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Electroacupuncture (EA) stimulation has been found to influence the brain (norepinephrine metabolism in experimental animals). Preliminary clinical research has shown that EA treatment is as effective as amitriptyline for patients with depression. In this study, two consecutive clinical studies on the treatment of depression with EA are conducted. The first study was double blind placebo controlled, in which 29 depressed inpatients were recruited. Patients were randomly divided into three groups: EA + placebo; amitriptyline; and EA + amitriptyline. They received EA and/or amitriptyline treatment for 6 weeks. The Hamilton Rating Scale for Depression, Clinical Global Impression and ASBERG scales for the side effect of antidepressants were used to evaluate the therapeutic efficacy and side effects. Based on the results and research protocol of the first study, a multi-centered collaborative study was conducted, in which 241 inpatients with depression were recruited. Patients were randomly divided into two treatment groups: the EA + placebo and the amitriptyline groups. The results from both studies showed that the therapeutic efficacy of EA was equal to that of amitriptyline for depressive disorders (P > 0.05). Electro-acupuncture had a better therapeutic effect for anxiety somatization and cognitive process disturbance of depressed patients than amitriptyline (P < 0.05). Moreover, the side effects of EA were much less than that of amitriptyline (P < 0.001). The article suggested that EA treatment was an effective therapeutic method for depressive disorders. Particularly, it was a treatment of choice for depressed patients who were unable to comply with the classic tricyclic antidepressants because of their anticholinergic side effects. The possible mechanism of EA treatment is discussed.
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PubMed/MEDLINE was searched for randomized, double-blind, placebo-controlled trials of antidepressants for treatment of both adult (nonelderly) MDD (patients aged < 65 years) and late-life MDD (patients aged ≥ 55 years). The search was limited to articles published between January 1, 1980, and March 3, 2010 (inclusive). The year 1980 was used as a cutoff in our search to decrease diagnostic variability, since the DSM-III was introduced in 1980. Our search cross-referenced the term placebo with each of the following antidepressants: amitriptyline, nortriptyline, imipramine, desipramine, clomipramine, trimipramine, protriptyline, dothiepin, doxepin, lofepramine, amoxapine, maprotiline, amineptine, nomifensine, bupropion, phenelzine, tranylcypromine, isocarboxazid, moclobemide, brofaromine, fluoxetine, sertraline, paroxetine, citalopram, escitalopram, fluvoxamine, zimelidine, tianeptine, trazodone, nefazodone, agomelatine, venlafaxine, desvenlafaxine, duloxetine, milnacipran, reboxetine, mirtazapine, and mianserin. We also reviewed the reference lists of all studies identified through the PubMed/MEDLINE search.
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We studied the inhibition of peroxidation by local anesthetics in an inflammatory animal model. Inflammatory lipid peroxidation was assessed by the thiobarbituric assay in plasma from rats injected or not injected with carrageenan (Carra) and killed 1, 2, 4, 6, 12, and 24 h thereafter. Thiobarbituric acid reactive substances (TBARS) values in inflammatory animals were maximal 6 h after Carra administration. This result, in accordance with the evolution of paw edema width during time, supports that TBARS reflect the intensity of inflammation. Local anesthetics (bupivacaine, lidocaine, ropivacaine, or bupivacaine-loaded microspheres) or amitriptyline were injected in clinically relevant concentrations as a sciatic nerve block or intraperitoneally in inflamed animals. Ropivacaine did not exhibit any protective effect on Carra-induced lipid peroxidation in rats. With all the other drugs administered as a sciatic nerve block, the maximal TBARS increase was not observed at 6 h. Our conclusion is that bupivacaine (plain or encapsulated), lidocaine, and amitriptyline in clinically relevant concentrations administered via the sciatic nerve showed antioxidant properties toward lipid peroxidation induced by Carra inflammation. Intraperitoneal injection of those drugs gave the same effect as nerve block; this result suggests that their mechanism of action is not strictly limited to the nerve. IMPLICATIONS. We investigated the antioxidant effects of local anesthetics and amitriptyline in an inflammatory rat model. Amitriptyline exhibits antioxidant properties per se, whereas lidocaine and bupivacaine (plain or encapsulated) seem to inhibit the peroxidation process. This may have future application in limiting toxic oxygen metabolite production during the inflammatory process.
