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Generic Anafranil is a tricyclic antidepressant. Generic Anafranil is used to treat symptoms of obsessive-compulsive disorder (recurrent thoughts or feelings and repetitive actions). Generic Anafranil works by affecting chemicals in the brain that may become unbalanced.

Other names for this medication:

Similar Products:
Anafranil SR, Clopran, Doxepin, Cymbalta, Elavil


Also known as:  Clomipramine.


Generic Anafranil is used to treat symptoms of obsessive-compulsive disorder (recurrent thoughts or feelings and repetitive actions).

Generic Anafranil is a tricyclic antidepressant.

Anafranil is also known as Clomipramine, Clonil, Clofranil, Clopram, Clopran, Clopress, Equinorm, Hydiphen.

Generic Anafranil works by affecting chemicals in the brain that may become unbalanced.

Generic name of Generic Anafranil is Clomipramine.

Brand name of Generic Anafranil is Anafranil.


Take Generic Anafranil orally.

Do not take Generic Anafranil in large amounts.

Take Generic Anafranil with food.

Take Generic Anafranil up to 4 weeks.

The dosage of tablets depends on the disease and its prescribed treatment.

If you want to achieve most effective results do not stop taking Generic Anafranil suddenly.


If you overdose Generic Anafranil and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Anafranil overdosage: uneven heart rate, extreme drowsiness, confusion, agitation, vomiting, blurred vision, sweating, muscle stiffness, increased or decreased urination, swelling, shortness of breath, blue lips or fingernails, feeling light-headed, fainting, seizure.


Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Anafranil are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Anafranil if you are allergic to Generic Anafranil components.

Do not take Generic Anafranil if you're pregnant or you plan to have a baby, or you are a nursing mother.

Do not take Generic Anafranil if you had recent heart attack.

Do not take Generic Anafranil if you use MAO inhibitor such as isocarboxazid (Marplan), phenelzine (Nardil), rasagiline (Azilect), selegiline (Eldepryl, Emsam) or tranylcypromine (Parnate) within the past 14 days.

Be careful with Generic Anafranil if you have heart disease or a history of heart attack, bipolar disorder, schizophrenia or other mental illness, kidney or liver disease, overactive thyroid or adrenal gland tumor, glaucoma, problems with urination.

Avoid using other medicines that make you sleepy while using Generic Anafranil.

Avoid drinking grapefruit juice and eating grapefruit while using Generic Anafranil.

Avoid exposure to sunlight or artificial UV rays while using Generic Anafranil.

Be careful if you drive or do anything that requires you to be awake and alert while using Generic Anafranil.

Avoid alcohol.

Do not stop taking Generic Anafranil suddenly.

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This paper reports, for the first time, the development of a modified Quick, Easy, Cheap Effective, Rugged and Safe (QuEChERS) combined with a dispersive SPE (d-SPE) based clean-up procedure as a new and powerful strategy for the simultaneous and efficient isolation of two different antidepressants, fluoxetine and clomipramine, and their active metabolites in human urine samples. A univariate experimental design with four independent variables such as sample volume, extraction solvent, buffered salts and clean-up step, was performed and used to investigate the effect of process variables on the extraction efficiency. Good linearity was achieved at the studied concentration range (0.1-5.0 µg mL(-1)), with correlation coefficients (R(2)) higher than 0.9961. Low detection limits, ranging between 0.060 and 0.092 μg mL(-1) were obtained for all analytes, whereas the lowest quantification limit was 0.1 μg mL(-1), corresponding to the lowest concentration of the standard curve. The method also showed good results for accuracy, with values ranging from 91% to 105%. Intra- and inter-day precision, expressed as the relative standard deviation (RSD), were also satisfactory (<10%). Consistent recoveries of antidepressants ranging from 86% to 109% were observed when urine samples were fortified at three concentrations, namely 0.1, 2.5 and 5.0 μg mL(-1) In order to evaluate the proposed method for clinical use, the QuEChERS/UHPLC-PDA method was applied to analysis of 12 urine samples from depressed patients.

