Helpless Behavior Research Articles

Mu-opioid receptor activation in the habenula modulates synaptic transmission and depression-like behaviors

Opioid system dysregulation in response to stress is known to lead to psychiatric disorders including major depression. Among three different types of opioid receptors, the mu-type receptors (mORs) are highly expressed in the habenula complex, however, the action of mORs in this area and its interaction with stress exposure is largely unknown. Therefore, we investigated the roles of mORs in the habenula using male rats of an acute learned helplessness (aLH) model. First, we found that mOR activation decreased both excitatory and inhibitory synaptic transmission onto the lateral habenula (LHb). Intriguingly, this mOR-induced synaptic depression was reduced in an animal model of depression compared to that of controls. In naïve animals, we found an unexpected interaction between mORs and the endocannabinoid (eCB) signaling occurring in the LHb, which mediates presynaptic alteration occurring with mOR activation. However, we did not observe presynaptic alteration by mOR activation after stress exposure. Moreover, selective mOR activation in the habenula before, but not after, stress exposure effectively reduced helpless behaviors compared to aLH animals. Our observations are consistent with clinical reports suggesting the involvement of mOR signaling in depression, and additionally reveal a critical time window of mOR action in the habenula for ameliorating helplessness symptoms.

Learned Helplessness As a Potential Transdiagnostic Therapeutic Mechanism of Classic Psychedelics

Background: Emerging literature suggests that classic psychedelics may have efficacy in treating mood and substance use disorders in humans. This has raised questions regarding the primary therapeutic mechanism of these compounds. Here, we hypothesize that the reversal of and resilience against learned helplessness may be an important driver of the therapeutic mechanisms of classic psychedelics. Furthermore, we argue that the learned helplessness paradigm can provide a robust model to investigate the behavioral and mechanistic effects of classic psychedelics in both clinical and preclinical experiments. Opinion: We highlight the learned helplessness model and its potential utility in the psychedelic sphere for several reasons. First, learned helplessness is a robust phenomenon observed across multiple mammalian species including humans, and has been well described in terms of its neurobiology, behavioral effects, and clinical implications; current efforts in psychedelic research and theories of psychedelic mechanisms have yet to achieve this level of integration. Interestingly, there is substantial overlap in the neural circuits governing resilience against learned helplessness and psychedelic actions—such as those involving the dorsal raphe nucleus. Furthermore, our hypothesis that classic psychedelics can reverse helplessness behavior fits with much of the current preclinical data, which has shown that psychedelics improve performance in behavioral despair tasks in rodents. Here we make the case for bringing attention to these congruencies in an effort to advance toward mechanistic, behavioral, and transdiagnostic insights into the therapeutic effects of classic psychedelics, with the potential for learned helplessness to help explain some positive effects across levels of analysis.

Fast antidepressant action of ketamine in mouse models requires normal VGLUT1 levels from prefrontal cortex neurons

The NMDA antagonist ketamine demonstrated a fast antidepressant activity in treatment-resistant depression. Pre-clinical studies suggest that de novo synthesis of the brain-derived neurotrophic factor (BDNF) in the PFC might be involved in the rapid antidepressant action of ketamine. Applying a genetic model of impaired glutamate release, this study aims to further identify the molecular mechanisms that could modulate antidepressant action and resistance to treatment.To that end, mice knocked-down for the vesicular glutamate transporter 1 (VGLUT1+/−) were used. We analyzed anhedonia and helpless behavior as well as the expression of the proteins linked to glutamate transmission in the PFC of mice treated with ketamine or the reference antidepressant reboxetine. Moreover, we analyzed the acute effects of ketamine in VGLUT1+/− mice pretreated with chronic reboxetine or those that received a PFC rescue expression of VGLUT1.Chronic reboxetine rescued the depressive-like phenotype of the VGLUT1+/− mice. In addition, it enhanced the expression of the proteins linked to the AMPA signaling pathway as well as the immature form of BDNF (pro-BDNF). Unlike WT mice, ketamine had no effect on anhedonia or pro-BDNF expression in VGLUT1+/− mice; it also failed to decrease phosphorylated eukaryote elongation factor 2 (p-eEF2). Nevertheless, we found that reboxetine administered as pretreatment or PFC overexpression of VGLUT1 did rescue the antidepressant-like activity of acute ketamine in the mice.Our results strongly suggest that not only do PFC VGLUT1 levels modulate the rapid-antidepressant action of ketamine, but also highlight a possible mechanism for antidepressant resistance in some patients.

