Alzheimer’s disease (AD) is a chronic neurodegenerative disorder of neural structures in different areas of the brain. Loss of synapses is a key stage in the development of AD and it precedes significant loss of neurons. However, the mechanisms of synapse loss are uncertain. Structural and functional changes in synapses are interrelated with the morphology of postsynaptic formations – dendritic spines. This paper describes the implementation of the technology of chronic imaging of dendritic spines in transgenic animals using the methods of multiphoton fluorescence microscopy. Mice of the 5xFAD-M hybrid line were used. 5xFAD-M was derived by crossing transgenic mice with expressions of green fluorescent protein GFP in individual neurons of the brain (M-Line) and a mouse model of AD (5xFAD line). Methodological achievements revealed the multi-day dynamics of the density of dendritic spines in M-Line and 5xFAD-M mice. Transformations of morphological types of spikes were revealed during a long period of observations.

In socially living species, including humans, social contacts’ deficit provokes chronic stress development, leading to disorders in the psychoemotional sphere, cognitive impairment, etc. Previously, we showed that spatial memory and passive avoidance impairments in rats exposed to months-long social isolation (SI) from an early age are more pronounced in females compared to males. There is lack research on females. This study aimed to evaluate learning in the two-way avoidance paradigm using the conditioned active avoidance reflex (CAAR) test and to assess skill retention in female rats exposed to SI, which started after the pups were taken from their dams and lasted for up to ten months. After 6.5 months of SI, rats were trained in the CAAR test when their anxiety level and grooming expression were lower than in rats housed in groups. Rats exposed to SI performed fewer avoidance but more escape responses and were less likely to achieve the learning criterion. In isolated rats compared to control rats, the escape latency was heightened, and the maximum number of avoidance reactions in a row was less after 24 hours after training. After 2 months after training, no differences in CAAR retention were revealed between rats kept in different housing conditions. After 10 months of SI, rat blood serum corticosterone levels were lower than in rats in the control group. The findings show worse learning and skill retention one day following training in the CAAR test in rats under the influence of long-term SI.

In a group of 49 young girls, the Stroop emotional task was used to study the effect of irrelevant information on attention bias and cognitive control of attention, depending on the severity of autonomic dysfunction (severe, moderate, absence). The subjects performed the task of identifying facial expressions of anger, fear and disgust, which was difficult by superimposing on the faces of words – names of emotions, congruent or incongruent to the presented facial expression. The results showed that autonomic dysfunction worsens attention control, makes it difficult to suppress irrelevant verbal information, and leads to an attention bias, quantified by the Stroop effect value. The most pronounced Stroop effect was found in the group of young girls with severe autonomic dysfunction. Among the negative emotions used in the work, disgust turned out to be the most effective for identifying the relationship between autonomic dysfunction and attention bias.

Social interactions in the context of cooperation and competition are the most important type of activity of people, determining their well-being and success in life. The neural bases of this activity, as well as the role of personality-related individual differences, are insufficiently studied. In particular, the literature lacks data on the relationship between neuroticism and individual differences in brain activity during cooperative and competitive interactions, and the aim of our work was to fill this gap. fMRI data were recorded during task performance in individual, cooperative, and competitive modes and analyzed using the inter-subject representative similarity analysis. The results indicate that in emotionally instable individuals, social interactions, in both cooperative and competitive contexts, are associated with greater strain, manifested in the activity of social brain, emotion regulation, and attentional centers. This can potentially lead to the accumulation of the effects of social stress and the emergence of symptoms of mental health problems.

Synaptic plasticity, which refers to long-term changes in the efficiency of synaptic transmission in the form of potentiation and depression, is thought to be a cellular mechanism of learning and memory. Long-term potentiation and depression can be induced under a variety of experimental conditions using different induction protocols. One such example is a protocol that follows Hebb’s rule, where induction of plasticity requires paired activation of a pre- and postsynaptic neuron that occur within a narrow temporal window relative to each other. Such plasticity is called homosynaptic plasticity because the same (homo-, Greek prefix meaning “same, identical”) synapses that participated in the induction of plasticity undergo long-term changes. However, as numerous experiments have shown, synapses that were inactive during the induction of plasticity also undergo long-term changes. This process has been termed heterosynaptic (hetero – “other, different”) plasticity in mammalian studies. Historically, however, the term heterosynaptic plasticity first appeared in studies of mollusks, where plastic changes in synaptic transmission were caused by a combination of stimulation of “weak” and “strong” synaptic inputs. As was later shown, the potentiating effect of stimulating the “strong” input in this case was associated with the release of neuromodulators, primarily serotonin. This type of plasticity was later demonstrated in mammals, where it was termed modulatory plasticity. The review considers different types of heterosynaptic plasticity, cellular and molecular mechanisms of its induction and maintenance, and explains the reasons for some terminological confusion related to this phenomenon in the literature.