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An analytical procedure for the subcellular fractionation of rat brain cortex is presented; it consists of a two-step procedure involving a differential centrifugation using the five-fraction scheme and an isopycnic centrifugation in continuous sucrose gradients. All fractions obtained were analyzed for their content of various constituents, such as receptor binding, uptake, and several marker enzymes. Special attention was paid to the subcellular distribution of the serotonin S2 receptors; they were mainly recovered in the microsomal P fraction, but a significant amount was also associated with the mitochondrial (M and L) fractions. After equilibration in density gradients, serotonin S2 receptors revealed two peaks, which were similarly affected after treatment with amitriptyline and/or yohimbine. There is no evidence to suggest that serotonin S2 receptors are associated with nerve endings containing the neurotransmitter serotonin. Although three main profiles, a microsomal, a mitochondrial, and a mixed one, clearly appear from the differential centrifugation, subgroups of these main profiles were also found. For instance, the microsomal distribution patterns of serotonin S2 receptors and 5'-nucleotidase are very similar, but differ from that of UDP-galactosyltransferase. Similarly, the mitochondrial profiles of cytochrome oxidase and 5-HT (serotonin) uptake are different. An analytical approach for brain fractionation, when performed with appropriate measurements (cytochrome oxidase, amine uptake, 5'-nucleotidase, and receptor binding), is rapid and clearly differentiates pre- and postsynaptic constituents.
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In the past 10 years, great strides have been made in the field of feline analgesia. A better understanding of the cat's unique metabolism has led researchers to realize that extrapolation across species boundaries is unwise,and this has resulted in feline-specific studies. The opioids are now used more commonly in cats, with good analgesic effect and few side effects. Excellent acute pain management is achievable in cats by using opioids, NSAIDs, alpha2-agonists, and local anesthetics. Although much of the research data has compared the use of single drugs, a multimodal approach using agents that work at different parts of the pain pathway is commonly used in clinical settings, with added benefit. Compared with dogs, few pain-scoring systems have been developed for cats, and this remains an important goal. Management of chronic pain in cats is a challenge because of the potential problems with long-term NSAID use; however, reports of low doses given at extended intervals are encouraging. As we gain experience with less traditional analgesics, such as amitriptyline, amantadine, and gabapentin, and critically evaluate complimentary therapies, our ability to provide comfort to this population of cats will improve.
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NP after definitive surgery for OS is frequently encountered, can persist for a significant time, and NP outcomes are similar in limb sparing and amputation groups.
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A prospective, double blind, randomised, placebo controlled study was initiated at two centres. Patients with vulvar vestibulitis were assigned to apply cromolyn or placebo cream to the vestibule. Symptoms (burning, irritation) and signs (erythema, extent of erythema, tenderness) were recorded on a 0-3 scale. In the sexually active patient subgroup, dyspareunia was also evaluated.
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Considering depression as a condition that damages physical, mental and social wellbeing, in the individual as well as in the community, research was made in the evolution of symptoms of depressive syndromes of 33 subjects, when treated with amytryptiline compounds. Treatment was begun with 25 mg daily and increased to 150 mg; doses were divided to avoid somnolence, and maintained for 8 to 14 weeks. Depressive syndromes showed improvement in 100% of cases, with resolution of clinical depression in 80%.
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Depression is a common and treatable condition among nursing facility residents, with low body weight being a frequent concomitant concern. A common prescribing dictum is that older tricyclic antidepressants (TCAs) enhance appetite and may facilitate weight gain, while newer selective serotonin reuptake inhibitors (SSRIs) cause anorexia and resultant weight loss in older adults. Evidence is lacking on whether the small weight changes noted during short-term antidepressant efficacy trials translate into larger weight changes during prolonged treatment periods. Our main objective was to compare weight outcomes at 6 months among users of three different antidepressant groups with a control group of non-antidepressant users. A secondary objective was to determine whether antidepressant selection was associated with weight pattern before drug initiation, to capture possible prescribing bias that would affect study inferences.
