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CNS Neuroscience & Therapeutics Mar 2024To explore the pharmacological treatment of vascular depression (VaDep) and whether the blood levels of neurotransmitters can reflect the VaDep severity. (Randomized Controlled Trial)
Randomized Controlled Trial
Efficacy and safety of venlafaxine hydrochloride combined with tandospirone citrate for patients with vascular depression accompanied by somatic symptoms: An open-labeled randomized control trial.
AIMS
To explore the pharmacological treatment of vascular depression (VaDep) and whether the blood levels of neurotransmitters can reflect the VaDep severity.
METHODS
VaDep patients with somatic symptoms were enrolled and randomly received venlafaxine + tandospirone (Combined Group) or venlafaxine (Monotherapy Group). The treatment efficacy was assessed by Hamilton Depression Scale (HAMD), Hamilton Anxiety Scale (HAMA), and Patient Health Questionnaire-15 (PHQ-15). The levels of blood monoamine neurotransmitters were measured by enzyme-linked immunosorbent assay.
RESULTS
Both groups reported a progressive decrease in HAMD, HAMA, and PHQ-15 scores to below the baseline after the respective treatment. Compared with the Monotherapy Group, the Combined Group reported a significant decrease in HAMD score at week 2 and markedly lower HAMA and PHQ-15 scores at weeks 1, 2, 4, and 8. Both groups showed a decrease in the levels of blood monoamine neurotransmitters at weeks 4 and 8 when compared with the baseline. A strong positive association was evident between the plasma 5-HT levels and the HAMD score.
CONCLUSION
The combined therapy rapidly acts on VaDep comorbid with anxiety and somatic symptoms and significantly alleviates the anxiety and somatic symptoms. The plasma levels of 5-HT may serve as potential objective candidates in evaluating VaDep severity and the efficacy of the undertaken treatment regimen.
Topics: Humans; Anti-Anxiety Agents; Citrates; Depression; Isoindoles; Medically Unexplained Symptoms; Piperazines; Pyrimidines; Selective Serotonin Reuptake Inhibitors; Serotonin; Treatment Outcome; Vascular Depression; Venlafaxine Hydrochloride; Drug Therapy, Combination
PubMed: 38514905
DOI: 10.1111/cns.14650 -
Journal of Psychiatry & Neuroscience :... Jan 2021Late-life depression is often associated with non-response or relapse following conventional antidepressant treatment. The pathophysiology of late-life depression likely... (Clinical Trial)
Clinical Trial
BACKGROUND
Late-life depression is often associated with non-response or relapse following conventional antidepressant treatment. The pathophysiology of late-life depression likely involves a complex interplay between aging and depression, and may include abnormalities in cortical inhibition and plasticity. However, the extent to which these cortical processes are modifiable by antidepressant pharmacotherapy is unknown.
METHODS
Sixty-eight patients with late-life depression received 12 weeks of treatment with open-label venlafaxine, a serotonin-norepinephrine reuptake inhibitor (≤ 300 mg/d). We combined transcranial magnetic stimulation of the left motor cortex with electromyography recordings from the right hand to measure cortical inhibition using contralateral cortical silent period and paired-pulse short-interval intracortical inhibition paradigms; cortical facilitation using a paired-pulse intracortical facilitation paradigm; and short-term cortical plasticity using a paired associative stimulation paradigm. All measures were collected at baseline, 1 week into treatment ( = 23) and after approximately 12 weeks of treatment.
RESULTS
Venlafaxine did not significantly alter cortical inhibition, facilitation or plasticity after 1 or 12 weeks of treatment. Improvements in depressive symptoms during treatment were not associated with changes in cortical physiology.
LIMITATIONS
The results presented here are specific to the motor cortex. Future work should investigate whether these findings extend to cortical areas more closely associated with depression, such as the dorsolateral prefrontal cortex.
CONCLUSION
These findings suggest that antidepressant treatment with venlafaxine does not exert meaningful changes in motor cortical inhibition or plasticity in late-life depression. The absence of changes in motor cortical physiology, alongside improvements in depressive symptoms, suggests that age-related changes may play a role in previously identified abnormalities in motor cortical processes in latelife depression, and that venlafaxine treatment does not target these abnormalities.
