Escitalopram Treatment Research Articles

Escitalopram Induced Hair Loss

Drug-induced hair loss is more common than many clinicians realize, because it can easily be overlooked and it can disturb a patient's treatment adherence. In this report, we present an interesting and rare hair loss case, which developed after the onset of escitalopram treatment and which resolved after cessation of the drug.

Effect of selective serotonin reuptake inhibitors on expression of 5-HT1AR and neurotransmitters in rats with vascular dementia.

5-hydroxytryptamine receptor 1A (5-HT1AR) is closely associated with cognitive functions. Selective serotonin reuptake inhibitors (SSRIs) can protect individuals from brain damage following ischemia/hypoxia. To investigate the function of SSRIs in vascular dementia (VD), we established a rat model of VD, and observed the effect of SSRIs on the expression of 5-HT1AR mRNA and neurotransmitters. Male SD rats (6 months) were randomly assigned into sham, model, and SSRI groups (N = 30). VD was achieved by permanent ligation of the bilateral common carotid artery. Escitalopram, a highly selective 5-HT reabsorption inhibitor, was ip injected into the rats for three consecutive weeks. The Morris water-maze was used to test learning and memory. H&E staining for neuronal injury was conducted on cortical and hippocampal tissues. HPLC was used to determine the levels of dopamine (DA), 5-HT, and norepinephrine (NE). RT-PCR was used to determine expression of 5-HT1AR mRNA. As compared to control rats, model animals demonstrated elongated escape latency, lower platform crossing times, and significant injuries to hippocampal CA1 neurons. This was accompanied by reductions in DA, 5-HT, and NE levels in hippocampal tissues, as well as reduced cortical 5-HT and decreased 5-HT1AR mRNA expression (P < 0.05). Escitalopram treatments reduced escape latency, elevated platform crossing times, improved CA1 neuronal damage, increased DA and 5-HT levels in hippocampal and cortical neurons, as well as elevated expression of 5-HT1AR mRNA (P < 0.05). Therefore, SSRIs may improve cognitive dysfunction of VD rats, possibly by stimulating expression of neurotransmitters and protecting neurons.

Effects of Escitalopram on a Rat Model of Persistent Stress-Altered Hedonic Activities: Towards a New Understanding of Stress and Depression.

Chronic mild stress (CMS) paradigm is a model to simulate clinical depression induced by long-term environmental stress. The present study investigated the effects of escitalopram, a specific serotonin reuptake inhibitor (SSRI), on depression-like activities in adult (18 week-old) Sprague-Dawley (SD) rats that underwent a total 8-week CMS. Body weight, locomotor activity and sucrose consumption of the rats were measured under CMS paradigm and following escitalopram treatment. The plasma level of corticosterone was also measured at the end of the experiment. Our results revealed that the CMS program reduced the body weight, but not the locomotor activity of the rats. Adult SD rats consumed less sucrose solution under CMS. However, chronic escitalopram regime (10 mg/kg/day for 4 weeks) appeared not helpful in reversing this CMS effect and, if any, the drug exaggerated anxiety profile of the animals. Unexpectedly, the stressed rats exhibited higher sucrose consumption than non-stressed rats after receiving repeated saline injections. Further, the stressed rats were found to have a higher plasma level of corticosterone after escitalopram treatment. Our results provide an example of the possibility that previously stressed individuals may develop an anti-depression ability that lessens the benefits of intervention with antidepressants. Finally, a separate group of rats that entered the CMS program at 10 week-old were used to examine possible effects of aging to interpret the stress coping ability observed in the 18 week-old rats. The younger rats developed less anti-anhedonia effects under repeated saline injections. The data of the present study provide a different perspective on stress-induced depression and possible interaction with antidepressants.

Effect of short-term escitalopram treatment on neural activation during emotional processing.

Recent functional magnetic resonance (fMRI) imaging studies have revealed that subchronic medication with escitalopram leads to significant reduction in both amygdala and medial frontal gyrus reactivity during processing of emotional faces, suggesting that escitalopram may have a distinguishable modulatory effect on neural activation as compared with other serotonin-selective antidepressants. In this fMRI study we aimed to explore whether short-term medication with escitalopram in healthy volunteers is associated with reduced neural response to emotional processing, and whether this effect is predicted by drug plasma concentration. The neural response to fearful and happy faces was measured before and on day 7 of treatment with escitalopram (10mg) in 15 healthy volunteers and compared with those in a control unmedicated group (n=14). Significantly reduced activation to fearful, but not to happy facial expressions was observed in the bilateral amygdala, cingulate and right medial frontal gyrus following escitalopram medication. This effect was not correlated with plasma drug concentration. In accordance with previous data, we showed that escitalopram exerts its rapid direct effect on emotional processing via attenuation of neural activation in pathways involving medial frontal gyrus and amygdala, an effect that seems to be distinguishable from that of other SSRIs.