It is well established that hypothalamic-pituitary-adrenal (HPA) axis dysregulation, characterized by elevated circulating cortisol concentrations and impaired negative feedback inhibition, is associated with affective disorders. As normalization of the HPA axis function and mood-stabilizing effects occur simultaneously during antidepressant treatment, it is likely that these effects are either directly or indirectly dependent. Although data concerning the outward transport of glucocorticoids from the brain by P-glycoprotein (Pgp) are inconsistent, it has been hypothesized that antidepressants exert their clinical activity in parts by inhibiting Pgp, subsequently leading to enhanced brain glucocorticoid levels and the normalization of the HPA axis function. Here, we report on the effects of different antidepressants (amitriptyline, fluoxetine, mirtazapine, St John's wort extract) on the brain/plasma distribution of corticosterone in mice after acute and subchronic treatment. The four antidepressants exerted different effects on the corticosterone concentration in brain and plasma. Changes in corticosterone levels were highly correlated, suggesting passive diffusion between both tissues. St John's wort extract and fluoxetine elevated brain and plasma corticosterone concentrations after subchronic treatment. Mirtazapine and amitriptyline had no effect on corticosterone concentration after subchronic treatment, possibly because both are also potent antagonists at the 5-HT2 receptor, which mediates HPA axis stimulation by serotonergic stimuli. In addition, St John's wort is the only antidepressant tested which slightly elevated Pgp protein level in the brain.
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Women formed 2/3 of each group, the mean age in both groups being similar. Psychological symptoms were noted in the majority of both groups, but South Asians presented more physical complaints than the White group (67.5% compared to 22%, Chi squared=18.86, P=0.00001). The South Asian group were significantly more likely to be prescribed amitriptyline at doses of 75 mg or less than the White group (Fisher exact 2 tailed test, P=0.008), had significantly shorter median durations of antidepressant treatment (60 days, compared with 160 days for the White group, Mann Whitney test P=0.005). No differences were found between the groups in their continuity of care.
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Preliminary reports suggested that the addition of lithium carbonate to the regimen of patients treated with, but not responding to, a tricyclic antidepressant (TCA) drug can induce a rapid alleviation of depression. We examined the effect of lithium carbonate addition in 39 patients with unipolar depression whose conditions were not improved by at least three weeks' TCA drug administration. In 30 of 42 observations, lithium carbonate brought about a greater than 50% improvement within 48 hours. In a second study, the effects of lithium carbonate addition were compared in five amitriptyline hydrochloride-pretreated and five placebo-pretreated patients who showed no improvement after a three-week treatment. All five patients receiving amitriptyline showed a greater than 50% improvement 48 hours after lithium carbonate addition, whereas only one patient in the placebo group showed a marked response. In a third study the effect of lithium carbonate withdrawal was studied in nine TCA-resistant patients who had shown a marked improvement 48 hours after lithium addition. Only five of these patients had a relapse five days after lithium discontinuation. Since animal studies have shown that TCA drugs sensitize forebrain neurons to serotonin and that lithium enhances the activity of serotonin-containing neurons, we propose that the antidepressant effect of lithium addition in TCA-resistant patients might be mediated by enhancing serotonin neurotransmission.
A significant positive correlation was observed between the plasma amitriptyline concentration and road-tracking performance (r = 0.543, P < 0.05). There was no significant correlation between the plasma amitriptyline concentration and other driving performance, cognitive functions, and subjective somnolence.
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Chiropractic was more beneficial than placebo in reducing pain and more beneficial than either placebo or muscle relaxants in reducing GIS.
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Data were independently extracted by two reviewers using a standard form. Responders to treatment were calculated on an intention-to-treat basis: drop-outs were always included in this analysis. When data on drop-outs were carried forward and included in the efficacy evaluation, they were analysed according to the primary studies; when dropouts were excluded from any assessment in the primary studies, they were considered as treatment failures. Scores from continuous outcomes were analysed including patients with a final assessment or with the last observation carried forward. Tolerability data were analysed by calculating the proportion of patients who failed to complete the study and who experienced adverse reactions out of the total number of randomised patients. The primary analyses used a fixed effects approach, and presented Peto Odds Ratio (PetoOR) and Standardised Mean Difference (SMD).