Topics: Aged; Aged, 80 and over; Depressive Disorder, Major; Electric Stimulation; Electromyography; Evoked Potentials, Motor; Female; Humans; Male; Middle Aged; Motor Cortex; Neural Inhibition; Neuronal Plasticity; Outcome Assessment, Health Care; Serotonin and Noradrenaline Reuptake Inhibitors; Transcranial Magnetic Stimulation; Venlafaxine Hydrochloride
PubMed: 33119493
DOI: 10.1503/jpn.200001 -
BMC Medical Informatics and Decision... Oct 2022Dementia is a group of symptoms that largely affects older people. The majority of patients face behavioural and psychological symptoms (BPSD) during the course of their...
BACKGROUND
Dementia is a group of symptoms that largely affects older people. The majority of patients face behavioural and psychological symptoms (BPSD) during the course of their illness. Alzheimer's disease (AD) and vascular dementia (VaD) are two of the most prevalent types of dementia. Available medications provide symptomatic benefits and provide relief from BPSD and associated health issues. However, it is unclear how specific dementia, antidepressant, antipsychotic, antianxiety, and mood stabiliser drugs, used in the treatment of depression and dementia subtypes are prescribed in hospital admission, during hospital stay, and at the time of discharge. To address this, we apply multi-dimensional data analytical approaches to understand drug prescribing practices within hospitals in England and Wales.
METHODS
We made use of the UK National Audit of Dementia (NAD) dataset and pre-processed the dataset. We evaluated the pairwise Pearson correlation of the dataset and selected key data features which are highly correlated with dementia subtypes. After that, we selected drug prescribing behaviours (e.g. specific medications at the time of admission, during the hospital stay, and upon discharge), drugs and disorders. Then to shed light on the relations across multiple features or dimensions, we carried out multiple regression analyses, considering the number of dementia, antidepressant, antipsychotic, antianxiety, mood stabiliser, and antiepileptic/anticonvulsant drug prescriptions as dependent variables, and the prescription of other drugs, number of patients with dementia subtypes (AD/VaD), and depression as independent variables.
RESULTS
In terms of antidepressant drugs prescribed in hospital admission, during stay and discharge, the number of sertraline and venlafaxine prescriptions were associated with the number of VaD patients whilst the number of mirtazapine prescriptions was associated with frontotemporal dementia patients. During admission, the number of lamotrigine prescriptions was associated with frontotemporal dementia patients, and with the number of valproate and dosulepin prescriptions. During discharge, the number of mirtazapine prescriptions was associated with the number of donepezil prescriptions in conjunction with frontotemporal dementia patients. Finally, the number of prescriptions of donepezil/memantine at admission, during hospital stay and at discharge exhibited positive association with AD patients.
CONCLUSION
Our analyses reveal a complex, multifaceted set of interactions among prescribed drug types, dementia subtypes, and depression.
Topics: Aged; Anticonvulsants; Antidepressive Agents; Antipsychotic Agents; Depression; Donepezil; Dothiepin; Frontotemporal Dementia; Hospitals; Humans; Lamotrigine; Memantine; Mirtazapine; NAD; Sertraline; Valproic Acid; Venlafaxine Hydrochloride; Wales
PubMed: 36207697
DOI: 10.1186/s12911-022-01892-9 -
Current Therapeutic Research, Clinical... Dec 2014Extracts of the plant Hypericum perforatum L. have been traditionally used in folk medicine for the treatment of depressive disorders. Xanthone, a component of Hypericum...
BACKGROUND
Extracts of the plant Hypericum perforatum L. have been traditionally used in folk medicine for the treatment of depressive disorders. Xanthone, a component of Hypericum perforatum L., has been shown to be effective in animal models of depression.
OBJECTIVE
We investigated if 2 xanthone derivatives (1101 and 1105) were as effective as venlafaxine, which is a serotonin-norepinephrine reuptake inhibitor and was used as a positive control, in animal models of depression.
METHODS
A series of derivatives from xanthone were designed and synthesized. After preliminary experiments, 2 xanthone derivatives (1101 and 1105) were considered to be effective in our mouse depression model. To further determine their effects on depression, classical behavioral despair animal models (forced swim and tail suspension tests) were used to assess the efficacies of these derivatives, whereas venlafaxine hydrochloride was used as a positive control. Oral acute toxicity studies were used to determine if the derivatives were toxic in mice.