The NOP antagonist BTRX-246040 increases stress resilience in mice without affecting adult neurogenesis in the hippocampus

Nociceptin/orphanin FQ (N/OFQ) is the endogenous ligand of an inhibitory G protein coupled receptor named N/OFQ peptide receptor (NOP). Clinical and preclinical findings suggest that the blockade of the NOP signaling induces antidepressant-like effects. Additionally, the blockade of the NOP receptor during inescapable stress exposure prevented the acquisition of the helplessness phenotype, suggesting that NOP antagonists are able to increase stress resilience. BTRX-246040 (aka LY2940094) is a NOP receptor antagonist with high affinity, potency and selectivity for the NOP over classical opioid receptors. BTRX-246040 is under development for the treatment of depression, eating disorders and alcohol abuse and it already entered clinical trials.In the present study, the antidepressant effects of BTRX-246040 were evaluated in mice subjected to the forced swimming test and to the learned helplessness model of depression. Additionally, the ability of BTRX-246040 to prevent the development of the helpless behavior and to modulate adult hippocampal neurogenesis has been investigated.BTRX-246040 (30 mg/kg, i.p.) produced antidepressant-like effects in the forced swimming test and in the learned helplessness model. More interestingly, when given before the stress induction sessions it was able to prevent the development of the helplessness behavior. Under these experimental conditions, BTRX-246040 did not modulate adult hippocampal neurogenesis, neither in naive nor in stressed mice.This study, performed with a clinically viable ligand, further corroborates growing evidence indicating that the blockade of the NOP signaling may provide an innovative strategy for the treatment of stress related psychopathologies.

The Duration of Stress Determines Sex Specificities in the Vulnerability to Depression and in the Morphologic Remodeling of Neurons and Microglia.

Stress exposure has been shown to induce a variety of molecular and functional alterations associated with anxiety and depression. Some studies suggest that microglia, the immune cells of the brain, play a significant role in determining neuronal and behavioral responses to chronic stress and also contribute to the development of stress-related psychopathologies. However, little is known about the impact of the duration of stress exposure upon microglia and neurons morphology, particularly considering sex differences. This issue deserves particular investigation, considering that the process of morphologic remodeling of neurons and microglia is usually accompanied by functional changes with behavioral expression. Here, we examine the effects of short and long unpredictable chronic mild stress (uCMS) protocols on behavior, evaluating in parallel microglia and neurons morphology in the dorsal hippocampus (dHIP) and in the nucleus accumbens (NAc), two brain regions involved in the etiology of depression. We report that long-term uCMS induced more behavioral alterations in males, which present anxiety and depression-like phenotypes (anhedonia and helplessness behavior), while females only display anxiety-like behavior. After short-term uCMS, both sexes presented anxiety-like behavior. Microglia cells undergo a process of morphologic adaptation to short-term uCMS, dependent on sex, in the NAc: we observed a hypertrophy in males and an atrophy in females, transient effects that do not persist after long-term uCMS. In the dHIP, the morphologic adaptation of microglia is only observed in females (hypertrophy) and after the protocol of long uCMS. Interestingly, males are more vulnerable to neuronal morphological alterations in a region-specific manner: dendritic atrophy in granule neurons of the dHIP and hypertrophy in the medium spiny neurons of the NAc, both after short- or long-term uCMS. The morphology of neurons in these brain regions were not affected in females. These findings raise the possibility that, by differentially affecting neurons and microglia in dHIP and NAc, chronic stress may contribute for differences in the clinical presentation of stress-related disorders under the control of sex-specific mechanisms.