Associations between Serotonergic Genes and Escitalopram Treatment Responses in Patients with Depressive Disorder and Acute Coronary Syndrome: The EsDEPACS Study.

Genes related to serotonin are associated with responses to treatment for depression. We examined associations between the serotonin transporter (5-HTT) and serotonin 2a receptor (5-HTR2a) genes and responses to treatment for depressive disorders in acute coronary syndrome (ACS). A total of 255 patients who met the DSM-IV major or minor depressive disorder and recently developed ACS were randomly assigned to the escitalopram (n=127) or placebo (n=128) group in this 24-week double-blind trial (ClinicalTrial.gov identifier: NCT00419471). Remission was defined as a Hamilton Rating Scale for Depression (HAMD) score ≤7. Assays were performed for the 5-HTTLPR, STin2 VNTR, 5-HTR2a 102T/C, and 5-HTR2a 1438A/G genotypes. Escitalopram was superior to placebo for treating depressive disorder with ACS but there were no significant associations between serotonergic genes and treatment responses even when considering ACS severity. The effect of escitalopram was independent of 5-HTT and 5-HTR2a polymorphisms.

Chronic P-glycoprotein inhibition increases the brain concentration of escitalopram: potential implications for treating depression.

Recent preclinical studies have revealed a functionally important role for the drug efflux pump P‐glycoprotein (P‐gp) at the blood–brain barrier in limiting brain levels and thus antidepressant‐like activity of certain antidepressant drugs. Specifically, acute administration of P‐gp inhibitors, such as verapamil and cyclosporin A (CsA), has been shown to augment brain concentrations and functional activity of the antidepressant escitalopram in rodents. However, depression is a chronic disorder and current treatments require prolonged administration to elicit their full therapeutic effect. Thus, it is important to investigate whether acute findings in relation to P‐gp inhibition translate to chronic paradigms. To this end, the present study investigates whether chronic treatment with the P‐gp inhibitor verapamil and the antidepressant escitalopram results in enhanced brain distribution and antidepressant‐like effects of escitalopram. Verapamil (10 mg·kg−1 i.p.) and escitalopram (0.1 mg·kg−1 i.p.) were administered once daily for 22 days. On the final day of treatment, brain regions and plasma were collected for analysis of cortical and plasma escitalopram concentrations, and to determine the hippocampal expression of genes previously reported to be altered by chronic antidepressant treatment. Verapamil treatment resulted in a greater than twofold increase in brain levels of escitalopram, without altering plasma levels. Neither gene expression analysis nor behavioral testing revealed an augmentation of responses to escitalopram treatment due to verapamil administration. Taken together, these data demonstrate for the first time that P‐gp inhibition can yield elevated brain concentrations of an antidepressant after chronic treatment. The functional relevance of these increased brain levels requires further elaboration.

Altered serotonin transporter binding potential in patients with obsessive-compulsive disorder under escitalopram treatment: [11C]DASB PET study.

Obsessive-compulsive disorder (OCD) is a chronic, relapsing mental illness. Selective serotonin reuptake inhibitors block serotonin transporters (SERTs) and are the mainstay of treatment for OCD. SERT abnormalities are reported in drug-free patients with OCD, but it is not known what happens to SERT levels during treatment. This is important as alterations in SERT levels in patients under treatment could underlie poor response, or relapse during or after treatment. The aim of the present study was first to validate a novel approach to measuring SERT levels in people taking treatment and then to investigate SERT binding potential (BP) using [11C]DASB PET in patients with OCD currently treated with escitalopram in comparison with healthy controls. Twelve patients and age- and sex-matched healthy controls were enrolled. The patients and healthy controls underwent serial PET scans after administration of escitalopram and blood samples for drug concentrations were collected simultaneously with the scans. Drug-free BPs were obtained by using an inhibitory E max model we developed previously. The inhibitory E max model was able to accurately predict drug-free SERT BP in people taking drug treatment. The drug-free BP in patients with OCD currently treated with escitalopram was significantly different from those in healthy volunteers [Cohen's d = 0.03 (caudate), 1.16 (putamen), 1.46 (thalamus), -5.67 (dorsal raphe nucleus)]. This result extends previous findings showing SERT abnormalities in drug-free patients with OCD by indicating that altered SERT availability is seen in OCD despite treatment. This could account for poor response and the high risk of relapse in OCD.