RESULTS
The oral acute toxicity studies of 2 xanthone derivatives (1101 and 1105) did not show any toxic effect until the dose at 1000 mg/kg body weight, and xanthone derivatives 1101 and 1105 resulted in a significant decrease of the immobility period (in seconds) compared with the untreated control group during the forced swim test with rats (dose = 12 mg/kg; P < 0.05) and mice (dose = 25 mg/kg; P < 0.001). At lower doses, derivatives 1101 and 1105 also decreased the immobility period of rats and mice during the forced swim test but significant differences were only found in mice compared with the untreated control group (P < 0.05). No difference was found between the groups treated with xanthone derivatives and the positive control group during the swimming period in both mice (dose = 25 mg/kg) and rats (dose = 12 mg/kg) (P > 0.05). In the tail suspension test, derivatives 1101 and 1105 produced marked effects with regard to the motion of mice (P < 0.01 or 0.001, respectively) and the derivatives were also noted to have some effects on rats at a dose of 12 mg/kg (P < 0.05). Compared with the positive venlafaxine control group, no differences were found between those treated with either derivative 1101 or derivative 1105 and venlafaxine (P > 0.05).
CONCLUSIONS
Within certain dose ranges, xanthone derivatives 1101 and 1105 have similar effects to venlafaxine hydrochloride in the treatment of depression as suggested by behavioral despair animal models using rats and mice.
PubMed: 25067986
DOI: 10.1016/j.curtheres.2014.04.003 -
Drug Design, Development and Therapy 2020The purpose of the present study was to investigate the effects of vonoprazan on the pharmacokinetics of venlafaxine in vitro and in vivo.
PURPOSE
The purpose of the present study was to investigate the effects of vonoprazan on the pharmacokinetics of venlafaxine in vitro and in vivo.
METHODS
The mechanism underlying the inhibitory effect of vonoprazan on venlafaxine was investigated using rat liver microsomes. In vitro, the inhibition was evaluated by determining the production of O-desmethylvenlafaxine. Eighteen male Sprague-Dawley rats were randomly divided into three groups: control group, vonoprazan (5 mg/kg) group, and vonoprazan (20 mg/kg) group. A single dose of 20 mg/kg venlafaxine was administrated to rats orally without or with vonoprazan. Plasma was prepared from blood samples collected via the tail vein at different time points and concentrations of venlafaxine and its metabolite, O-desmethylvenlafaxine, were determined by ultra-performance liquid chromatography-tandem mass spectrometry.
RESULTS
We observed that vonoprazan could significantly decrease the amount of O-desmethylvenlafaxine (IC = 5.544 μM). Vonoprazan inhibited the metabolism of venlafaxine by a mixed inhibition, combining competitive and non-competitive inhibitory mechanisms. Compared with that in the control group (without vonoprazan), the pharmacokinetic parameters of venlafaxine and its metabolite, O-desmethylvenlafaxine, were significantly increased in both 5 and 20 mg/kg vonoprazan groups, with an increase in MR.
CONCLUSION
Vonoprazan significantly alters the pharmacokinetics of venlafaxine in vitro and in vivo. Further investigations should be conducted to check these effects in humans. Therapeutic drug monitoring of venlafaxine in individuals undergoing venlafaxine maintenance therapy is recommended when vonoprazan is used concomitantly.
Topics: Administration, Oral; Animals; Chromatography, High Pressure Liquid; Desvenlafaxine Succinate; Male; Microsomes, Liver; Pyrroles; Rats; Rats, Sprague-Dawley; Sulfonamides; Tandem Mass Spectrometry; Venlafaxine Hydrochloride
PubMed: 33204067
DOI: 10.2147/DDDT.S276704 -
PLoS Medicine Nov 2021The prevalence of depression and the exposure to antidepressants are high among women of reproductive age and during pregnancy. Duloxetine is a selective...
BACKGROUND
The prevalence of depression and the exposure to antidepressants are high among women of reproductive age and during pregnancy. Duloxetine is a selective serotonin-norepinephrine reuptake inhibitor (SNRI) approved in the United States and Europe in 2004 for the treatment of depression. Fetal safety of duloxetine is not well established. The present study evaluates the association of exposure to duloxetine during pregnancy and the risk of major and minor congenital malformations and the risk of stillbirths.