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These data indicate a significant influence of the CYP2D6 genotype, minor influence of the CYP2C19 genotype and no influence of the CYP2C9 genotype on plasma concentrations of patients taking mainly second-generation antidepressants. Because of the good tolerability of the latter and the flat dose-response relationship, genotyping should only be considered in cases of suspected side effects.

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34 patients with diagnosis of depressive episode (ICD-10) were treated for 8 weeks with tricyclic antidepressants (TCA) 22 patients were treated with clomipramine 75-175 mg daily, 11 with imipramine 75-150 mg and 1 with amitriptyline 150 mg. Following parameters were analysed: plasma concentration (FPIA, HPLC), pharmaco-EEG (spectrum power for delta, theta, alfa1, 2, beta 1, 2, 3 by the use of FFT), clinical improvement (HAMD, HARS, SGI, SERS). 50% reduction in HAMD was regarded as improvement.

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Several studies reported a decreased pain sensitivity in patients with depression, but the underlying neurobiological mechanisms of this phenomenon are unclear. While there is extensive evidence that the serotoninergic system plays a key role in pain modulation, especially in pain inhibitory mechanisms via descending pathways, as well as in the pathophysiology of depression, no study so far has examined its potential relevance in mediating the alteration of pain processing. The present study addresses the question of whether indices of serotoninergic dysfunction, as investigated by a neuroendrocine challenge paradigm, are related to pain sensitivity. Nineteen drug-free inpatients with unipolar major depression underwent a neuroendocrine challenge test by measuring cortisol and prolactin in response to intravenously administered clomipramine (12.5mg). Heat/cold pain thresholds, warmth/cold detection thresholds, measures of current pain complaints and mood were assessed the day before and three day after challenge procedure. When patients were classified in subgroups based on a median split of their cortisol response values, the low-responsive group showed significantly elevated heat pain thresholds and nearly significantly elevated cold pain thresholds compared to the high-responsive group. No such group differences were found with regard to somatosensory thresholds, measures of pain complaints and mood. Subgrouping on the basis of prolactin responsiveness did not reveal significant differences in any parameter. In summary, a decreased pain sensitivity was demonstrated in patients characterized by a reduced neuroendocrine responsiveness to clomipramine, suggesting an involvement of serotoninergic dysfunction underlying altered pain perception in depression.

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A sleep deprivation/chlorimipramine therapy was compared to chlorimipramine therapy in endogenous depression. In the sleep deprivation/chlorimipramine group a quick and long-lasting remission of depressive symptoms could be demonstrated. In the chlorimipramine group a marked prolonged onset of action was seen.

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The effectiveness mechanism of the chlomipramine treatment was evaluated by sacral evoked response (SER) and dorsal nerve somatosensory cortical evoked potential (DN-SEP) testings in 15 patients with true premature ejaculation (TPE). We couldn't demonstrate any significant difference between the values of either latency times or amplitudes of the evoked responses determined just before and at the end of the treatment with chlomipramine in these patients. However, the sensory thresholds were 24.4 +/- 4.3 V in the pretreatment term and 30.2 +/- 7.3 V at the end of the treatment. This difference is statistically significant (P = 0.0031). Our results suggest that chlomipramine increases the sensory threshold for the stimuli in the genital area.

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Adhesion dependent mechanisms are increasingly recognized to be important for a wide range of biological processes, diseases and therapeutics. This has led to a rising demand of pharmaceutical modulators. However, most currently available adhesion assays are time consuming and/or lack sensitivity and reproducibility or depend on specialized and expensive equipment often only available at screening facilities. Thus, rapid and economical high-content screening approaches are urgently needed.