Primer progressive aphasia: a case report

Background: Primaryprogressive aphasia (PPA) is known as subtype of frontotemporal dementia with evident language impairment. There is a progressive disorder in finding and understanding words at least for two years. Mental functions like memory, visuospatial functions, personality traits are generally preserved. Objective: We want to share a quite rare case, PPA by reporting a woman having difficulty in recognizing words and uttering long sentences. Patient and methods: A 65-year-old-woman was admitted to the hospital with complaints with difficult in speaking and fixing long sentences. She stated that she had gathered the sentences in her mind but was not able to find suitable words to express them. On the neurological examination , she could easily transfer her thoughts to writing as well as she could read long sentences, but there were pauses during her speech while using long sentences. She had difficulties in finding the right words to express her thoughts. Insight, judgement, personal care were preserved . In neuropsychological testing, the range of attention was slightly deteriorated and the complex attention was clearly deteriorated. Results: On brain MRI, there were atrophic changes in the perisylvian regions bilaterally. In brain PET hypoperfusion was observed particularly in the left temporal and frontal lobes. She was given donepezil and escitalopram treatment for 6 months and there were no changes on control examination. Conclusion: PPA may not be diagnosed for many years due to the insidious progressive loss of language functions. Neuropsychological testing and neuroimaging is important to diagnose. PPA seemed worth presenting since it was a rare case.

The Effects of Escitalopram Treatment on Oxidative/ Antioxidative Parameters in Patients with Depression

ABS TRACT: The effects of escitalopram treatment on oxidative/antioxidative parameters in patients with depression Objective: In this study, we aimed to investigate the effects of escitalopram, an antidepressant drug of the selective serotonin reuptake inhibitor group, on lipid peroxidation, nitric oxide (NO) level and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities in patients with major depressive disorder. Method: Eighteen patients (11 women, 7 men) diagnosed with major depressive disorder (MDD) according to DSM-IV criteria and eighteen healthy controls (10 women, 8 men) were included in the study. The relevant parameters were measured before and after treatment with 20 mg/day escitalopram for 6 weeks in patients and only once in the controls. Results: Plasma SOD, CAT, malondialdehyde (MDA) and NO levels were significantly higher before treatment in patients with major depression compared to healthy controls; there was no significant differences in GPx levels. Treatment with 20 mg/day escitalopram for 6 weeks reduced plasma SOD, CAT, MDA and NO levels statistically significantly; it had no effect on GPx levels. Conclusion: The results provide evidence for the role of oxidative stress in the pathogenesis of MDD and revealed that subchronic treatment with escitalopram significantly decreased the activity of antioxidant enzymes and MDA values. It may be argued that antioxidant enzymes such as SOD, CAT and oxidative stress markers such as MDA and NO are state markers of MDD, because values came close to the results of healthy subjects after treatment.

Escitalopram and Intermenstrual Vaginal Bleeding: A Probable Association

A 21 year-old woman started experiencing intermenstrual vaginal bleeding on the 6th day of initiation of escitalopram treatment for major depression which ceased 1 day after she stopped taking the drug. On escitalopram rechallenge the patient re-experienced vaginal spotting which resolved after discontinuation. There are no published reports on intermenstrual vaginal bleeding associated with escitalopram, although there are pre and postmarketing data mentioning this adverse effect. Multiple cases of menstrual disorders and vaginal bleeding with other antidepressants had been reported previously. This case supports previous unpublished data indicating escitalopram as a potential cause of intermenstrual vaginal bleeding.