METHODS AND FINDINGS
A population-based observational study was conducted based on data from registers in Sweden and Denmark. All registered births and stillbirths in the medical birth registers between 2004 and 2016 were included. Malformation diagnoses were identified up to 1 year after birth. Logistic regression analyses were used. Potential confounding was addressed through multiple regression, propensity score (PS) matching, and sensitivity analyses. Confounder variables included sociodemographic information (income, education, age, year of birth, and country), comorbidity and comedication, previous psychiatric contacts, and birth-related information (smoking during pregnancy and previous spontaneous abortions and stillbirths). Duloxetine-exposed women were compared with 4 comparators: (1) duloxetine-nonexposed women; (2) selective serotonin reuptake inhibitor (SSRI)-exposed women; (3) venlafaxine-exposed women; and (4) women exposed to duloxetine prior to, but not during, pregnancy. Exposure was defined as redemption of a prescription during the first trimester and throughout pregnancy for the analyses of malformations and stillbirths, respectively. Outcomes were major and minor malformations and stillbirths gathered from the national patient registers. The cohorts consisted of more than 2 million births with 1,512 duloxetine-exposed pregnancies. No increased risk for major malformations, minor malformations, or stillbirth was found across comparison groups in adjusted and PS-matched analyses. Duloxetine-exposed versus duloxetine-nonexposed PS-matched analyses showed odds ratio (OR) 0.98 (95% confidence interval [CI] 0.74 to 1.30, p = 0.909) for major malformations, OR 1.09 (95% CI 0.82 to 1.45, p = 0.570) for minor malformation, and 1.18 (95% CI 0.43 to 3.19, p = 0.749) for stillbirths. For the individual malformation subtypes, some findings were statistically significant but were associated with large statistical uncertainty due to the extremely small number of events. The main limitations for the study were that the indication for duloxetine and a direct measurement of depression severity were not available to include as covariates.
CONCLUSIONS
Based on this observational register-based nationwide study with data from Sweden and Denmark, no increased risk of major or minor congenital malformations or stillbirth was associated with exposure to duloxetine during pregnancy.
Topics: Abnormalities, Drug-Induced; Adolescent; Adult; Cohort Studies; Congenital Abnormalities; Denmark; Duloxetine Hydrochloride; Female; Humans; Maternal Exposure; Middle Aged; Pregnancy; Risk Factors; Stillbirth; Sweden; Young Adult
PubMed: 34807906
DOI: 10.1371/journal.pmed.1003851 -
BMJ (Clinical Research Ed.) Feb 2020To evaluate the risk of adverse maternal and infant outcomes following in utero exposure to duloxetine.
OBJECTIVE
To evaluate the risk of adverse maternal and infant outcomes following in utero exposure to duloxetine.
DESIGN
Cohort study nested in the Medicaid Analytic eXtract for 2004-13.
SETTING
Publicly insured pregnancies in the United States.
PARTICIPANTS
Pregnant women 18 to 55 years of age and their liveborn infants.
INTERVENTIONS
Duloxetine exposure during the etiologically relevant time window, compared with no exposure to duloxetine, exposure to selective serotonin reuptake inhibitors, exposure to venlafaxine, and exposure to duloxetine before but not during pregnancy.
MAIN OUTCOME MEASURES
Congenital malformations overall, cardiac malformations, preterm birth, small for gestational age infant, pre-eclampsia, and postpartum hemorrhage.
RESULTS
Cohort sizes ranged from 1.3 to 4.1 million, depending on the outcome. The number of women exposed to duloxetine varied by cohort and exposure contrast and was around 2500-3000 for early pregnancy exposure and 900-950 for late pregnancy exposure. The base risk per 1000 unexposed women was 36.6 (95% confidence interval 36.3 to 36.9) for congenital malformations overall, 13.7 (13.5 to 13.9) for cardiovascular malformations, 107.8 (107.3 to 108.3) for preterm birth, 20.4 (20.1 to 20.6) for small for gestational age infant, 33.6 (33.3 to 33.9) for pre-eclampsia, and 23.3 (23.1 to 23.4) for postpartum hemorrhage. After adjustment for measured potential confounding variables, all baseline characteristics were well balanced for all exposure contrasts. In propensity score adjusted analyses versus unexposed pregnancies, the relative risk was 1.11 (95% confidence interval 0.93 to 1.33) for congenital malformations overall and 1.29 (0.99 to 1.68) for cardiovascular malformations. For preterm birth, the relative risk was 1.01 (0.92 to 1.10) for early exposure and 1.19 (1.04 to 1.37) for late exposure. For small for gestational age infants the relative risks were 1.14 (0.92 to 1.41) and 1.20 (0.83 to 1.72) for early and late pregnancy exposure, respectively, and for pre-eclampsia they were 1.12 (0.96 to 1.31) and 1.04 (0.80 to 1.35). The relative risk for postpartum hemorrhage was 1.53 (1.08 to 2.18). Results from sensitivity analyses were generally consistent with the findings from the main analyses.