Extensive global use of the serotonin-norepinephrine reuptake inhibitor Amitriptyline (AMI) for treatment of mental health problems has led to its common occurrence in the aquatic environment. To assess AMI bioconcentration factors, tissue distribution, and metabolite formation in fish, we exposed gilt-head bream (Sparus aurata) to AMI in seawater for 7 days at two concentrations (0.2 μg/L and 10 μg/L). Day 7 proportional bioconcentration factors (BCFs) ranged from 6 (10 μg/L dose, muscle) to 127 (0.2 μg/L dose, brain) and were consistently larger at the low dose level. The relative tissue distribution of AMI was consistent at both doses, with concentrations decreasing in the order brain ≈ gill > liver > plasma > bile ≫ muscle. Using a suspect screening workflow based on liquid chromatography-high resolution (Orbitrap) mass spectrometry we identified 33 AMI metabolites (both Phase I and Phase II), occurring mostly in bile, liver and plasma. Ten structures are reported for the first time. Remarkably, all 33 metabolites retained the tricyclic ring structure common to tricyclic antidepressants, which may be toxicologically relevant. Collectively these data indicate that, in addition to AMI, a broad suite of metabolites should be included in biomonitoring campaigns in order to fully characterize exposure in aquatic wildlife.
Fifty-eight actively psychotic inpatients who initially met criteria for long-standing schizophrenia and subsequently met Research Diagnostic Criteria for a current episode of schizoaffective disorder (mainly schizophrenic) with a depressive syndrome, and who scored at least 30 (mean = 55, SEM = 1.6) on the Brief Psychiatric Rating Scale and 17 (mean = 23, SEM = 0.7) on the Hamilton Rating Scale for Depression, were treated for 5 weeks with haloperidol hydrochloride and benztropine. Haloperidol and benztropine treatment was continued, while those patients who consistently scored greater than 17 on the Hamilton Rating Scale for Depression were randomly assigned to the following double-blind treatment groups for 4 weeks: adjunctive amitriptyline hydrochloride, desipramine hydrochloride, or placebo. Adjunctive desipramine or amitriptyline showed no significant therapeutic advantage, when compared with haloperidol and placebo, on the Brief Psychiatric Rating Scale or the Hamilton Rating Scale for Depression. After 4 weeks of combine therapy, patients receiving adjunctive amitriptyline or desipramine, as compared with those receiving adjunctive placebo, tended to score higher on the Brief Psychiatric Rating Scale hallucinatory behavior item and on the thinking disturbance factor than patients receiving placebo. These results suggest that adjunctive antidepressants are not indicated for the treatment of depressive symptoms in actively psychotic schizophrenic inpatients. Adjunctive antidepressants may retard the rate of resolution of psychosis in this population.
Disruption of normal neuronal networks and neurotransmitters like serotonin and norepinephrine levels in post traumatic brain injury (TBI) are observed to be the primary causative agent for depression/anxiety. This communication reports the efficacy of various classes' anti-depressants in the treatment of depression/anxiety following TBI in rats. Chronic treatment with anti-depressants (escitalopram and venlafaxine) leads to improvement in the depressive/anxiogenic-like behaviour in the TBI rat and corroborates the notion of the involvement of serotonin and norepinephrine in the behavioural consequences of post-TBI. Chronic treatments with escitalopram and venlafaxine significantly reversed the effect of TBI as compared to vehicle-treated TBI group. The results showed a quantitative battery of neuro-behavioural functional assessments that correlates with neuronal damage following traumatic brain injury.
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We conducted a series of definitive systematic reviews and meta-analyses of RCTs. Claims data from the MEDLINE, EMBASE, LILACS, CBM, CNKI, VIP, Wan Fang, and Cochrane Library databases were used. We also reviewed articles and reference lists of relevant articles pertaining to human subjects published prior to March 26, 2016. No language restrictions were imposed. Two authors independently reviewed the titles and abstracts of the retrieved studies, which were matched using Review Manager 5.3 software. Disagreements were resolved by consensus. The outcome data were the number of subjects whose symptoms declined, measured by cough or Leicester Cough Questionnaire (LCQ) score. Random effect meta-analyses were used to pool the findings. Publication bias was assessed using funnel plots.
