Introduction. To study the regularities of formation of individual experience we summarize the results of research in consolidation, reconsolidation of memory, extinction and forgetting within a unified idea that considers them in the frames of systems psychophysiology as manifestations of two coordinated processes: formation of new experience and modification of previously formed experience. Theoretical Justification. Within the framework of the theory of functional systems, it had been proposed that systemogenesis also takes place in adults, since the formation of a new behavioral act is the formation of a new system. In studies with single-neuron activity recording it was shown that during performance of new behavior the simultaneous activation of multiple earlier formed systems occurs along with activation of new systems formed during learning. Therefore, we consider consolidation, reconsolidation, extinction, and forgetting as manifestations of reorganization of individual experience as a whole. The results of research in the neurophysiology of memory show that the processes of memory formation (including its consolidation) and forgetting are not mutually exclusive and can take place independently. Some forms of forgetting are caused by the inability to use memory, rather than by its removal, that makes forgetting similar to the formation of extinction. Discussion. We argue that (re)consolidation, extinction and forgetting may be based on similar long-term changes in previously formed experience, in particular those that do not let some elements of this experience to be utilized further.

The results of the study of assessing the contribution of the acute alcohol administration factor to the indicators of analyticity–holism on the AHS scale are presented. The study was conducted on

The high attrition rates in glioblastoma (GB) therapeutic development stem largely from preclinical models that fail to adequately recapitulate the dynamic tumor–host ecosystem. Unlike previous reviews that characterize glioma cell lines in isolation, this article integrates tumor biology with the distinct neuro-immune–endocrine landscapes of major laboratory rat strains. We critically evaluate standard rat malignant glioma cell lines (C6, F98, RG2, 9L) alongside transplantable tissue models (GB 101.8, GB 15/47), which offer enhanced translational relevance, demonstrating that the predictive value of any model is contingent upon the specific “glioma model and host strain” pairing and the individual physiological characteristics of the host. We provide evidence that strain-specific hypothalamic–pituitary–adrenal (HPA) axis reactivity (e.g., hyper-reactive Fischer 344 versus normo-reactive Wistar) acts as a decisive, yet often overlooked, modulator of the tumor microenvironment and therapeutic response. The review delineates the utility and limitations of these models, specifically addressing the MHC incompatibilities of the widely used C6 model in immunotherapy research, while contrasting it with the immune-evasive phenotypes of RG2 and the GB 101.8 tissue model. Furthermore, we highlight the superiority of tissue transplants in preserving cellular polyclonality and diffuse infiltration patterns compared to the circumscribed growth often observed in cell line-derived tumors. Consequently, we propose a strategic selection paradigm wherein immunogenic models serve as bioindicators of host immunocompetence, while invasive, non-immunogenic systems (F98, RG2, and GB 101.8) are utilized to investigate therapeutic resistance and systemic host-tumor interactions.

A method has been developed and tested to study the processes of acquisition/improvement of a skill. The method is based on the Signal Detection Theory and the “Yes-No” task and involves the evaluation of short time intervals. The theoretical justification of the use of this technique for studying the acquisition/improvement of a skill was given from the standpoint of the system-evolutionary approach. The main factors that can act as side variables during the use of this technique were taken into account and leveled, especially the so-called «sensory» adaptation and existing experience. Two experimental series was conducted, each of which was aimed at checking the factors that distorted the results. In the first series, the focus was on the «sensitization” factor. The phenomenon of sensitization for the task of distinguishing short time intervals and the method of accounting for this factor was described. In the second series, the discriminativity of the method was investigated, and the parameters of the complexity of the task were selected for further empirical research of skill acquisition/improvement.

The high attrition rates in glioblastoma (GB) therapeutic development stem largely from preclinical models that fail to adequately recapitulate the dynamic tumor-host ecosystem. Unlike previous reviews that characterize glioma cell lines in isolation, this article integrates tumor biology with the distinct neuro-immune-endocrine landscapes of major laboratory rat strains. We critically evaluate standard rat malignant glioma cell lines (C6, F98, RG2, 9L) alongside transplantable tissue models (GB 101.8, GB 15/47), which offer enhanced translational relevance, demonstrating that the predictive value of any model is contingent upon the specific "glioma model and host strain" pairing and the individual physiological characteristics of the host. We provide evidence that strain-specific hypothalamic-pituitary-adrenal (HPA) axis reactivity (e.g., hyper-reactive Fischer 344 versus normo-reactive Wistar) acts as a decisive, yet often overlooked, modulator of the tumor microenvironment and therapeutic response. The review delineates the utility and limitations of these models, specifically addressing the MHC incompatibilities of the widely used C6 model in immunotherapy research, while contrasting it with the immune-evasive phenotypes of RG2 and the GB 101.8 tissue model. Furthermore, we highlight the superiority of tissue transplants in preserving cellular polyclonality and diffuse infiltration patterns compared to the circumscribed growth often observed in cell line-derived tumors. Consequently, we propose a strategic selection paradigm wherein immunogenic models serve as bioindicators of host immunocompetence, while invasive, non-immunogenic systems (F98, RG2, GB 101.8) are utilized to investigate therapeutic resistance and systemic host-tumor interactions.