \\ Hypoxia (\(n=6\)) & 13.83 \(\pm\) 1.30 & 20.34 \(\pm\) 1.85 & 11.58 \(\pm\) 0.62 \({}^{*}\) \\ Hypoxia + IKK\(\beta\) inhibitor (\(n=6\)) & 13.17 \(\pm\) 2.58 & 14.39 \(\pm\) 1.87 & 36.16 \(\pm\) 6.05 \({}^{*}\) \\ Hypoxia + SRC inhibitor (\(n=6\)) & 13.83 \(\pm\) 1.30 & 52.78 \(\pm\) 8.21 \#\$ & 28.71 \(\pm\) 4.18 \$ \\ \hline \end{tabular} \({}^{*}\)—the differences are significant compared to the Intact group, \(p\leq 0.05\), \(\$\)—the differences are significant compared to the Hypoxia group, \(p\leq 0.05\), \(\#\)—the differences are significant compared to baseline, two-way repeated measures ANOVA. A—Average number of small network bursts/10 min, \(F=1030.563\), \(p=5.51\times 10^{-7}\). Bonferroni post-hoc level revealed significant differences between the following groups: Intact 7 days vs. Intact baseline \(p=2.2167\times 10^{-6}\), Intact 7 days vs. Intact 1 day \(p=1.5776\times 10^{-5}\), On 7 th day: Hypoxia vs. Intact \(p=5.4456\times 10^{-6}\); Hypoxia + IKK\(\beta\) inhibitor vs. Intact \(p=0.0051\); Hypoxia + SRC inhibitor vs. Intact \(p=3.5323\times 10^{-4}\). B—Average number of spikes in a network burst, \(F=135.699\), \(p=8.1877\times 10^{-5}\). Bonferroni post-hoc test revealed significant differences between the following groups: Intact 7 days vs. Intact baseline \(p=4.72\times 10^{-11}\), Intact 7 days vs. Intact 1 day \(p=6.2394\times 10^{-11}\), Hypoxia + SRC inhibitor vs. Hypoxia 1 day \(p=8.0157\times 10^{-5}\), Hypoxia + SRC inhibitor 7 day vs. Hypoxia 1 day \(p=0.0309\). On 1 st day: Hypoxia + SRC inhibitor vs. Intact \(p=0.0005\), Hypoxia + SRC inhibitor vs. Hypoxia \(p=3.5878\times 10^{-5}\). On 7 th day: Hypoxia vs. Intact \(p=1.2062\times 10^{-11}\); Hypoxia + IKK\(\beta\) inhibitor vs. Intact \(p=8.5271\times 10^{-8}\); Hypoxia + SRC inhibitor vs. Intact \(p=4.134\times 10^{-9}\), Hypoxia + IKK\(\beta\) inhibitor vs. Hypoxia \(p=0.0309\); Hypoxia + SRC inhibitor vs. Hypoxia \(p=0.0051\).  
\end{table} 
Table 1: Key parameters of spontaneous bioelectrical activity of primary hippocampal cultures against the background of kinase blockade under physiological conditions in vitro. Inhibition of SRC kinase in hypoxic damage supported the partial maintenance of neural network activity at a functional level. Despite the fact that the level of spontaneous bioelectrical activity was reduced relative to intact cultures, on day 7 of the posthypoxic period, the number of spikes forming a burst in the Hypoxia + IKK\(\beta\) inhibitor group and Hypoxia + SRC inhibitor group was significantly higher than in the Hypoxia group (36.16 \(\pm\) 6.05 and 28.71 \(\pm\) 4.18 respectively). Blockade of the IKK\(\beta\) kinase also partially maintained bioelectrical activity during hypoxia modeling (7 th posthypoxic day number spikes in burst 36.16 \(\pm\) 6.05). The analysis of activation patterns shows an increase in the time of impulse propagation between the electrodes in the posthypoxic period. Blockade of IKK\(\beta\) and SRC kinases does not lead to maintenance of the structure of network activity in the late posthypoxic period (Figure 2).