Stress-related Disorders Research Articles

A Critical Review on Stress Management through Ayurveda

In today's competitive society, everyone is rushing about day and night to be the greatest in their own terms. There are a lot of demands, goals, chores, deadlines, frustrations, and annoyances in life that results into the various stress related disorders like hypertension, irritable bowel syndrome and behavioral disorders like Oppositional defiant disorder, Conduct disorder, Attention-deficit hyperactivity disorder. Stress is a state of worries or mental tension caused by a difficult situation. Both the body and the psyche are impacted by stress. Stress in moderation can be beneficial and even useful in carrying out daily tasks. But excessive stress can leads to problems with mental and physical health. In ayurveda stress is referred to as a root cause of Krodha. Krodha arises due to practice of Raktakopak Nidan which vitiate Raja Guna causing stress. Ayurveda emphasize on maintaining a healthy balance between mind and body. Today's altered human lifestyle is interfering with the balance and is a major source of stress. A balanced diet, yoga, meditation, and physical activity may be helpful in reducing stress. It purges on all levels - physical, mental, and emotional - and is similar to rejuvenation. Ayurvedic management for stress include Nidanparivarjan, Yoga, Nidra, Dincharya, Rritucharya, Sadvrut, Naishthiki Chikitsa (Satvavajaya Chikitsa) and Aushadh Sevan.

Post-traumatic stress disorder: molecular mechanisms of the intergenerational and transgenerational inheritance

Post-traumatic stress disorder is a mental disorder that is closely associated with dysfunction of the hypothalamic-pituitary-adrenal axis, and for its development is required the experience of a traumatic event that causes negative emotions and memories that persist for quite a long time. The likelihood of development of post-traumatic stress disorder is influenced both environmental factors, and genetic and epigenetic characteristics of the body. In this case epigenetic modifications act as dynamic biomarkers (“nanotags”) of the impact of the environment on the genome (epigenome), which can, under certain conditions, disappear or remain not only in an individual directly exposed to psychogenic trauma, but also transmitted over a number of generations. Review focuses on the possible mechanisms of intergenerational and transgenerational inheritance of the biological effects of post-traumatic and stress-related disorders.

A narrative review on emerging issues about war-related trauma in perinatal women: good practice for assessment, prevention, and treatment.

Wars, in addition to causing death and destruction, have a negative impact on mental health, especially on perinatal women. The literature has identified psychological trauma as one of the most prevalent mental health issues associated with wars, but few studies have summarized how to assess, prevent, or treat this problem in perinatal women. To address this gap, the purpose of this study is to provide a narrative review of the current state of assessment, prevention, and treatment interventions of trauma among perinatal women living in war conditions or displaced as a result of a war. A literature search was performed in different research databases (e.g., Medline, PsycInfo). The search terms include a combination of trauma and stressor-related disorders and focused on diagnosis, prevention, and treatment. Most of the results were related to post traumatic stress disorder (PTSD) more than acute stress disorder, although there are not many assessments, and interventions (prevention or treatment) dedicated specifically to perinatal women affected by war conditions. Research in this area is still scarce. Recommendations for evidence-based practices in assessment and prevention and treatment interventions and future directions in research and clinical practice are provided. • The literature on trauma in perinatal women is sparse, and especially among perinatal women living in conditions of war. • This paper presents a narrative review of evidence-based assessment and treatment for perinatal women victims of war who experience trauma.

From brain to blood and back again: Linking chronic stress, myelopoiesis, and depression

In this issue of Cell Stem Cell, Mou etal. identified a brain-bone marrow axis reinforcing myelopoiesis and neuroinflammation during psychological stress, culminating in depression. The identification of this pathway provides insights into hematopoietic stem cell homeostasis and regulatory neuronal function with potentially significant implications for the treatment of stress-related disorders.