Cognitive and psychomotor effects of three months of escitalopram treatment in elderly patients with major depressive disorder

BackgroundAlthough psychomotor retardation (PR) and cognitive disfunctioning are essential symptoms of elderly depressed patients, the differential effect of treatment with an SSRI in the elderly on these symptoms has hardly got any attention in studies with objective experimental measures. Since effects appear relatively slower in elderly, this study evaluates the effect on cognitive and psychomotor functioning as compared to mood, on four points during a twelve week follow up of monotreatment with escitalopram. Method28 non-demented elderly unipolar depressive patients on 5–20mg escitalopram were compared to 20 matched healthy elderly. All participants underwent a test battery containing clinical depression measures, cognitive measures of processing speed, executive function and memory, clinical ratings of PR, and objective computerized fine motor skill-tests at the start and after 2, 6 and 12 weeks. Statistical analysis consisted of a General Linear Model (GLM) repeated measures multivariate analysis of variance of completers to compare the psychomotor and cognitive outcomes of the two groups. ResultsAlthough, apart from the significant mood effect, no interaction effects were found for the psychomotor and cognitive tasks, the means in general show a trend of differential effects in cognitive and psychomotor functions, with smaller effects and delayed timeframes and with presence of subgroups compared to mood effects. LimitationLonger follow up studies are necessary to evaluate differential long term effects. ConclusionIn elderly, moderate effects of SSRI treatment on mood precede slow or limited effects on cognition and psychomotor retardation.

Treatment with escitalopram improves the attentional bias toward negative facial expressions in patients with major depressive disorders

We hypothesized that treatment with escitalopram would improve cognitive bias and contribute to the recovery process for patients with major depressive disorder (MDD). Many previous studies have established that patients with MDD tend to pay selective attention to negative stimuli. The assessment of the level of cognitive bias is regarded as a crucial dimension of treatment outcomes for MDD. To our knowledge, no prior studies have been reported on the effects of treatment with escitalopram on attentional bias in MDD, employing a dot probe task of facial expression. We studied 25 patients with MDD and 25 controls, and used a dot probe task of facial expression to measure cognitive bias. The patients’ psychopathologies were rated using the Hamilton Depression Scale (HAMD) at baseline and after 8weeks of treatment with escitalopram. All participants performed the facial expression dot probe task. The results revealed that the 8week escitalopram treatment decreased the HAMD scores. The patients with MDD at baseline exhibited an attentional bias towards negative faces, however, no significant bias toward either negative or happy faces were observed in the controls. After the 8week escitalopram treatment, no significant bias toward negative faces was observed in the patient group. In conclusion, patients with MDD pay more attention to negative facial expressions, and treatment with escitalopram improves this attentional bias toward negative facial expressions. This is the first study, to our knowledge, on the effects of treatment with escitalopram on attentional bias in patients with MDD that has employed a dot probe task of facial expression.

Correlates and Escitalopram Treatment Effects on Sleep Disturbance in Patients with Acute Coronary Syndrome: K-DEPACS and EsDEPACS.

To investigate the correlates of sleep disturbance and to assess escitalopram treatment effects of depression on sleep disturbance in patients with acute coronary syndrome (ACS). A cross-sectional study in patients with ACS within 2 w post-ACS, and a 24-w double-blind controlled trial of escitalopram against placebo for patients with ACS who have comorbid depressive disorders. A university hospital in South Korea. There were 1,152 patients with ACS who were consecutively recruited. Of 446 patients with comorbid depressive disorders, 300 were randomized to the trial. Sleep disturbance was evaluated by the Leeds Sleep Evaluation Questionnaire. Demographic and clinical characteristics were assessed, including cardiovascular risk factors, current cardiac status, and depressive symptoms. Depressive symptoms were most strongly and consistently associated with sleep disturbance. In addition, older age, female sex, hypertension, and more severe ACS status were associated with certain aspects of sleep disturbance. Escitalopram was significantly superior to placebo for improving sleep disturbance over the 24-w treatment period. These effects were substantially explained by improvement in depressive symptoms. Depression screening is indicated in patients with acute coronary syndrome with sleep disturbance. Successful treatment of depression has beneficial effects on sleep outcomes in these patients. ClinicalTrial.gov identifier for the 24-w drug trial, NCT00419471.

Prenatal stress, regardless of concurrent escitalopram treatment, alters behavior and amygdala gene expression of adolescent female rats