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The relationship between delayed gastric emptying and symptom pattern in gastroparesis and, related to it, its separation from functional dyspepsia remains an area of controversy and uncertainty. Pathophysiological studies have focused on the role of pyloric resistance and duodenal motility in generation of symptoms. In diabetic patients, glycemic control did not determine short-term changes in gastric emptying rate in type 2 diabetes, but poor glycemic control was a major risk factor for long-term development of gastroparesis in type 1 diabetes. At the cellular level, diabetic gastroparesis is characterized by loss of interstitial cells of Cajal (ICCs), and this is inversely correlated to the number of CD206+ macrophages, which are thought to have a protective effect on ICCs. Treatment trials have focused on dietary factors and a nasal spray formulation of metoclopramide. A meta-analysis of prokinetic studies found no association between symptom improvement and enhancement of gastric emptying in gastroparesis. Two controlled studies showed no benefit of tricyclic antidepressants (nortriptyline, amitriptyline) in idiopathic gastroparesis and functional dyspepsia with delayed emptying.
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The majority of those affected were adolescent Caucasian females. Subjects with chronic nausea had a more severe presentation with daily 88% (vs 26%) and constant 60% (vs 10%) nausea (P < .001), one-half with peak morning intensity. In the chronic nausea group, 62% had migraines, and 71% (vs 22%) had familial migraines (P < .001), 36% had postural tachycardia syndrome and 27% cyclic vomiting syndrome. Both groups suffered comorbid symptoms (anxiety, dizziness, fatigue, and sleep problems). The chronic nausea cohort underwent extensive, negative medical evaluations.
In this communication two cases of possibly drug induced hyponatremia secondary to amitriptyline and thioridazine have been reported. What is particularly important is the fact that in one, irreversible neurological symptoms were left as sequelae and in the other, the patient was in a coma and thus suffered from a potentially lethal complication. The physicians should be aware of this disturbing side effect while treating their patients with antidepressant and neuroleptic medications.
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A total of 36 subjects were randomized; 34 completed both dosing periods (1 subject was lost to follow-up, 1 withdrew consent). Steady state was reached for CER 30 mg on day 7. Mean C(max,ss), C(min,ss), and C(avg,ss) were 41.1, 21.4, and 31.4 ng/mL, respectively. The median T(max,ss) for CER 30 mg was 7.0 hours, with a mean t(½) of 34.8 hours. At steady state, CER produced a sustained plasma cyclobenzaprine concentration with a single peak in plasma concentration during the 24-hour dose interval. The R(ac) for CER was 2.65. Because of a protocol violation (insufficient data), no steady-state pharmacokinetic assessments could be performed for CIR. Most adverse events were mild or moderate in intensity. Somnolence was the most frequently reported adverse event (100% of subjects) in those receiving CER, followed by dry mouth (58%), dizziness (19%), and headache (17%).
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A total of 12% of residents were prescribed one or more of 10 presumptively inappropriate medications on a standing basis, a figure that differed substantially between states (14.0% vs 7.4% (P < .001)). The most prevalent inappropriate medications were dipyridamole (5.4% of residents), amitriptyline (3.3%), and methyldopa (1.8%). Among patients receiving 0 to 3, 4 to 6, and 7+ medications, 5%, 12%, and 19%, respectively, were receiving at least one inappropriate medication. In multivariate logistic regression analyses, the strongest predictors of inappropriate medication use were state and the total number of standing medications prescribed. Including other statistically significant predictors of inappropriate medication use (age > 65 years, never having been married, severe functional limitations, being a long-stay patient, and medical diagnosis) did not substantially improve the overall predictive ability of the model.