C1q deletion exacerbates stress-induced learned helplessness behavior and induces neuroinflammation in mice

Increased levels of pro-inflammatory cytokines have been reported in postmortem brain samples and in the blood of depressed subjects. However, the inflammatory pathways that lead to depressive-like symptoms are not well understood. Using the learned helplessness (LH) model of depression, we examined the role of C1q, the initiator of classical complement pathway in mediating stress-induced depressive-like behavior in mice. We observed no significant changes in social behavior, despair behavior, spatial memory, and aggressive behavior between the wild type (WT) and C1q knockout (KO) mice. However, C1q deletion exacerbated the inescapable electric foot shock-induced learned helplessness behavior in mice. We found significant reductions in C1q mRNA levels in the prefrontal cortex (PFC) of WT helpless mice as compared to the naïve mice. Increased levels of pro-inflammatory cytokines were found in the PFC of C1q KO mice. These findings suggest that classical complement pathway-mediated learned helplessness behavior is accompanied by neuroinflammatory changes under stressful conditions.

GENDER PECULIARITIES OF STUDENT YOUTH PREDISPOSITION TO VICTIM BEHAVIOR

The article represents theoretical and practical workouts concerning the main gender peculiarities of predisposition and manifestation of student youth victim behavior. Psychological factors and peculiarities of victim behavior in elder juvenile age have been analyzed in the article. Particular attention has been given to gender specificity of manifestation of victim behavior in elder juvenile age. Meaningful value has been given to the solution of the indicated problems of student youth in the context of preparation of a professional specialist, sufficient to self-realization of a personality. A person’s gender as oneself and in combination with other characteristics, profession or kind of occupation has a high coefficient of victimhood. It has been determined, that young boys are more inclined to aggressive victim, self-destructive hyper social behavior than young girls.Two-way behavior is peculiar for them: provocative, when another person is involved in causing harm, and self-inflicted, which is characterized by predisposition to risk, thoughtless actions, often dangerous for a person itself and for surrounding people. And also young girls are more inclined to dependent and helpless behavior than young boys. In other words young girls are not inclined to stand against in case of danger for various reasons: first of all, due to physical weakness, fear, misgiving of responsibility about own illegal or immoral actionsї, and secondly, because of setting on helplessness. Young girls, who are involved in crisis situations, seek for compassion and support of others, are in a role position of a victim, they more often are shy and conformal, experience subjective difficulties in activity organization and have low frustration tolerance. Peculiarities concerning the prophylactic work on preventing of victimhood have been highlighted. The main tasks of victimhood prophylaxis is detection and fixing of positive personality traits, formation of ability to make a choice independently, awareness of responsibility, timely resolution of conflicts.

Changes in the Orexin System in Rats Exhibiting Learned Helplessness Behaviors.

Orexin-A (OX-A) and orexin-B (OX-B) are neuropeptides produced in the hypothalamus. Preclinical and clinical studies suggest that depression and anxiety are associated with the orexin system. In the current study, we used the learned helplessness (LH) animal model of depression to identify rats displaying LH behaviors (LH rats) and those that did not (No-LH rats). We compared the number of orexin-containing neurons in the hypothalamus of LH, No-LH, and control rats. Orexin peptides, orexin receptor 1 (OXR1) and 2 (OXR2) in brain areas involved in major depression and serum OX-A and corticosterone (CORT) concentrations were quantified and compared between rat groups. We found that LH and No-LH rats displayed higher serum OX-A concentrations compared with control rats. Comparison between LH and No-LH rats revealed that No-LH rats had significantly higher OX-A levels in the brain, more OX-A neurons, and more OX-A neuron activation. LH rats had more OX-B neurons and more OX-B neuron activation. Orexin peptides and receptors in the brain areas involved in major depression exhibited different patterns in LH and NoLH rats. Our findings revealed that activation of OX-A neurons could promote resilient behaviors under stressful situations and OX-A and OX-B neuropeptides exhibit dissimilar functions in LH behaviors.

