The genetic model of diabetes mellitus was studied on mutant C57Bl/KsLepr(db/+) mice. These mice were characterized by high concentrations of glucose and glycosylated hemoglobin in the blood, polyuria, polyphagia, polydipsia, progressive obesity, biphasic morphological changes in insular islets of the pancreas (hyperplasia and atrophy), fatty degeneration of the liver, and hypoplasia of the spleen tissue and lymph nodes. Our results indicate that C57Bl/KsLepr(db/+) mice serve as an adequate model of type 2 diabetes mellitus. This model is suitable for testing of therapeutic methods for type 2 diabetes mellitus.

Analysis of intracentral brain relationships, cognitive and psychopathological processes in animals by means of pharmacological modulation is an optimal method of cognition, determining the possibilities of correlation with similar processes in humans. New methods and approaches to biomodulation of psychopathologies, based on the principles of pharmaco-EEG standardization using fast Fourier-transformed brain electrograms and elements of systemic behavior, allow to identify quantitative parameters of fundamental mechanisms of neuropsychoactive agents in the cat brain.

The accumulation of scientific data in the field of pharmacogenetics requires the creation of adequate biomodels to reflect the immunogenetic characteristics of different population groups. We have obtained the ancestors of a new humanized transgenic mouse line carrying the human HLA-A*02:01:01:01 gene, which is characteristic of the Russian population. The new biomodels was created using the pronuclei microinjection method of a linearized fragment of genetically engineered DNA construct into zygotes, followed by overnight cultivation in CO2 incubator and transfer of potentially modified embryos at the stage of two 4.0 blastomere to pseudopregnant foster females. A total of 91 living offspring were obtained and analyzed, with 18 pups carrying the target genome modification. The resulting transgenic animals were used to create a new line of mouse biomodels carrying the human HLA-A*02:01:01:01 gene.

A high-frequency electrical activity across the range of 30–100 Hz, known as gamma rhythms, is observed in many regions of the brain. This phenomenon serves to synchronize the activity of various neural networks intended to process, transmit, store and receive information. Gamma rhythms play a key role in such processes of higher nervous activity as attention, sensory perception and memory formation. Impairment of gamma rhythms is a common symptom of diseases associated with cognitive impairment, including Alzheimer’s disease, epilepsy and schizophrenia. Recent studies have shown that a particular population of GABAergic-inhibiting neurons, i.e. parvalbumin-positive (PV+) interneurons, is the source of high-frequency oscillations. Maintenance of gamma rhythms is an extremely energy-intensive process that relies on a high rate of oxidative phosphorylation in the mitochondria of neurons and is limited by the presence of glucose. Insulin may be involved in the metabolic control of gamma oscillations, since PV+ interneurons selectively express the insulin-dependent glucose transporter GLUT4, which can provide an additional glucose influx under near-limit functioning conditions as in the case of high-frequency gamma oscillations. This review generalized available literature data on the relationship between metabolism and a high-frequency electrical brain activity, with an emphasis on the possible contribution of central insulin resistance to disturbances of gamma rhythms in the brain.