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Single doses of amitriptyline (50 mg) and zimelidine (100 mg) were administered orally to 4 young and 4 elderly healthy volunteers (aged 21--26 and 68--75 respectively) in a comparative study of the two drugs. Systolic time intervals, supine and standing blood pressure, salivary flow and indices of sedation were measured at regular intervals up to 6 hours post dose. No conclusive changes in the QS2 interval, left ventricular ejection time (LVETc) LVET index, pre-ejection period (PEPc), resting heart rate, or blood pressures were observed with either drug. Salivary flow was reduced by about 40% at 3.5 hours and 50% at 5.5 hours after ingestion of amitriptyline. No change in salivary flow was observed after zimelidine (significant difference between treatments; P less than 0.01 at 3.5 and 5.5 hours). Subjective drowsiness as measured by visual analogue ratings was significantly greater for amitriptyline at 3.5 hours (P less than 0.01). Postural sway was also increased by amitriptyline but not zimelidine (difference between treatments significant at 3.5 and 5.5 hours; P less than 0.01 and 0.05 respectively). Auditory reaction time increased with amitriptyline, the difference between treatments achieving significance at 5.5 hours. No differences in response to either drug between young and elderly volunteers were demonstrable in these small groups, although variability was greater in the older group. Possible implications of these findings for the treatment of depression in the elderly are discussed.
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Of nine studies of manipulation for tension-type headaches that reported quantitative outcomes, four were randomized clinical trials and five were case series designs. These studies reported on 729 subjects, 613 of whom received manipulation. Outcomes ranged from good to excellent. Manipulation seems to be better than no treatment, some types of mobilization and ice, and it seems to be equivalent to amitriptyline but with greater durability of effect than this medication. Of three studies on migraine, only one was a randomized clinical trial. These studies reported on 202 subjects, 156 of whom received manipulation. The outcomes ranged from fair to very good.
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The objective of this study was to provide a quantitative analysis (meta-analysis) of the efficacy and harms of antidepressants in the management of adult FMS patients.
The current study examines the effects of amitriptyline administration on extracellular levels of monoamines and their metabolites in hypothalamus of conscious rat using in vivo microdialysis. Systemic amitriptyline (30 mg/kg, i.p.) maximally increased extracellular norepinephrine to nearly 19 times, dopamine 12 times, and serotonin 2.5 times that of their respective basal values. Local administration of amitriptyline (10 microM) in the perfused artificial cerebrospinal fluid increased extracellular serotonin levels to 2.7 times basal levels - a similar increase to that observed with systemic administration. In contrast, local administration of amitriptyline (10 microM) increased extracellular norepinephrine and dopamine to only 5.3 and 3.8 times basal levels. Systemic administration of amitriptyline (30 mg/kg, i.p.) during local amitriptyline perfusion increased norepinephrine and dopamine levels to 28 and 12.9 times their respective basal levels without affecting serotonin levels. Systemic amitriptyline administration preferentially increases extracellular norepinephrine and dopamine levels over serotonin levels in the rat hypothalamus and the effects on the catecholamine levels may be partially due to mechanisms other than local uptake inhibition.
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Clinical, preclinical, and pharmacological studies have suggested that decreased enkephalin tone is associated with depression-like symptoms and increase in enkephalin signaling could have a therapeutic value in the treatment of depression. In this study we demonstrate that, surprisingly, animals lacking enkephalin (preproenkephalin, Penk1(-/-)) showed no depression-related phenotype in the Porsolt forced swimming or tail suspension tests. Moreover, Penk1(-/-) mice had a lower frequency of depression-related behavior in stress-induced hypoactivity and ultrasonic vocalization models of depression, similar to animals treated with antidepressant drugs, although this effect was specific to the genetic background. In addition, there was no significant difference in the efficacy of antidepressant reference compounds in wild-type and knockout animals. Nialamide and amitriptyline were even slightly more effective in animals with genetic deletion of Penk1, whereas the minimal effective dose of imipramine and fluoxetine was the same in the two genotypes. The dual peptidase inhibitor RB-101 was also effective in Penk1(-/-) as well as in Penk1(-/-)/Pdyn(-/-) animals, although its efficacy was somewhat reduced compared with wild-type animals. This result was also surprising because the antidepressant effects of RB-101 were thought to be due to the elevation of enkephalin levels.