In this review, based on our own and literature data, the temporal course of long-term memory formation, the duration of consolidation and reconsolidation processes, the temporal parameters of the interaction of glial and neuronal elements of the neural network, and possible mechanisms of neuro-glial interactions are analyzed. Based on the analysis, an assumption was made that allows us to explain the duration of the period of consolidation and reconsolidation of long-term memory (4–6 hours) by the need for the contribution of glia to the local epigenetic regulation of plasticity gene expression in the neurons of the memory engram.

The description of the developed experimental set, permitting to evaluate rats solution of the “object permanence” test (be J. Piaget), which reflects animal capacity to operate one of the most simple empirical rules (by Krushinsky), i.e. capacity to solve elementary logic task. An animal, being placed in the brightly lit part of the box, is eager to run into the dark one via underpass, although after the first attempts the underpass was hidden by several means, and now an animal can solve the task overcoming the obstacle in case it operates the object permanence rule. The test solution does not require the previous learning, and it is similar to the test used in mice experiments. The test was applied in experiments with rats of five genetic groups – outbred Wistar and Long-Evans rats, rats of inbred audiogenic-prone Krushinsky – Molodkina (KM) strain, the strain derived from KM rats, selected for audiogenic non-proneness and inbred SHR strain with spontaneous arterial hypertension. The preliminary experiments (performed with an animal during one experimental day) revealed interstrain differences with the test solution prevalence in SHR strain. This test could be used in pharmacological and neurophysiological experiments with rats.

Glial cell line-derived neurotrophic factor (GDNF) is under extensive investigation as a therapeutic agent for treating age-related neurodegenerative diseases and traumatic neuronal injury. The compelling results from preclinical studies contrast with the disappointing outcomes of phase II clinical trials in Parkinson’s disease, highlighting the need for further fundamental research. Several hypotheses have been proposed to explain these discrepancies, including challenges with the delivery of high molecular weight drugs, GDNF’s high affinity for heparin and heparin-like molecules, which limits its biodistribution in the brain parenchyma, the use of protein forms differing from the native GDNF, and the existence of multiple isoforms of the protein. These issues underscore the necessity for further investigation into GDNF at the genetic, RNA, and protein levels. This review aims to consolidate the latest data on GDNF, address the challenges identified, and explore its potential for therapeutic application in human neurodegenerative diseases.

The plasticity of inhibitory resposes during CA3-CA1 long-term potentiation (LTP) in the rat hippocampal slices was studied by the method of paired-pulse stimulation. Coefficients of inhibition were estimated by the differences between IPSP dependent and independent paired-pulse plasticity. In the experimental group high frequency stimulation of Schaffer collaterals was delivered under jasplakinolide exposure, this inhibitor of actin depolymerization is used also as activator of actin polymerization. It was shown that the feature of LTP development after induction with blockade of actin depolymerization include altered modification profile of inhibition, specifically involved in resposes to paired-pulse stimulation. Initial enhancement of inhibition depended on the value before tetanization. Therefore this factor may be responsible for between-group differences and it was taken into account in the evaluation of specific for posttetanic depolymerization changes. In result, this phase is related to disinhibition disorder during LTP consolidation and maintenance. It may be assumed that coordinating role of actin cytoskeleton is essential for balanced modifications of excitatory and inhibitory transmission during long-term plasticity.

Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized by impaired cognitive functions, from minor deviations to dementia, as well as altered behavior. Typical features of this disease include the presence of senile plaques, neurofibrillary tangles, synaptic damage, and neuronal loss. Many factors contribute to cognitive decline in patients with AD. According to the cholinergic hypothesis, which prevailed at the end of the last century and remains relevant today, a key event in the pathogenesis of AD is the loss of cholinergic neurons in the basal forebrain (BFB), found in this region in AD patients. However, the death of neurons deprives the brain of a range of other neurochemical agents. In addition, the occurrence of AD may also be caused also caused by other morphofunctional abnormalities in this area of the brain. In modern literature there is no summary information about the role of BFB in the pathogenesis of AD. The functions of the BFB and the mechanisms of regulation of the neural network of this part of the brain in normal conditions and in neuropathologies remain unclear. This review comprehensively examines the involvement of the BFB and its connections with other brain regions in the development of AD. The article includes data from clinical observations and experiments conducted both on healthy animals and on those with models of this disease. The analysis of the available literature data will improve the understanding of the functioning of the BFB normally and its disturbances during the development of AD, which can advance the development of therapeutic approaches for the treatment of this disease.