CONCLUSIONS
On the basis of the evidence available to date, duloxetine is unlikely to be a major teratogen but may be associated with an increased risk of postpartum hemorrhage and a small increased risk of cardiac malformations. While continuing to monitor the safety of duloxetine as data accumulate over time, these potential small increases in risk of relatively uncommon outcomes must be weighed against the benefits of treating depression and pain during pregnancy in a given patient.
TRIAL REGISTRATION
EUPAS 15946.
Topics: Abnormalities, Drug-Induced; Adolescent; Adult; Cohort Studies; Duloxetine Hydrochloride; Female; Heart Defects, Congenital; Humans; Infant, Small for Gestational Age; Middle Aged; Postpartum Hemorrhage; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Premature Birth; Prenatal Exposure Delayed Effects; Serotonin and Noradrenaline Reuptake Inhibitors; United States; Young Adult
PubMed: 32075794
DOI: 10.1136/bmj.m237 -
Pain Practice : the Official Journal of... Feb 2018To examine medication adherence and healthcare costs for combination prescription initiators (duloxetine/milnacipran/venlafaxine with pregabalin) vs. monotherapy...
OBJECTIVE
To examine medication adherence and healthcare costs for combination prescription initiators (duloxetine/milnacipran/venlafaxine with pregabalin) vs. monotherapy initiators (duloxetine, milnacipran, venlafaxine, and pregabalin) among patients with fibromyalgia syndrome (FMS).
METHODS
Our retrospective cohort study used claims data for the South Carolina Blue Cross Blue Shield State Health Plan (SHP). Patients with FMS ≥ 18 years of age, with prescription initiation from July 1, 2007, through June 30, 2010, and SHP enrollment for 12 months pre- and post-index periods were included (combination: n = 100; pregabalin: n = 665; duloxetine: n = 713; milnacipran: n = 131; venlafaxine: n = 272). Medication adherence measures included high adherence (medication possession ratio ≥ 80%) and total supply days. Healthcare costs comprised direct medical expenditures. Propensity score methods of inverse probability of treatment weights were used to control for selection bias due to differing pre-index characteristics.
RESULTS
Odds ratios for high adherence were significantly increased (P < 0.05) among the combination cohort vs. the venlafaxine (2.15), duloxetine (1.39), and pregabalin (2.20) cohorts. Rate ratios for total supply days were significantly higher (P < 0.05) for combination vs. venlafaxine (1.23), duloxetine (1.08), and pregabalin (1.32) cohorts. Expenditures for total health care were significantly higher (P < 0.05) for combination vs. duloxetine ($26,291 vs. $17,190), milnacipran ($33,638 vs. $22,886), and venlafaxine ($26,586 vs. $16,857) cohorts.
CONCLUSIONS
Medication adherence was considerably better for combination prescription initiators; however, expenditures for total health care were higher. Still, our findings suggest important clinical benefits with the use of combination prescription therapy, and prospective studies of medication adherence are warranted to examine causal relationships with outcomes not captured by healthcare claims databases.
Topics: Adolescent; Adult; Aged; Cohort Studies; Databases, Factual; Drug Therapy, Combination; Duloxetine Hydrochloride; Female; Fibromyalgia; Health Care Costs; Humans; Male; Medication Adherence; Middle Aged; Milnacipran; Pregabalin; Retrospective Studies; Venlafaxine Hydrochloride
PubMed: 28419725
DOI: 10.1111/papr.12585 -
Chest Aug 2020One of the key mechanisms underlying OSA is reduced pharyngeal muscle tone during sleep. Data suggest that pharmacologic augmentation of central serotonergic/adrenergic... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND
One of the key mechanisms underlying OSA is reduced pharyngeal muscle tone during sleep. Data suggest that pharmacologic augmentation of central serotonergic/adrenergic tone increases pharyngeal muscle tone.
RESEARCH QUESTION
We hypothesized that venlafaxine, a serotonin-norepinephrine reuptake inhibitor, would improve OSA severity.