Capturing inter-individual variability in stress dynamics with heart rate traces reveals activity in the bilateral hippocampus, amygdala, and insula

Abstract Abnormalities in the neural mechanisms of the stress response have the potential to serve as a transdiagnostic marker for stress-related disorders. This potential is rooted in the highly individual and dynamic stress response, which poses a challenge to classical experimentally informed models that focus on specific phases, conditions, or stimuli during a stress task. Here, we integrate individual heart rates (HR) as an immanent index of the stress-response and combine these with functional magnetic resonance imaging (fMRI) data. In this study, 83 healthy participants completed a multimodal psychosocial imaging stress task comprising three different task phases (PreStress, Stress, and PostStress), with each phase consisting of five 60 s blocks of active task interleaved with 40 s of rest, and simultaneous recordings of pulse plethysmography. Participants were asked to solve mental calculations and were exposed to negative social feedback during the Stress phase. We estimated a general linear model (GLM) with individual heart rates averaged per active block as a single parametric modulator of the task regressor across all 15 active blocks irrespective of the task phase. Results revealed a negative correlation between HR and activation in the bilateral amygdala and anterior hippocampus as well as deactivation in the default mode network. Positive correlations with HR were detected in the bilateral insular cortex, bilateral angular gyrus, and parts of the inferior and superior parietal lobes. In summary, our findings emphasize the utility of integrating the commonly assessed cardiovascular stress response (here: HR) as an immediate index of the participant’s stress status. We conclude that by such integration, brain regions involved in regulating the acute stress response, such as the anterior hippocampus and amygdala, are detected more sensitively by tracking the individual’s “stress wave” rather than treating every experimental block uniformly. Our approach may serve as a complementary analysis to the task-regressor based model.

Asoprisnil as a Novel Ligand Interacting with Stress-Associated Glucocorticoid Receptor

Background/objective: The glucocorticoid receptor (GR) is critical in regulating cortisol production during stress. This makes it a key target for treating conditions associated with hypothalamic–pituitary–adrenal (HPA) axis dysregulation, such as mental disorders. This study explores novel ligands beyond mifepristone for their potential to modulate GR with improved efficacy and safety. By investigating these interactions, we seek to identify new pharmacotherapeutic options for stress-related mental illness. Methods: The ligands asoprisnil, campestanol, and stellasterol were selected based on structural similarities to mifepristone (reference ligand) and evaluated for pharmacological and ADME (absorption, distribution, metabolism, and excretion) properties using the SwissADME database. Molecular docking with AutoDock 4.2.6 and molecular dynamics simulations were performed to investigate ligand–protein interactions with the human glucocorticoid receptor, and binding free energies were calculated using MMPBSA. Results: Pharmacokinetic analysis revealed that asoprisnil exhibited high gastrointestinal absorption and obeyed Lipinski’s rule, while mifepristone crossed the blood–brain barrier. Toxicological predictions showed that mifepristone was active for neurotoxicity and immunotoxicity, while asoprisnil, campestanol, and stellasterol displayed lower toxicity profiles. Asoprisnil demonstrated the highest stability in molecular dynamics simulations, with the highest negative binding energy of −62.35 kcal/mol, when compared to mifepristone, campestanol, and stellasterol, with binding energies of −57.08 kcal/mol, −49.99 kcal/mol, and −46.69 kcal/mol, respectively. Conclusion: This makes asoprisnil a potentially favourable therapeutic candidate compared to mifepristone. However, further validation of asoprisnil’s interaction, efficacy, and safety in stress-related mental disorders through experimental studies and clinical trials is needed.

Synergy of rehabilitation for stress-related disorders and ARIs in school-age children under the war condition in Ukraine

Synergy of rehabilitation for stress-related disorders and ARIs in school-age children under the war condition in Ukraine

The Iatrogenic Consequences of Medicalising Grief: Resetting the Research Agenda.

When the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) was published in 2013, there was a firestorm of controversy about the elimination of the bereavement exclusion. Proponents of this change and of the proposed "complicated grief" designation believed that this change would help clinicians recognise major depression in the context of recent bereavement. Other researchers and clinicians have raised concerns about medicalising grief. In 2022 "prolonged grief disorder" (PGD) was officially included in the DSM-5-TR in the trauma- and stressor-related disorders section. Not surprisingly, there has been a push to identify biomarkers and to use neuroimaging to identify the neurobiological basis of PGD. Some researchers have even suggested that PGD is a 'reward circuit disorder' akin to addiction and that naltrexone, an opioid antagonist, may be a promising treatment. The purpose of this paper is to show how medicalising grief reinforces a research agenda dedicated to the search for pharmaceutical and psychological 'magic bullets.' Following George and Whitehouse (2021), we propose that an ecopsychosocial approach-one that incorporates environmental and contextual factors-is needed.

Enduring modulation of dorsal raphe nuclei regulates (R,S)-ketamine-mediated resilient stress-coping behavior.