Post-stress glucose consumption facilitates hormesis and resilience to severe stress

Oral ingestion of a glucose solution following severe stress is a simple and effective way of preventing several of the negative sequelae of stress in rats. Similar resilience is obtained through hormetic training – pre-exposure to mild-to-moderate stress prior to severe stress. Here, we examined whether hormetic training is facilitated when a glucose solution is available following each hormetic training session. In Experiment 1, all rats were pre-exposed to a 30 min hormetic session of 25 inescapable tailshocks on each of 3 days. The schedule or hormesis differed between groups. The hormetic sessions occurred on either 3 consecutive days or with an interpolated day of rest between each hormetic session. Furthermore, in each of these conditions, one group had access to water and one group had access to a 40% glucose solution immediately after each hormetic session to complete a 2x2 factorial design. All groups were exposed to 100 inescapable tailshocks on the day following the end of hormetic training. Shuttle-escape testing occurred 24 h later. In Experiment 2, rats received two consecutive days of 100 inescapable tailshocks. Water or glucose was available following each session. Testing occurred 24 h after the second shock exposure. Experiment 1 replicated previous findings that rats exposed to hormetic training with interpolated rest did not show exaggerated fear responding or shuttle-escape deficits that normally result from 100 inescapable tailshocks, but training was ineffective if no rest was given between stress sessions. However, all post-stress glucose groups showed an elimination of helpless behavior. In Experiment 2, it was revealed that even 100 tailshocks can be made hormetic by post-stress glucose consumption.

Ophn1 regulation of prefrontal inhibition: A mechanism for stress susceptibility in intellectual disability

Wang etal. (2021) characterize the molecular, cellular, and circuit-level role of Oligophrenin-1 in prefrontal parvalbumin interneurons, demonstrating that loss of Ophn1 function in these neurons is a mechanism for increased susceptibility to stress in intellectual disability caused by OPHN1 mutations.

Oligophrenin-1 moderates behavioral responses to stress by regulating parvalbumin interneuron activity in the medial prefrontal cortex

Ample evidence indicates that individuals with intellectual disability (ID) are at increased risk of developing stress-related behavioral problems and mood disorders, yet a mechanistic explanation for such a link remains largely elusive. Here, we focused on characterizing the syndromic ID gene oligophrenin-1 (OPHN1). We find that Ophn1 deficiency in mice markedly enhances helpless/depressive-like behavior in the face of repeated/uncontrollable stress. Strikingly, Ophn1 deletion exclusively in parvalbumin (PV) interneurons in the prelimbic medial prefrontal cortex (PL-mPFC) is sufficient to induce helplessness. This behavioral phenotype is mediated by a diminished excitatory drive onto Ophn1-deficient PL-mPFC PV interneurons, leading to hyperactivity in this region. Importantly, suppressing neuronal activity or RhoA/Rho-kinase signaling in the PL-mPFC reverses helpless behavior. Our results identify OPHN1 as a critical regulator of adaptive behavioral responses to stress and shed light onto the mechanistic links among OPHN1 genetic deficits, mPFC circuit dysfunction, and abnormalities in stress-related behaviors.

СОЦІАЛЬНО-ПСИХОЛОГІЧНІ ЧИННИКИ СХИЛЬНОСТІ ОСОБИСТОСТІ ДО УТВОРЕННЯ СПІВЗАЛЕЖНИХ СТОСУНКІВ

У статті представлено результати теоретичного та емпіричного дослідження чинників утворення співзалежних стосунків. Проаналізовані різні підходи до визначення співзалежності та визначений деструктивний вплив міжособистісної залежності на структуру особистості. Отримані результати розширили уявлення про зв`язок між невпевненістю в собі, емоційною опорою на інших, безпомічною поведінкою, реалізованою віктимністю та схильністю до співзалежної поведінки. 
 Ключові слова: адикція; міжособистісна залежність; співзалежність; стосунки; особистість.

Stress Resilience is Associated with Hippocampal Synaptoprotection in the Female Rat Learned Helplessness Paradigm

