Among the responses in the early stages of stroke, activation of neurodegenerative and proinflammatory processes in the hippocampus is of key importance for the development of negative post-ischemic functional consequences. However, it remains unclear which genes are involved in these processes. The aim of this work was a comparative study of the expression of genes encoding glutamate and GABA transporters and receptors, as well as inflammation markers in the hippocampus one day after two types of ischemic exposure (according to Koizumi - MCAO-MK, and Longa - MCAO-ML), as well as after direct pro-inflammatory activation by central administration of lipopolysaccharide (LPS). The results obtained revealed both differences and similarities between the responses to the impacts applied in the work. A greater number of genes that changed the expression associated with the activation of apoptosis and neuroinflammation, glutamate reception, and markers of the GABAergic system were found after MCAO-ML and LPS, than after MCAO-MK. In turn, MCAO-MK and LPS were characterized, in comparison with MCAO-ML, by changes in a larger number of genes involved in glutamate transport. The most pronounced difference between MCAO-ML and MCAO-MK and LPS was changes in the expression of genes for calmodulin and calmodulin-dependent kinases. The revealed features of the responses of the hippocampal transcriptome to two types of ischemia and a pro-inflammatory stimulus will contribute to further understanding of the causes of the diversity of stroke consequences, both in model studies and in the clinic.