THE INFLUENCE OF INVESTMENT INTERMEDIARIES ON THE CORPORATE SECTOR DEVELOPMENT OF UKRAINE

As the world experience shows, countries with the developed market economy are characterized by a high level of investment intermediation, as well as by an effective cooperation and interdependence of investors and corporations. The practice of domestic corporations shows also the objective dependence of the development level of intermediation and corporate sector that is stipulated. So in this study, the impact of investment intermediaries on the corporate sector development was estimated on the basis of econometric modeling. The result of the research is a proof of investment intermediaries operation in the domestic corporate sector that generally requires finding the way to increase the impact of their activities on the development level of the corporate sector. Investment intermediators’ activation opportunities as to corporate sector investments with some challenges are shown in their investments into the Ukrainian corporate sector

Improved Reversal Learning and Working Memory and Enhanced Reactivity to Novelty in Mice with Enhanced GABAergic Innervation in the Dentate Gyrus

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Excitation of Diverse Classes of Cholecystokinin Interneurons in the Basal Amygdala Facilitates Fear Extinction

There is growing evidence that interneurons (INs) orchestrate neural activity and plasticity in corticoamygdala circuits to regulate fear behaviors. However, defining the precise role of cholecystokinin-expressing INs (CCK INs) remains elusive due to the technical challenge of parsing this population from CCK-expressing principal neurons (CCK PNs). Here, we used an intersectional genetic strategy in CCK-Cre;Dlx5/6-Flpe double-transgenic mice to study the anatomical, molecular and electrophysiological properties of CCK INs in the basal amygdala (BA) and optogenetically manipulate these cells during fear extinction. Electrophysiological recordings confirmed that this strategy targeted GABAergic cells and that a significant proportion expressed functional cannabinoid CB1 receptors; a defining characteristic of CCK-expressing basket cells. However, immunostaining showed that subsets of the genetically-targeted cells expressed either neuropeptide Y (NPY; 29%) or parvalbumin (PV; 17%), but not somatostatin (SOM) or Ca2+/calmodulin-dependent protein kinase II (CaMKII)-α. Further morphological and electrophysiological analyses showed that four IN types could be identified among the EYFP-expressing cells: CCK/cannabinoid receptor type 1 (CB1R)-expressing basket cells, neurogliaform cells, PV+ basket cells, and PV+ axo-axonic cells. At the behavioral level, in vivo optogenetic photostimulation of the targeted population during extinction acquisition led to reduced freezing on a light-free extinction retrieval test, indicating extinction memory facilitation; whereas photosilencing was without effect. Conversely, non-selective (i.e., inclusive of INs and PNs) photostimulation or photosilencing of CCK-targeted cells, using CCK-Cre single-transgenic mice, impaired extinction. These data reveal an unexpectedly high degree of phenotypic complexity in a unique population of extinction-modulating BA INs

Identification of a novel gene regulating amygdala-mediated fear extinction.

Recent years have seen advances in our understanding of the neural circuits associated with trauma-related disorders, and the development of relevant assays for these behaviors in rodents. Although inherited factors are known to influence individual differences in risk for these disorders, it has been difficult to identify specific genes that moderate circuit functions to affect trauma-related behaviors. Here, we exploited robust inbred mouse strain differences in Pavlovian fear extinction to uncover quantitative trait loci (QTL) associated with this trait. We found these strain differences to be resistant to developmental cross-fostering and associated with anatomical variation in basolateral amygdala (BLA) perineuronal nets, which are developmentally implicated in extinction. Next, by profiling extinction-driven BLA expression of QTL-linked genes, we nominated Ppid (peptidylprolyl isomerase D, a member of the tetratricopeptide repeat (TPR) protein family) as an extinction-related candidate gene. We then showed that Ppid was enriched in excitatory and inhibitory BLA neuronal populations, but at lower levels in the extinction-impaired mouse strain. Using a virus-based approach to directly regulate Ppid function, we demonstrated that downregulating BLA-Ppid impaired extinction, while upregulating BLA-Ppid facilitated extinction and altered in vivo neuronal extinction encoding. Next, we showed that Ppid colocalized with the glucocorticoid receptor (GR) in BLA neurons and found that the extinction-facilitating effects of Ppid upregulation were blocked by a GR antagonist. Collectively, our results identify Ppid as a novel gene involved in regulating extinction via functional actions in the BLA, with possible implications for understanding genetic and pathophysiological mechanisms underlying risk for trauma-related disorders

Restoration of synaptic plasticity and learning in young and aged NCAM-deficient mice via elevation of neurotransmission mediated by the GluN2A-containing NMDA receptors

The neural cell adhesion molecule NCAM is the predominant carrier of the unusual polysialic acid (PSA). Deficits in PSA and/or NCAM expression cause impairments in hippocampal longterm potentiation and depression (LTP and LTD), and are associated with schizophrenia and aging. Here, we show that impaired LTP in adult NCAM deficient (NCAM-/-) mice is restored by increasing the activity of the NMDA subtype of glutamate receptors (GluN) by either elevation of extracellular Ca2+ and reduction of extracellular Mg2+ concentrations, or by Dcycloserine (DCS), a partial agonist of the GluN glycine binding site. Pharmacological inhibition of the GluN2A subtype reduced LTP to the same level in NCAM-/- and wild-type (NCAM+/+) littermate mice and abolished the rescue by DCS in NCAM-/- mice, suggesting that the effects of DSC are mediated by GluN2A. In NCAM-/- and NCAM+/+ mice, LTD was impaired in the presence of GluN2A or GluN2B antagonists, suggesting that both GluN2A and GluN2B are required for this form of plasticity. Remarkably, insufficient contribution of GluN to LTD in NCAM-/- mice was compensated by DCS. Furthermore, impaired contextual and cued fear conditioning was restored in NCAM-/- mice by administration of DCS before conditioning. In 1- year-old NCAM+/+ mice, LTP matched that of 3-month-old mice, but was further reduced in 1- year-old NCAM-/- mice when compared to 3-month-old NCAM-/- mice. DCS fully restored LTP at this age and partially rescued LTP in 2-year-old NCAM-/- mice. Thus, several deficiencies in synaptic plasticity and learning of NCAM-/- mice can be abrogated by enhancement of GluN2Amediated neurotransmission