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Substance P (SP) is possibly involved in the pathophysiology of depression and anxiety. We investigated interactions between antidepressants on SP-induced effects and their potential calcium-blocking activity in the isolated guinea pig ileum. All the antidepressants tested, except pargyline, moclobemide, mianserin, and reboxetine, were able to inhibit in a concentration-dependent manner the contraction induced by 100 nmol/L SP. Clomipramine, fluoxetine, maprotiline, and amitriptyline (all at 3 mumol/L) flattened the concentration-response curves to SP, resulting in a reduction of up to 59%, 63%, 32%, and 23%, respectively, of the maximum contractile effect. All the antidepressants tested (3 mumol/L), except pargyline, moclobemide, and mianserin, produced a rightward parallel shift of the concentration-response curve to CaCl2. The L-type selective calcium blocker nifedipine and the T-type selective mibefradil showed similar behaviour against both agonists used, SP and CaCl2. The relative order of potency was nifedipine (pA2, 7.6 +/- 0.1) > clomipramine (pA2, 7.0 +/- 0.1) > fluoxetine (pKB, 6.5 +/- 0.1) = mibefradil (pKB, 6.6 +/- 0.1) > amitriptyline (pKB, 6.3 +/- 0.1) = maprotiline (pKB, 6.2 +/- 0.1) > fluvoxamine (pKB, 5.9 +/- 0.1). The data reported in the present study suggest that the antidepressants tested did not behave as competitive antagonists versus NK1-receptor subtypes, but their inhibitory action seems to be related to their calcium-blocking properties.

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Visceral leishmaniasis affects people from 70 countries worldwide, mostly from Indian, African and south American continent. The increasing resistance to antimonial, miltefosine and frequent toxicity of amphotericin B drives an urgent need to develop an antileishmanial drug with excellent efficacy and safety profile. In this study we have docked series of febrifugine analogues (n = 8813) against trypanothione reductase in three sequential docking modes. Extra precision docking resulted into 108 ligands showing better docking score as compared to two reference ligand. Furthermore, 108 febrifugine analogues and reference inhibitor clomipramine were subjected to ADMET, QikProp and molecular mechanics, the generalized born model and solvent accessibility study to ensure the toxicity caused by compounds and binding-free energy, respectively. Two best ligands (FFG7 and FFG2) qualifying above screening parameters were further subjected to molecular dynamics simulation. Conducting these studies, here we confirmed that 6-chloro-3-[3-(3-hydroxy-2-piperidyl)-2-oxo-propyl]-7-(4-pyridyl) quinazolin-4-one can be potential drug candidate to fight against Leishmania donovani parasites.

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9-HC-6-one relaxed significantly phenylephrine (PE)-precontracted CC. Such response was not attenuated by endothelium disruption, N(G) -nitro-L-arginine methyl ester, or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one treatment, suggesting that a nitric oxide/cyclic guanosine monophosphate-dependent pathway was precluded. 9-HC-6-one attenuated PE-induced contraction by blocking cell surface and internal calcium channels with a higher potency for internal calcium release. This compound also antagonized calcium-evoked contraction in Ca2+ -free, high K+ -depolarizing condition, suggesting that interfering with the entry of calcium through voltage-dependent channels also contributed to 9-HC-6-one-induced corporal relaxation. After IC application of 9-HC-6-one, a significant rise in ICP was observed as compared with the application of normal saline. 9-HC-6-one relaxed significantly norepinephrine (NE)- and KCl-precontracted SV, and antagonized NE-induced oscillatory contraction as potent as clomipramine. Finally, the HNS-evoked increase in ILP was dose-dependently repressed after challenge by 9-HC-6-one.

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Four human studies and nine experimental models were found. The human studies showed a transiently statistically significant positive association between amitriptyline and liver cancer and a negative association with pancreatic cancer; and that the antidepressants amitriptyline, nortriptyline, desipramine, and phenelzine may increase risk of breast cancer. Results of the experimental studies differed depending on which antidepressants were examined and which model was used. Amitriptyline was found to promote tumour growth, fluoxetine and clomipramine were reported to be both tumour promoters and antineoplastic agents, and imipramine and citalopram both demonstrated antineoplastic properties.