Ketamine may be a novel pharmacologic approach to enhance resilience and protect against stress-related disorders, but the molecular targets underlying this response remain to be fully characterized. The multifunctional protein p11 is crucial in the pathophysiology of depression and antidepressant responses. However, it is still unclear whether p11 plays a role in the pro-resilience effects induced by ketamine. Here, we demonstrated that prophylactic administration of ketamine buffers passive stress-induced maladaptive phenotypes induced by chronic stress exposure. Spatial neurotransmitter and metabolite analysis revealed that prophylactic ketamine was also effective in blunting stress-induced disturbances of tryptophan metabolism in dorsal raphe nuclei (DRN). Additionally, we demonstrated that ketamine prevented chronic restraint stress-induced p11 reduction in DRN, a highly p11-enriched region. Furthermore, we provide novel evidence indicating that p11 deficiency regulates susceptibility to stress-induced depression-related phenotypes, and these behavioral maladaptations are dependent, at least in part, on p11 function in serotonergic neurons. Spatial neurotransmitter and metabolite analysis also showed a reduction of tryptophan and dopamine metabolism in DRN of serotonergic p11-deficient mice. Viral-mediated downregulation of p11 within DRN induced a stress-susceptible phenotype. Finally, our results also unveiled that the ability of ketamine to elicit a pro-resilience response against stress-induced maladaptive phenotypes was occluded when p11 was selectively deleted in serotonergic neurons. Altogether, we showed a previously unexplored role of the DRN circuit in regulating stress susceptibility and resilience-enhancing actions of ketamine.

ASPECTOS EMOCIONAIS E DESAFIOS NA PRÁTICA DOS PROFISSIONAIS DE SAÚDE

Introduction: The emotional challenges faced by healthcare professionals are frequent and significantly impact the quality of care provided and individual well-being. This study addresses factors such as workload, constant exposure to suffering, and the stigmatization of emotional care, highlighting the effects exacerbated by the COVID-19 pandemic. Material and Methods: A literature review was conducted based on PRISMA guidelines, covering articles published between 2016 and 2024. The consulted databases included PubMed, Scopus, Web of Science, and Google Scholar. Articles analyzing emotional aspects and coping strategies related to healthcare professionals were included, while studies outside the scope or duplicates were excluded. Results and Discussion: The review highlighted the prevalence of burnout, anxiety, and other stress-related disorders among healthcare professionals. Psychological support strategies, resilience training, and practices such as mindfulness proved effective in reducing emotional impacts. However, barriers such as stigma and the lack of adequate institutional policies limit the implementation of preventive and corrective interventions. Conclusions: Promoting the emotional well-being of healthcare professionals is an ethical and strategic priority. Public policies and integrated institutional actions, combined with the use of psychological monitoring technologies, can mitigate the identified challenges, strengthening the sustainability of healthcare systems and the quality of care provided.

Salivary alpha-amylase: A marker of stress in gynecological residents during a shoulder dystocia simulation scenario.

Salivary alpha-amylase (sAA) has been recently proposed as biomarker of stress responsiveness within the sympathetic nervous system, preferable to cortisol, since limitations related to cortisol measurement (e.g. diurnal and seasonal rhythms, drugs interferences). Several factors, as age, collection device and analytical methods, also influence sAA levels and interpretation. This study aims to assess whether sAA could be useful to evaluate the stress response, also verifying some sources of variability. To identify any sources of sAA variability, saliva samples were collected from eight healthy subjects at five different times (8:00, 10:00, 12:00, 14:00 and 16:00) over five consecutive days using two different collection devices. Saliva was then collected from 35 obstetric residents before and after a simulated shoulder dystocia scenario, one of the most traumatic birth events in the professional life of gynecologists, to assess the stress levels. Samples were analysed throughout two different assays. Heart rate (HR) of residents was also measured before and after simulation scenario. Residents self-collected two saliva samples 10 min apart on a typical day. Overall, sAA levels increased significantly from morning to afternoon. Levels varied between subjects, but no differences were found between days or sampling devices. sAA activity levels in samples from 35 residents were significantly higher than those obtained before the scenario took place (about ten minutes later). These results were confirmed by two different assays. Moreover, a similar trend was observed when HR was considered. No differences were observed between samples collected 10 minutes apart on a typical day. Salivary alpha-amylase activity is a reliable, quick, and efficient marker for stress response, then its measurement will be of potential interest in the field of stress-related disorders. However, it is important to consider the timing of sample collection before introducing sAA in a clinical setting.