Depression during pregnancy has been linked to in utero stress and is associated with long-lasting symptoms in offspring, including anxiety, helplessness, attentional deficits, and social withdrawal. Depression is diagnosed in 10–20% of expectant mothers, but the impact of antidepressant treatment on offspring development is not well documented, particularly for females. Here, we used a prenatal stress model of maternal depression to test the hypothesis that in utero antidepressant treatment could mitigate the effects of prenatal stress. We also investigated the effects of prenatal stress and antidepressant treatment on gene expression related to GABAergic and serotonergic neurotransmission in the amygdala, which may underlie behavioral effects of prenatal stress. Nulliparous female rats were implanted with osmotic minipumps delivering clinically-relevant concentrations of escitalopram and mated. Pregnant dams were exposed to 12 days of mixed-modality stressors, and offspring were behaviorally assessed in adolescence (postnatal day 28) and adulthood (beyond day 90) to determine the extent of behavioral change. We found that in utero stress exposure, regardless of escitalopram treatment, increased anxiety-like behavior in adolescent females and profoundly influenced amygdala expression of the chloride transporters KCC2 and NKCC1, which regulate GABAergic function. In contrast, prenatal escitalopram exposure alone elevated amygdala expression of 5-HT1A receptors. In adulthood, anxiety-like behavior returned to baseline and gene expression effects in the amygdala abated, whereas deficits emerged in novel object recognition for rats exposed to stress during gestation. These findings suggest prenatal stress causes age-dependent deficits in anxiety-like behavior and amygdala function in female offspring, regardless of antidepressant exposure.

Does escitalopram reduce neurotoxicity in major depression?

A pro-inflammatory state and a dysregulation in the tryptophan/kynurenine pathway have been documented in depression. This study examined whether treatment with the SSRI, escitalopram (ESC), could suppress inflammation and favorably shift metabolites of the kynurenine pathway in patients with major depressive disorder (MDD) within the utilized treatment period. Twenty seven healthy control subjects were included for comparison. Thirty patients were enrolled after completing baseline assessments. They received a 12-week ESC monotherapy. Twenty subjects were completers. Clinical assessments were carried out at each visit using the HAM-D, HAM-A, CGI and BDI rating scales. Blood samples were collected at each assessment and stored until analyzed. Cytokines were analyzed with Randox multiplex assay and tryptophan and kynurenine metabolites were analyzed using HPLC/GCMS. Baseline plasma concentrations of hsCRP, TNFα, IL6 and MCP-1 were significantly higher in patients compared to healthy controls. IL10 trended toward an increase. Baseline plasma IL1β correlated significantly with IL1α, and IL4. Patients showed significant improvement in all outcome measures with a high remission rate. Significant correlations were obtained between specific symptoms and certain biomarkers at baseline but these correlations must be viewed as very preliminary. During ESC treatment concentrations of inflammatory biomarkers did not change except for TNFα that trended lower. Metabolites and ratios of the tryptophan/kynurenine pathway showed reductions of the neurotoxic metabolites, 3-hydroxykynurenine and quinolinic acid, 3-hydroxykynurenine/kynurenine, quinolinic acid/tryptophan, kynurenic acid/quinolinic acid and quinolinic acid/3-hydroxykynurenine. The results indicate that ESC may exert its antidepressant effect in part through inhibition of synthesis of certain neurotoxic kynurenine metabolites and possibly also through reduction of the inflammatory response, although there was no concordance in the time course of changes between antidepressant efficacy and reversal of the pro-inflammatory status.

Effects of depression screening on psychiatric outcomes in patients with acute coronary syndrome: Findings from the K-DEPACS and EsDEPACS studies

BackgroundIt has been controversial whether routine screening for depression should be recommended in all patients with acute coronary syndrome (ACS) due to lack of evidence for psychiatric as well as for cardiac outcomes. This study aimed to evaluate the result of screening for treatment and subsequent treatment of depression on one-year psychiatric outcomes in ACS. MethodsAt baseline 1152 patients with recently developed ACS were screened with the Beck Depression Inventory (BDI) and depressive disorder diagnoses were applied according to DSM-IV criteria. Of the 446 patients with depressive disorder, 300 were randomized to a 24-week double-blind trial of escitalopram or placebo, while the remaining 146 received conventional medical treatment only (MTO) without randomization. Of all baseline participants, 828 were followed up one year later. Psychiatric outcomes included BDI, Hamilton Depression Rating Scale (HAMD), Montgomery Asberg Depression Rating Scale (MADRS), Social and Occupational Functioning Assessment Scale (SOFAS) and the World Health Organization Disability Assessment Schedule-12 (WHODAS-12). ResultsBDI screen-positive ACS patients showed worse one-year outcomes on MADRS, SOFAS, and WHODAS scores (p-values<0.01) compared to BDI screen-negative patients. Escitalopram treatment was associated with beneficial effects compared to placebo and MTO on one-year outcomes on HAMD, MADRS and SOFAS (p-values<0.01). Of patients screening positive on the BDI, those with depressive disorder treated with escitalopram had similar outcomes to those without depressive disorder. ConclusionsRoutine screening of depressive symptom in ACS patients is helpful to plan further management. Moreover, successive accurate diagnosis of depressive disorder with appropriated treatment is effective at least for psychiatric outcomes.