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Serotonin (5-HT) is considered to be an important transmitter underlying mood and behaviour. Abnormalities of the 5-HT transporter have been suggested in mood disorders, since it is one of the major binding sites of antidepressants. A number of ligands have been developed to visualise the 5-HT transporter in vivo, but only a few have successfully visualised specific binding in vivo. In this study, we comparatively evaluated two ligands for 5-HT transporter, [(11)C](+)McN5652 and [(11)C]cyanoimipramine, in the human brain. Brain uptake of [(11)C](+)McN5652 and [(11)C]cyanoimipramine was measured with PET in 15 healthy volunteers. Second PET scans were performed after pretreatment with the potent 5-HT reuptake inhibitor clomipramine. Data were analysed as regional brain uptake as well as whole brain uptake. In six healthy volunteers uptake of the two ligands was also measured in the lung since it is one of the high-uptake organs in the body. In the brain, high accumulation was observed in the thalamus and striatum, the regions known to contain high densities of 5-HT transporter, for both [(11)C](+)McN5652 and [(11)C]cyanoimipramine. The average ratio of thalamus to cerebellum uptake at 90 min after the tracer injection was approximately 1.6 for [(11)C](+)McN5652 and 1.7 for [(11)C]cyanoimipramine, while the ratios obtained after pretreatment with clomipramine were approximately 1.2. However, the whole brain uptake of [(11)C](+)McN5652 was approximately twice that of [(11)C]cyanoimipramine, while the lung uptake of [(11)C](+)McN5652 was approximately half that of [(11)C]cyanoimipramine. Both [(11)C](+)McN5652 and [(11)C]cyanoimipramine showed sufficient specific binding for performance of a quantitative analysis in the brain. [(11)C](+)McN5652 could be superior because of its higher distribution to the brain.

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Most of the 125 (84.0%) analyzed cases were associated with a recent change in a serotonergic drug (introduction, increasing the dose or overdose). Antidepressants were the most often involved serotonergic drugs, mostly serotonin reuptake inhibitors (SRIs, 42.1%) and to a lesser extent serotonin-noradrenalin reuptake inhibitors (9.1%, mainly venlafaxine), tricyclic antidepressants (8.6%, mainly clomipramine), and some monoamine oxidase inhibitors (6.2%, mainly moclobemide). Nonpsychotropic medications were also involved, generally opioids (14.8%, mainly tramadol). Most of the cases (59.2%) resulted from pharmacodynamic DDIs, most often involving SRIs + opioids (mostly paroxetine + tramadol). However, SS also occurred with a single serotonergic drug in a significant number of cases (40.8%), most often SRIs (mainly fluoxetine) or venlafaxine at usual doses. Lastly, a major pharmacokinetic DDI could have played a role in 1/5 (20.8%) of cases.

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Records of patients with OCD were analyzed for clinical features, medication used, extent of behavior modification, and outcome.

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The contractile responses of 17 circular smooth muscle strips of human vas deferens to 10-4 M. norepinephrine were observed in the absence and presence of clomipramine, and the selective serotonin re-uptake inhibitors fluoxetine, sertraline and paroxetine. The intraluminal pressure response of rat vas deferens to electrical stimulation of the hypogastric nerve was measured in 5 rats in the central plus peripheral effect group before and after the intravenous injection of 4.2 mg./kg. clomipramine or 8.3 mg./kg. sertraline. The pressure response to each agent was also observed after the transection of all proximal sympathetic input to the hypogastric nerve in 5 animals in the peripheral effect group.

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Treatment of obsessive compulsive disorder has not changed a lot since 2000. Following a cautious assessment of the patient, using adequate scales, OCD patients require a step by step hierarchical treatment. A syndrome of low intensity (Yale-Brown Obsessive Compulsive Score [Y-BOCS] around 15) will be mainly treated by behavioural and cognitive therapy (BCT) especially exposition with prevention of response technique; for a more severe disorder, a drug treatment is required. Selective serotonin reuptake inhibitors (SSRI) are firstly recommended. They should be used in monotherapy with daily doses higher than those used for depression. Response is slow and usually delayed comparing to the alleviation of the depressive syndrome. A full response with disappearance of the symptoms is an exception. A good response to an antiobsessive treatment affords a 50% reduction of the intensity of OCD. Clomipramine may be slightly more effective than SSRI. Once, an improvement has been obtained, the drug titration should be kept for at least 18 to 24 months before attempting to discontinue medication. In case of non response, switching SSRI drug, combination with BCT may contribute to resolve the problem. In treatment refractory OCD, combination with either risperidone or olanzapine has shown some effective results in controlled trials. Finally, for several infrequent patients with a "malignant syndrome", functional neuro-surgery using deep brain stimulation might be a safe and hopeful therapeutic technique.