Ocular Side Effects of Medications for Anxiety, Depression, and Stress: A Review

Background: The COVID-19 pandemic has led to a global rise in mental health disorders, prompting increased usage of psychotropic medications. This study examines the ocular side effects associated with these medications in patients diagnosed with anxiety, depression, and stress-related disorders. Methods: A total of 100 patients were enrolled in this one-year study conducted at ESIC Medical College & Hospital, Bihta, Patna. Ocular evaluations were performed to assess the prevalence of dry eye disease (DED), mydriasis, elevated intraocular pressure (IOP), and other ocular complications of psychotropic medication use. Results: The study found that 75% of participants exhibited symptoms of dry eye disease, while 50% experienced mydriasis. Elevated intraocular pressure was observed in 15% of the patients. Additionally, 5% of participants developed acute angle-closure glaucoma, highlighting the significant ocular risks associated with psychotropic medication use. Conclusions: The findings indicate a high prevalence of ocular side effects among patients receiving treatment for anxiety and depression with psychotropic medications. Routine ocular assessments and patient education regarding these side effects are essential for improving patient outcomes and quality of life. Further research is needed to explore the long-term implications of these medications on ocular health. Keywords: Ocular Side Effects, Psychotropic Medications, Anxiety Disorders, Depression

Noradrenergic Projections from the Locus Coeruleus to the Medial Prefrontal Cortex Enhances Stress Coping Behavior in Mice Following Long-Term Intermittent Fasting.

Intermittent fasting has been shown to alleviate stress, anxiety, and depressive symptoms. Although noradrenaline, also known as norepinephrine (NE), is implicated in stress regulation, the dynamics of NE release and the associated neural pathways during stress coping behaviors in fasting mice remain poorly understood. In this study, we employed the forced swimming test (FST) to evaluate the effects of intermittent fasting on stress coping behavior in mice. Our results demonstrate that mice subjected to long-term intermittent fasting exhibited significantly more active coping behaviors in the FST compared to control mice. In contrast, acute fasting did not produce similar effects. Using the fluorescent GRAB-NE sensor to measure NE release with sub-second temporal resolution during the FST, we found that intermittent fasting modulates the locus coeruleus-medial prefrontal cortex (LC-mPFC) pathway, which underlies these behavioral adaptations. Moreover, chemogenetic activation of LC-mPFC projections strongly promoted active coping in the FST. These findings suggest that enhanced LC-mPFC activity mediates the increased active coping behavior observed in fasting mice. This study provides new insights into the neural mechanisms through which intermittent fasting may ameliorate depressive-like behaviors, offering potential therapeutic targets for stress-related disorders.

Efficacy of fluoxetine and (R,S)-ketamine in attenuating conditioned fear behaviors in male mice

Post-traumatic stress disorder (PTSD) is caused by exposure to a traumatic or stressful event. Symptoms related to this disorder include persistent re-experiencing of memories and fear of generalization. Current pharmacological treatments for PTSD are insufficient, with fewer than 30% of patients reporting symptom remission. This study aims to determine the efficacy of acute (R,S)-ketamine and chronic fluoxetine (FLX) in reducing fear memory and fear generalization. In rodents, fear conditioning (FC) is commonly used in the literature to induce behaviors related to symptoms of PTSD, and the open field test (OFT) can assess anxiety and fear generalization behaviors during the exploration of a novel environment. In this study, FC consisted of a white noise cue stimulus and 4 inescapable foot shocks. Treatments began 4 hours after FC. Fear and anxiety behaviors were recorded during re-exposure to the FC stimuli at 24 hours and 2 weeks. The OFT was conducted 1 day before the last FC re-exposure. Results support the combined use of acute ketamine and chronic FLX as a treatment for reducing behaviors indicative of fear memory during re-exposure at 2 weeks, but not behaviors indicative of anxiety and fear generalization in the OFT. FLX alone was most effective in reducing behaviors related to fear generalization. This study contributes to the existing literature on pharmacological treatment for fear and anxiety behaviors relating to fear memory and fear generalization. Continued research is necessary to replicate results, optimize treatment protocols, and investigate the molecular adaptations to trauma and treatment. Significance StatementUp to 6% of people in the United States will develop PTSD within their lifetime, and less than half of those individuals will find relief from their symptoms given the current therapeutic options. This study offers preliminary support for the efficacy of ketamine and FLX in reducing PTSD-like behaviors induced by fear-conditioning in mice. Compared with current standard treatments, the results of the current study indicate the potential for a more effective therapeutic option for those with stress-related disorders, such as PTSD.