The synaptogenic hypothesis of major depressive disorder implies that preventing the onset of depressive-like behavior also prevents the loss of hippocampal spine synapses. By applying the psychoactive drugs, diazepam and fluoxetine, we investigated whether blocking the development of helpless behavior by promoting stress resilience in the rat learned helplessness paradigm is associated with a synaptoprotective action in the hippocampus. Adult ovariectomized and intact female Sprague-Dawley rats (n = 297) were treated with either diazepam, fluoxetine, or vehicle, exposed to inescapable footshocks or sham stress, and tested in an active escape task to assess helpless behavior. Escape-evoked corticosterone secretion, as well as remodeling of hippocampal spine synapses at a timepoint representing the onset of escape testing were also analyzed. In ovariectomized females, treatment with diazepam prior to stress exposure prevented helpless behavior, blocked the loss of hippocampal spine synapses, and muted the corticosterone surge evoked by escape testing. Although fluoxetine stimulated escape performance and hippocampal synaptogenesis under non-stressed conditions, almost all responses to fluoxetine were abolished following exposure to inescapable stress. Only a much higher dose of fluoxetine was capable of partly reproducing the strong protective actions of diazepam. Importantly, these protective actions were retained in the presence of ovarian hormones. Our findings indicate that stress resilience is associated with the preservation of spine synapses in the hippocampus, raising the possibility that, besides synaptogenesis, hippocampal synaptoprotection is also implicated in antidepressant therapy.

Antidepressant effects of 3-(3,4-methylenedioxy-5-trifluoromethyl phenyl)-2E-propenoic acid isobutyl amide involve TSPO-mediated mitophagy signalling pathway.

Piper laetispicum C. DC is one of the Chinese herbal medicines used for alleviating depressive disorders. G11-5 [3-(3, 4-methylenedioxy-5-trifluoromethyl phenyl)-2E-propenoic acid isobutyl amide] is synthesized based on the chemical structure of an activeintegrant of Piper laetispicum C. DC. The present study assessed the antidepressant effect of G11-5 and investigated the underlying mechanism with learned helplessness (LH) and social defeat stress (SDS) mice model of depression. In the LH model, mice were exposed to 60 inescapable electric shocks once a day for three consecutive days followed by 2-week drug administration and helpless behaviour assessment. In the SDS model, mice were subjected to repeated social defeat by an aggressive CD-1 mouse once a day for consecutive 10days. Following oral administration for 2weeks, the mice were subjected to a series of behavioural tests including social interaction test. G11-5 significantly decreased the number of escape failures induced by LH paradigm, meanwhile increased the social interaction ratio and shortened the immobility time in forced swimming test for the SDS-exposed mice, suggesting remarkable antidepressant effect. Moreover, G11-5 ameliorated the changes in mitophagy-related proteins induced by two stress exposures and restored retrograde axonal transport and neurotransmitter release. Our findings suggested that G11-5 exhibited an obvious antidepressant through TSPO-mediated mitophagy pathway.

The gut microbiota metabolite indole increases emotional responses and adrenal medulla activity in chronically stressed male mice

Background and aimsThe gut microbiota produces metabolites that are an integral part of the metabolome and, as such, of the host physiology. Changes in gut microbiota metabolism could therefore contribute to pathophysiological processes. We showed previously that a chronic and moderate overproduction of indole from tryptophan in male individuals of the highly stress-sensitive F344 rat strain induced anxiety-like and helplessness behaviors. The aim of the present study was to extend the scope of these findings by investigating whether emotional behaviors of male mice that are moderately stress-sensitive but chronically exposed to environmental stressors would also be affected by indole. MethodsWe colonized germ-free male C3H/HeN mice with a wild-type indole-producing Escherichia coli strain, or with the non-indole producing mutant. Gnotobiotic mice were subjected to an unpredictable chronic mild stress procedure, then to a set of tests aimed at assessing anxiety-like (novelty and elevated plus maze tests) and depression-like behaviors (coat state, splash, nesting, tail suspension and sucrose tests). Results of the individual tests were aggregated into a common z-score to estimate the overall emotional response to chronic mild stress and chronic indole production. We also carried out biochemical and molecular analyses in gut mucosa, plasma, brain hippocampus and striatum, and adrenal glands, to examine biological correlates that are usually associated with stress, anxiety and depression. ResultsChronic mild stress caused coat state degradation and anhedonia in both indole-producing and non-indole producing mice, but it did not influence behaviors in the other tests. Chronic indole production did not influence mice behavior when tests were considered individually, but it increased the overall emotionality z-score, specifically in mice under chronic mild stress. Interestingly, in the same mice, indole induced a dramatic increase of the expression of the adrenomedullary Pnmt gene, which is involved in catecholamine biosynthesis. By contrast, systemic tryptophan bioavailability, brain serotonin and dopamine levels and turnover, as well as expression of gut and brain genes involved in cytokine production and tryptophan metabolism along the serotonin and kynurenine pathways, remained similar in all mice. ConclusionsChronic indole production by the gut microbiota increased the vulnerability of male mice to the adverse effects of chronic mild stress on emotional behaviors. It also targeted catecholamine biosynthetic pathway of the adrenal medulla, which plays a pivotal role in body’s physiological adaptation to stressful events. Future studies will aim to investigate the action mechanisms responsible for these effects.