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Munchausen syndrome by proxy (MSBP) is a rare form of child abuse in which a parent, usually the mother, fabricates or produces illness in a child, so causing them unnecessary medical investigations, treatments and hospitalizations. One of the commonest false presenting symptom is 'seizures'.

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Panic disorder is a common psychiatric disorder characterized by recurrent anxiety attacks and anticipatory anxiety. Due to the severity of the symptoms of the panic attacks and the frequent additional occurrence of agoraphobia, panic disorder is an often debilitating disease. Elevation of central serotonin levels by drugs such as clomipramine represents one of the most effective treatment options for panic disorder. This points to an important role of dysregulation of the serotonergic system in the genetic etiology of panic disorder. The novel brain-specific 5-HT synthesizing enzyme, tryptophan hydroxylase-2 (TPH2), which represents the rate-limiting enzyme of 5-HT production in the brain, may therefore be of particular importance in panic disorder. We focused on the putative transcriptional control region of TPH2 and identified two novel common single nucleotide polymorphisms (SNPs) of TPH2 in and close to this region. Moreover, a recently described loss-of-function mutation of TPH2 which results in an 80% reduction of serotonin production, was assessed. In an analysis of the putative transcriptional control region SNPs in a sample of panic disorder patients and controls no association of the disorder with the TPH2 SNPs or haplotypes was found. Moreover, the loss-of-function R441H mutation of TPH2 was not present in the panic disorder patients. The results of this first study of TPH2 in panic disorder argue against an importance of allelic variation of TPH2 in the pathogenesis of panic disorder with or without agoraphobia.

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Long-term clomipramine administration (CMI: 2.5 mg/kg IP, 25 days) effects on 274 identified hippocampus-septal neurons was assessed in rats. Stimulation of CA 1/dentate areas produced a biphasic response in 61% of lateral septal neurons. A brief activation was followed by a period of suppression of firing. In CMI-treated rats, the neurons showing this biphasic response increased their firing rate about fourfold, while the suppression of firing shortened around threefold. Other septal neurons (36%), in which only the burst of activation appeared but not suppression of firing, did not change their firing rate even after long-term CMI. In conclusion, CMI produces an increase of firing rate in lateral septal neurons receiving inhibitory hippocampal influence which is likely to be mediated by a disinhibitory process.

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1. Binding of the novel radioligand (3)H-2-(2-dimethylaminomethyl-phenylsulphanyl)-5-methyl-phenylamine ((3)H-MADAM) to the serotonin transporter (SERT) was used to characterise a range of selective serotonin re-uptake inhibitors (SSRIs) in vitro and in vivo. 2. (3)H-MADAM bound with high affinity in a saturable manner to both human SERT expressed in CHO cells (K(d)=0.20 nm (pK(d)=9.74+/-0.12), B(max)=35+/-4 fmol mg(-1) protein) and mouse cerebral cortex membranes (K(d)=0.21 nm (pK(d)=9.66+/-0.10), B(max)=50+/-24 fmol mg(-1) protein). 3. Binding of (3)H-MADAM was highly selective for SERT in vitro as demonstrated by the in vitro profile of MADAM tested at 75 different receptors, ion channels and transporters. This was further substantiated by the pharmacological profile of the binding. Hence, the binding of (3)H-MADAM was potently inhibited by SSRIs but not by selective inhibitors of noradrenaline transport and dopamine transport. Likewise, a 5-HT(2A/2C) receptor antagonist did not inhibit (3)H-MADAM binding. 4. (3)H-MADAM binding in vivo was inhibited only by compounds which also inhibited the binding of (3)H-MADAM in vitro (the SSRIs, mixed SERT/noradrenaline transport inhibitors and clomipramine), confirming the selectivity of (3)H-MADAM for SERT also in vivo. Moreover, compounds effective in inhibiting (3)H-MADAM binding were the only ones found to be active in the mouse 5-HTP potentiation test confirming the model as a behavioural correlate to in vivo 5-HT uptake. 5. Finally, it was found that a SERT occupancy of 85-95% was necessary to produce 50% of the maximum behavioural response (ED(50)).

