## 4 Discussion  
Our previous work showed that the blockade of SRC and IKK\(\beta\) kinases positively affects nerve cell viability when modeling ischemia factors [8,9]. However, IKK\(\beta\) inhibition did not allow the main parameters of calcium activity to be maintained at the proper level, and SRC blockade only partially preserved the share of active cells. In this work, we investigated the effect of SRC and IKK\(\beta\) kinase blockade in more detail and evaluated the effects of inhibition of the studied kinases in vivo. In our work, we investigated the previously undescribed effect of SRC and IKK\(\beta\) kinase inhibitors on neural network bioelectrical activity. It is important to evaluate not only cell viability but also the integrity of the neural network during the blockade of these kinases and modeling of ischemia factors. Nerve cells form neural networks providing intercellular communication, exchanging molecules and information, thereby exhibiting spontaneous electrical and chemical activity. The registration and analysis of signals between neurons allow the obtainment of necessary information about the properties of neural networks and their functional architecture [17]. Figure 9: Representative MR-images of the brains of mice in the modeling of acute ischemic brain injury. (**A**)—Intact, (**B**)—Control, (**C**)—SRC inhibitor, (**D**)—IKK\(\beta\) inhibitor. Arrows show traces of inhibitor injection. Using the multielectrode arrays for the extracellular action potentials' registration we can assess the functional integrity of neural networks, which is an additional parameter for evaluating the efficiency of the adaptive capabilities of nerve cells. In addition to calcium imaging, the assessment of functional neural network activity using multielectrode arrays will create a comprehensive picture of the preservation of synaptic contacts and neuronal signaling. Inhibition of IKK\(\beta\) and SRC kinases cause a neuroprotection effect that contributes to the maintenance of viability. However, despite the preservation of neuronal viability, SRC kinase blockade partially maintains the number of spikes in a network impulse burst but does not allow for the preservation of the number of network bursts. IKK\(\beta\) kinase blockade does not support the spontaneous bioelectrical activity of primary neuronal cultures in the late posthypoxic period. Recent studies have shown that SRC kinase inhibition can attenuate hypoxia-induced overactivation of CaM kinase IV, which in turn attenuates apoptotic cell death and improves neurological status in modeling of hypoxia in piglets [18]. SRC is also involved in receptor-mediated mitophagy (removal of unwanted or damaged mitochondria in response to energy demand) [19]. There is evidence that kinases of the SRC family regulate the functioning of the NMDA receptor and are involved in the development of damage during ischemia/reperfusion. Blockade of p-SRC kinase improves neurological functions in hypoxic-ischemic injury [20]. Our results obtained in vivo to verify the experiments on cell cultures are consistent with these data and indicate that the administration of an SRC kinase inhibitor to experimental animals increases the survival time of animals in the modeling of AHH, increases the share of high- and medium-resistant animals, and contributes to the reduction of morphological changes during hypoxic brain damage. Thus, studies in vivo confirmed the neuroprotective effect of SRC inhibition revealed in studies in vitro. However, the protective effect of IKK\(\beta\) kinase inhibition has not been confirmed in the in vivo study. This may be due to the fact that the action of this kinase is associated with the activation of the transcription factor NF-\(\kappa\)B, which has highly diverse pleiotropic effects that may differ when implemented in cell culture and in vivo.