Depressed children of depressed mothers: Escitalopram for mothers improves symptoms in both

In a trial of medications, researchers found that depressed children of depressed mothers improved when the mothers received escitalopram treatment. However, results are preliminary, as there were no comparisons with psychotherapy or placebo groups. Most notably, though, mothers with anxiety and irritability, based on a very preliminary measure, had the greatest improvement in parenting functionality based on both their and their children's reports.

Presynaptic plasticity as a hallmark of rat stress susceptibility and antidepressant response.

Two main questions are important for understanding and treating affective disorders: why are certain individuals susceptible or resilient to stress, and what are the features of treatment response and resistance? To address these questions, we used a chronic mild stress (CMS) rat model of depression. When exposed to stress, a fraction of rats develops anhedonic-like behavior, a core symptom of major depression, while another subgroup of rats is resilient to CMS. Furthermore, the anhedonic-like state is reversed in about half the animals in response to chronic escitalopram treatment (responders), while the remaining animals are resistant (non-responder animals). Electrophysiology in hippocampal brain slices was used to identify a synaptic hallmark characterizing these groups of animals. Presynaptic properties were investigated at GABAergic synapses onto single dentate gyrus granule cells. Stress-susceptible rats displayed a reduced probability of GABA release judged by an altered paired-pulse ratio of evoked inhibitory postsynaptic currents (IPSCs) (1.48 ± 0.25) compared with control (0.81 ± 0.05) and stress-resilient rats (0.78 ± 0.03). Spontaneous IPSCs (sIPSCs) occurred less frequently in stress-susceptible rats compared with control and resilient rats. Finally, a subset of stress-susceptible rats responding to selective serotonin reuptake inhibitor (SSRI) treatment showed a normalization of the paired-pulse ratio (0.73 ± 0.06) whereas non-responder rats showed no normalization (1.2 ± 0.2). No changes in the number of parvalbumin-positive interneurons were observed. Thus, we provide evidence for a distinct GABAergic synaptopathy which associates closely with stress-susceptibility and treatment-resistance in an animal model of depression.

Dopamine Receptor D2 and Associated microRNAs Are Involved in Stress Susceptibility and Resistance to Escitalopram Treatment.

Background:Early life stress has been demonstrated to increase the risk of developing depression in adulthood. However, the roles and associated molecular mechanisms of stresses in the onset and relapse of depression have yet to be fully elucidated.Methods:Depression-like behaviors were induced in rats by maternal deprivation and chronic unpredictable stress. Depression- and anxiety-like behaviors of rats, dopamine receptor D2 level, and microRNAs expression in rats’ brain tissues were measured.Results:Chronic unpredictable stress alone induced depression-like behaviors in rats, but maternal deprivation enhanced the effect of chronic unpredictable stress. Escitalopram significantly decreased depression-like behaviors in chronic unpredictable stress rats but was less effective in maternal deprivation with chronic unpredictable stress rats. Maternal deprivation increased dopamine receptor D2 messenger RNA expression and decreased microRNA-9 expression in the striatum. Chronic unpredictable stress increased dopamine receptor D2 mRNA and protein levels and decreased microRNA-9 expression in the nucleus accumbens. Furthermore, maternal deprivation enhanced the effect of chronic unpredictable stress on dopamine receptor D2 gene and microRNA-9 expression. Chronic unpredictable stress increased the expression of microRNA-326 in the nucleus accumbens but decreased it in the striatum, whereas maternal deprivation elevated microRNA-326 expression in the striatum. Escitalopram normalized microRNA-326 expression but had no effect on the expression of microRNA-9, dopamine receptor D2 mRNA, and dopamine receptor D2 protein in both the nucleus accumbens and striatum. The in vitro study showed that only microRNA-9 directly targeted the 3’ untranslated region of dopamine receptor D2 mRNA and inhibited dopamine receptor D2 protein expression.Conclusion:Early life stress enhanced the susceptibility to late life stress and resistance to escitalopram treatment through decreasing microRNA-9 expression and subsequently upregulating dopamine receptor D2 expression in the nucleus accumbens. microRNA-326 may be a novel target of escitalopram.

Rhabdomyolysis After Escitalopram Treatment in a Young Adult With Melancholic Depression

Rhabdomyolysis After Escitalopram Treatment in a Young Adult With Melancholic Depression