A descriptive analysis of Aboriginal adolescents admitted to a regional inpatient mental health unit: Was culture considered?

To describe the characteristics of Aboriginal adolescents admitted to a Child and Adolescent Mental Health (CAMH) inpatient unit and assess if cultural identity was acknowledged, and what proportion received cultural support. A retrospective chart review of adolescents who identified as Aboriginal and were admitted to a regional CAMH Unit over 10years. Medical records were reviewed for demographics, diagnosis, details of admission, acknowledgement of Aboriginal identity, cultural information and cultural support provided. A total of 172 patients who identified as Aboriginal were admitted during this period, comprising a total of 266 admissions. Most frequent admission reason was suicidal ideation or self-harm (66%), then psychosis (14%) and 49% were admitted involuntarily. Most frequent discharge diagnosis was a stress-related disorder (23%) followed by post-traumatic stress disorder (18%). A referral for Aboriginal clinician cultural support was made for 30%. Thirty patients (23%) had any detail regarding cultural identity documented. Amongst young Aboriginal people admitted to a psychiatric inpatient unit, the minority had cultural identity acknowledged or were provided cultural support. There is a need for increased access to Aboriginal Mental Health Clinicians and improved training for the broader workforce in the provision of culturally considered care.

PTSD Increases Risk for Hypertension Development Through PVN Activation and Vascular Dysfunction in Sprague Dawley Rats.

This study investigates the impact of single prolonged stress (SPS), a model of post-traumatic stress disorder (PTSD), on cardiovascular responses, hypothalamic paraventricular nucleus (PVN) activity, and vascular function to elucidate the mechanisms linking traumatic stress to hypertension. Although SPS did not directly cause chronic hypertension in male Sprague Dawley (SD) rats, it induced acute but transient increases in blood pressure and heart rate and significantly altered the expression of hypertension-associated genes, such as vasopressin, angiotensin II type 1 receptor (AT1R), and FOSL1 in the PVN. Notably, mitochondrial reactive oxygen species (mtROS) were predominantly elevated in the pre-autonomic regions of the PVN, colocalizing with AT1R- and FOSL1-expressing cells, suggesting that oxidative stress may amplify sympathetic activation and stress responses. SPS also increased mRNA levels of pro-inflammatory cytokines (TNFα and IL1β) and inducible nitric oxide synthase (iNOS) in the aorta, and impaired vascular reactivity to vasoconstrictor and vasodilator stimuli, reflecting compromised vascular function. These findings suggest that SPS-sensitize neuroendocrine, autonomic, and vascular pathways create a state of cardiovascular vulnerability that could predispose individuals to hypertension when exposed to additional stressors. Understanding these mechanisms provides critical insights into the pathophysiology of stress-related cardiovascular disorders and underscores the need for targeted therapeutic interventions that address oxidative stress and modulate altered PVN pathways to mitigate the cardiovascular impact of PTSD and related conditions.

Examining threat responses through a developmental lens.

Adolescence has been characterized by risk taking and fearlessness. Yet, the emergence of anxiety disorders that are associated with fear peaks during this developmental period. Moreover, adolescents show heightened sensitivity to stress relative to children and adults. To address inconsistencies between the common characterization of adolescents as fearless and the evidence of heightened anxiety and stress during this time, we build upon foundational discoveries of threat-related circuitry and behavior in adult rodents by Joseph LeDoux and colleagues. Specifically, theconservation of this circuitry across species has provided opportunities for identifying mechanisms underlying threat responses that we have extended to developing humans and rodents. We elucidate situations in which adolescents show heightened threat responses and others where they appear fearless and link them to developmental changes of threat circuitry during this period. We discuss the potential adaptiveness of these threat responses for survival of the individual and species but also the potential risks for anxiety and stress. We end by offering potential new ways in which behavioral treatments for youth with anxiety and stress-related disorders may be optimized to target the developing vs developed brain.