Vulnerability to helpless behavior is regulated by the circadian clock component CRYPTOCHROME in the mouse nucleus accumbens

The nucleus accumbens (NAc), a central component of the midbrain dopamine reward circuit, exhibits disturbed circadian rhythms in the postmortem brains of depressed patients. We hypothesized that normal mood regulation requires proper circadian timing in the NAc, and that mood disorders are associated with dysfunctions of the NAc cellular circadian clock. In mice exhibiting stress-induced depression-like behavior (helplessness), we found altered circadian clock function and high nighttime expression of the core circadian clock component CRYPTOCHROME (CRY) in the NAc. In the NAc of helpless mice, we found that higher expression of CRY is associated with decreased activation of dopamine 1 receptor-expressing medium spiny neurons (D1R-MSNs). Furthermore, D1R-MSN-specific CRY-knockdown in the NAc reduced susceptibility to stress-induced helplessness and increased NAc neuronal activation at night. Finally, we show that CRY inhibits D1R-induced G protein activation, likely by interacting with the Gs protein. Altered circadian rhythms and CRY expression were also observed in human fibroblasts from major depressive disorder patients. Our data reveal a causal role for CRY in regulating the midbrain dopamine reward system, and provide a mechanistic link between the NAc circadian clock and vulnerability to depression.

Prelimbic medial prefrontal cortex disruption during adolescence increases susceptibility to helpless behavior in adult rats

Major depressive disorder (MDD) is a disabling mental disorder worldwide. Several animal models have been used to study the neurobiology of this disorder, including the learned helplessness (LH) paradigm, in which susceptible animals show helpless behavior indicated by fails to escape a controllable footshock. This behavior has been associated with a downregulation of ventral tegmental area (VTA) dopamine (DA) system activity. The prelimbic portion of the prefrontal cortex (plPFC) plays an important role in the modulation of helpless behavior, but so far there is no evidence indicating that its developmental disruption alters susceptibility to helpless behavior. We investigated the impact of plPFC lesion performed at adolescence (postnatal day 31–33) or adulthood (postnatal day 70–72) on anxiety responses (elevated plus-maze), susceptibility to helpless behavior, and the VTA DA system activity in adult Sprague-Dawley rats. Whereas adult plPFC lesions induced neither anxiety responses nor increased susceptibility to helpless behavior (plPFC lesion: 33.3% of helplessness; controls: 30.8% of helplessness rats), adolescent plPFC lesions induced anxiety responses and increased the proportion of rats showing helpless at adulthood (plPFC lesion: 92.3% helplessness; controls: 42.1% helplessness rats). Moreover, only helpless rats in the groups showed a decreased VTA DA system population activity that was confined to the medial portion of the VTA. These findings suggest that the impairment of plPFC activity during adolescence occurs during a critical window for the development of helpless behavior in adult rats, indicating that predisposition or early life adverse events that impair plPFC activity may enhance susceptibility to depression in adulthood.