STUDY DESIGN AND METHODS
In this mechanistic, randomized, double-blind, placebo-controlled crossover trial, 20 patients with OSA underwent two overnight polysomnograms ≥ 4 days apart, receiving either 50 mg of immediate-release venlafaxine or placebo before bedtime. Primary outcomes were the apnea-hypopnea index (AHI) and peripheral oxygen saturation (Spo) nadir, and secondary outcomes included sleep parameters and pathophysiologic traits with a view toward understanding the impact of venlafaxine on mechanisms underlying OSA.
RESULTS
Overall, there was no significant difference between venlafaxine and placebo regarding AHI (mean reduction, -5.6 events/h [95% CI, -12.0 to 0.9]; P = .09) or Spo nadir (median increase, +1.0% [-0.5 to 5]; P = .11). Venlafaxine reduced total sleep time, sleep efficiency, and rapid eye movement (REM) sleep, while increasing non-REM stage 1 sleep (P < .05). On the basis of exploratory post hoc analyses venlafaxine decreased ("improved") the ventilatory response to arousal (-30%; P = .049) and lowered ("worsened") the predicted arousal threshold (-13%; [P = .02]; ie, more arousable), with no effects on other pathophysiologic traits (P ≥ .3). Post hoc analyses further suggested effect modification by arousal threshold (P = .002): AHI improved by 19% in patients with a high arousal threshold (-10.9 events/h [-3.9 to -17.9]) but tended to increase in patients with a low arousal threshold (+7 events/h [-2.0 to 16]). Other predictors of response were elevated AHI and less collapsible upper airway anatomy at baseline (|r| > 0.5, P ≤ .02).
INTERPRETATION
In unselected patients, venlafaxine simultaneously worsened and improved various pathophysiologic traits, resulting in a zero net effect. Careful patient selection based on pathophysiologic traits, or combination therapy with drugs countering its alerting effects, may produce a more robust response.
TRIAL REGISTRY
ClinicalTrials.gov; No.: NCT02714400; URL: www.clinicaltrials.gov.
Topics: Adult; Cross-Over Studies; Double-Blind Method; Female; Humans; Male; Middle Aged; Pharyngeal Muscles; Polysomnography; Serotonin and Noradrenaline Reuptake Inhibitors; Severity of Illness Index; Sleep Apnea, Obstructive; Venlafaxine Hydrochloride
PubMed: 32278781
DOI: 10.1016/j.chest.2020.02.074 -
Behavioral and Brain Functions : BBF Dec 2016Accumulating evidence has indicated that S100B may be involved in the pathophysiology of depression. No published study has examined the effect of the antidepressant...
BACKGROUND
Accumulating evidence has indicated that S100B may be involved in the pathophysiology of depression. No published study has examined the effect of the antidepressant drug venlafaxine on S100B in animal models of depression. This study investigated S100B expression in the hippocampus and assessed the effect of venlafaxine on S100B mRNA level and protein expression in rats exposed to chronic unpredictable mild stress (CUMS).
METHODS
Forty Sprague-Dawley rats were randomly divided into four groups as control, 0, 5 and 10 mg venlafaxine groups. The venlafaxine groups were exposed to CUMS from day 2 to day 43. Venlafaxine 0, 5 and 10 mg/kg were then administered from day 23 to day 43. We performed behavioral assessments with weight change, open-field and sucrose preference, and analyzed S100B protein expression and mRNA level in the hippocampus.
RESULTS
The CUMS led to a decrease in body weight, locomotor activity and sucrose consumption, but venlafaxine treatment (10 mg) reversed these CUMS-induced decreases Also, CUMS increased S100B protein expression and mRNA level in the hippocampus, but venlafaxine treatment (10 mg) significantly decreased S100B protein expression and mRNA level, which were significantly lower than the other treatment groups, without significant difference between the 10 mg venlafaxine and the control groups.
CONCLUSIONS
Our findings showed that venlafaxine treatment (10 mg) may improve the depression-like behaviors and decrease over-expression of S100B protein and mRNA in the hippocampus in a rat model of depression.
Topics: Animals; Antidepressive Agents, Second-Generation; Body Weight; Depression; Disease Models, Animal; Gene Expression Regulation; Hippocampus; Male; Random Allocation; Rats; Rats, Sprague-Dawley; S100 Calcium Binding Protein beta Subunit; Stress, Psychological; Venlafaxine Hydrochloride
PubMed: 27931233
DOI: 10.1186/s12993-016-0116-x