Aromatic Serenity: How Lavender Eases Stress and Anxiety - A Literature Review

In today's fast-paced society, rising stress levels necessitate effective management strategies. While pharmacological treatments are common, their side effects have spurred interest in alternative therapies, particularly those rooted in natural remedies. Lavender (Lavandula angustifolia), long esteemed for its calming properties, has emerged as a promising non-pharmacological option. Historical use in herbal medicine for anxiety and stress-related disorders has inspired modern scientific research to explore its potential. This review synthesizes recent studies on lavender essential oil, examining its mechanisms—such as neurotransmitter modulation—and its effectiveness in diverse settings, from reducing stress among healthcare professionals to improving sleep quality. Despite promising results, limitations like small sample sizes and variability in application methods highlight the need for more rigorous research to establish lavender's efficacy and optimize its therapeutic use in stress management and mental health care.

Sex-specific GABAergic microcircuits that switch vulnerability into resilience to stress and reverse the effects of chronic stress exposure.

Clinical and preclinical studies have identified somatostatin (SST)-positive interneurons as critical elements that regulate the vulnerability to stress-related psychiatric disorders. Conversely, disinhibition of SST neurons in mice results in resilience to the behavioral effects of chronic stress. Here, we established a low-dose chronic chemogenetic protocol to map these changes in positively and negatively motivated behaviors to specific brain regions. AAV-hM3Dq-mediated chronic activation of SST neurons in the prelimbic cortex (PLC) had antidepressant drug-like effects on anxiety- and anhedonia-like motivated behaviors in male but not female mice. Analogous manipulation of the ventral hippocampus (vHPC) had such effects in female but not male mice. Moreover, the activation of SST neurons in the PLC of male mice and the vHPC of female mice resulted in stress resilience. Activation of SST neurons in the PLC reversed prior chronic stress-induced defects in motivated behavior in males but was ineffective in females. Conversely, activation of SST neurons in the vHPC reversed chronic stress-induced behavioral alterations in females but not males. Quantitation of c-Fos+ and FosB+ neurons in chronic stress-exposed mice revealed that chronic activation of SST neurons leads to a paradoxical increase in pyramidal cell activity. Collectively, these data demonstrate that GABAergic microcircuits driven by dendrite targeting interneurons enable sex- and brain-region-specific neural plasticity that promotes stress resilience and reverses stress-induced anxiety- and anhedonia-like motivated behavior. The data provide a rationale for the lack of antidepressant efficacy of benzodiazepines and superior efficacy of dendrite-targeting, low-potency GABAA receptor agonists, independent of sex and despite striking sex differences in the relevant brain substrates.

Transcriptome signatures of the medial prefrontal cortex underlying GABAergic control of resilience to chronic stress exposure.

Analyses of postmortem human brains and preclinical studies of rodents have identified somatostatin (SST)-positive, dendrite-targeting GABAergic interneurons as key elements that regulate the vulnerability to stress-related psychiatric disorders. Conversely, genetically induced disinhibition of SST neurons (induced by Cre-mediated deletion of the γ2 GABAA receptor subunit gene selectively from SST neurons, SSTCre:γ2f/f mice) results in stress resilience. Similarly, chronic chemogenetic activation of SST neurons in the medial prefrontal cortex (mPFC) results in stress resilience but only in male and not in female mice. Here, we used RNA sequencing of the mPFC of SSTCre:γ2f/f mice to characterize the transcriptome changes underlying GABAergic control of stress resilience. We found that stress resilience of male but not female SSTCre:γ2f/f mice is characterized by resilience to chronic stress-induced transcriptome changes in the mPFC. Interestingly, the transcriptome of non-stressed SSTCre:γ2f/f (stress-resilient) male mice resembled that of chronic stress-exposed SSTCre (stress-vulnerable) mice. However, the behavior and the serum corticosterone levels of non-stressed SSTCre:γ2f/f mice showed no signs of physiological stress. Most strikingly, chronic stress exposure of SSTCre:γ2f/f mice was associated with an almost complete reversal of their chronic stress-like transcriptome signature, along with pathway changes suggesting stress-induced enhancement of mRNA translation. Behaviorally, the SSTCre:γ2f/f mice were not only resilient to chronic stress-induced anhedonia - they also showed an inversed, anxiolytic-like behavioral response to chronic stress exposure that mirrored the chronic stress-induced reversal of the chronic stress-like transcriptome signature. We conclude that GABAergic dendritic inhibition by SST neurons exerts bidirectional control over behavioral vulnerability and resilience to chronic stress exposure that is mirrored in bidirectional changes in the expression of putative stress resilience genes, through a sex-specific brain substrate.