Аутоагрессия как предиктор виктимного поведения личности

The article focuses on autoaggressive behaviour in the context of victimisation risks. The authors consider a number of approaches that define autoaggressive manifestations in Russian and foreign psychology. It is noted that a tendency towards self-aggression may be induced by various causes found within an individual’s personality and in the external environment. Particularly, the efforts of the parents to restrain and control a child’s aggression by using corporal punishment only reinforce and increase the risk of self-injurious behaviour. The main purpose of the research is to study autoaggression as a predictor of victim behaviour. In order to address the issue identified as the main focus of the study, the authors present the results of empirical research conducted at Novosibirsk State Pedagogical University on a sample group of students, both male and female, aged 18–23 years. In total, the study involved 70 people. Regression analysis was applied to determine the predictors contributing to different manifestations of victim behaviour. As a result, the propensity for non-critical behaviour was linked to neurotic spontaneous aggression, injurious reactive aggression, and suppression of anger. The tendency towards highly social victimisation behaviour was connected to anger, irritability, reactive aggression, and self-injurious behaviour. The propensity for dependent and helpless behaviour correlates with the levels of hopelessness, inhibition of aggression, and suppression of anger. The tendency towards self-injurious behaviour and self-destruction is influenced by auto-aggression, depression, irritability, and inhibition of aggression. In conclusion, the collected results suggest that there is a set of variables associated with the different manifestations of victim behaviour.

STYLE CHARACTERISTICS OF BEHAVIOR SELF-REGULATION IN STUDENTS WITH VARIOUS VICTIMITY

Aim. In the present work, victimity is considered as a psychological deviation manifestingin specific behavioral responses that characterize the type of potential victim. The emphasis ismade on the necessity of taking into account a realized victimity of a person, the formation of itsadequate forms and its correction at the stage of professional training. The article is aimed at establishingthe style characteristics of behavior self-regulation in students with various victimity.Materials and methods. Based on the analysis of the results obtained according to the “Realizedvictimity” scale (the “Tendency to victim behavior” questionnaire) all subjects were divided intotwo groups: an average (n = 36) and below-average (n = 53) victimity. The data on victimity, behaviorself-regulation and emotional intelligence in students of the pedagogical university wereobtained using the corresponding questionnaires: “Tendency to victim behavior”, “Style of behaviorself-regulation”, “Emotional intelligence”. Results. In the structure of students’ victimity,high values are observed on scales that assess the tendency to addictive and helpless behavior, toaggressive victim behavior, to self-damaging and self-destructive behavior, and to non-criticalbehavior. When comparing groups of students with various victimity, the following features wereregistered expressed in the differences in the style characteristics of behavior self-regulation (inthe implementation of modeling, assessment and flexible interaction); in the absence of differencesin the parameters of emotional intelligence. Conclusion. Features of behavior selfregulationin students are determined by their victimity. Subjects with low victimity are twice aslikely to show high behavior self-regulation compared to respondents with average victimity. Theidentified risk group of students who are prone to addictive and helpless behavior requires specialmeasures to accompany their social adaptation at the university. When it comes to the formationof professional competencies of the future teacher, it is advisable to include in the program ofelective courses the analysis of the results of studies of victimity in students, pedagogical workers,as well as ways to correct victim identity deformation.

Prospective associations between children's depressive symptoms and peer victimization: The role of social helplessness.

Investigating precursors to peer victimization, a particularly damaging form of peer maltreatment, represents an important research objective. This study's purpose was to evaluate the hypothesis that social helplessness is one mechanism underlying the pathway from early depressive symptoms to subsequent peer victimization among preadolescents in the third through fifth grades (N=230; 126 girls; Mage at recruitment=9.48; SD=0.68). We collected self-reports of depressive symptoms and peer victimization and teacher reports of social helplessness in the fall of 2015 or 2016 (T1) and at two subsequent time points (T2 and T3) separated by 6-month lags. Results from a random intercepts cross-lagged panel model provided evidence for our hypothesized model in which T2 social helplessness partially mediated the effect of T1 depressive symptoms on T3 peer victimization. Findings underscore the importance of school-based prevention and youth development programmes that promote social-emotional learning for youth who are symptomatic for depression. Statement of contribution What is already known on the subject? Children's depressive symptoms and interpersonal dysfunction are related in a transactional way. Children who are symptomatic for depression tend to exhibit social-behavioural deficits. Depression-linked, social-behavioural deficits are associated with relationship disturbances. What does this study add? Children's socially helpless behaviour mediated the contribution of depressive symptoms to subsequent peer victimization. Depressive symptoms predicted, and were predicted by, socially helpless behaviour. Socially helpless behaviour increased risk for, but did not result from, peer victimization.