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A case is reported of seizure development after combined use of bupropion and clomipramine. Electroencephalography revealed frequent generalized spike and wave complexes prominent on both frontal areas. These newly developed epileptiform discharges persisted even after discontinuation of both drugs.

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There is currently available evidence that suggests that drugs combining 2 synergistic mechanisms of action (e.g., enhancement of both noradrenergic and serotonergic neurotransmission) may yield superior therapeutic efficacy compared with a single therapeutic mechanism of highly selective agents such as selective serotonin reuptake inhibitors (SSRIs). The differences in antidepressant efficacy favoring dual-acting drugs may exist in particular for 3 difficult-to-treat groups of patients: those with endogenous depression, those with severe depression, or hospitalized depressed patients. Mirtazapine differs from other new dual-acting antidepressants by not being a reuptake inhibitor. Its antidepressant activity may be related to a direct enhancement of noradrenergic neurotransmission by blockade of alpha2-autoreceptors. The rapid increase in serotonin (5-HT) synaptic levels by blockade of alpha2-heteroreceptors indirectly enhances 5-HT1A-mediated neurotransmission since 5-HT2 and 5-HT3 are blocked by mirtazapine. The antidepressant efficacy of mirtazapine was established in several placebo-controlled trials. Currently available evidence suggests that mirtazapine is effective in all levels of severity of depressive illness, as well as is in a broad range of symptoms associated with depression.

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Depression is one of the frequently-observed psychiatric symptoms associated with nicotine (NC) use. In the present study, considering the unique effects of NC (e.g. antidepressant effects have also been reported), the time course of the NC-induced depressive behavioral alterations in a mouse model was compared with a typical depression-inducing stressor. Furthermore, based on the involvement of cannabinoid (CB) receptors in the behavioral effects of NC, the effects of antidepressants including CB ligands (CBs) against the NC-induced behavioral alterations were also investigated. Repeated subcutaneous NC treatments (0.3 mg/kg, 4 days), like repeated immobilization stress (IM) treatments (10 min, 4 days), caused prolonged depressive effects (increased immobility time) at both 2 hr and 1 day time points after the last treatment in the tail suspension test. However, in the NC group, depressive effects (suppressed swimming behaviors) were observed only at the 2 hr time point in the forced swimming test. The antidepressants amitriptyline, clomipramine and fluvoxamine, the endogenous mixed CB agonist/antagonist virodhamine and the anandamide-like cannabimimetic O-2093 provided antagonistic effects against the depressive behaviors in the tail suspension test. However, in the forced swimming test, NC-induced depressive behaviors were antagonized only by the CBs virodhamine and O-2093. The present results demonstrated depressive effects of NC in two typical behavioral tests, which support the risk of repeated NC use. The shortened behavioral alterations in the forced swimming test, as compared to the IM group, seemed to reflect the neuronal modifications peculiar to NC, which are antagonized by some CBs.

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Two review authors independently selected and appraised the studies for inclusion and risk of bias. All data were continuous.

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In an open clomipramine dose finding study, 33 depressed indigenous African outpatients were randomly assigned to two regimens of treatment with 125 mg and 75 mg oral medications daily. At the end of eight weeks of treatment, 16 patients (48.5 pc) were on the 75 mg regime, and 17 (54.8 pc) were on 125 mg. Analysis of depression scores on the Beck-Rafaelsen scale indicated improvements of depression in both regimes of equal magnitude. Analysis of variance showed no statistically significant difference on dose response between the two regimes. The higher doses, however, were associated with more drowsiness and tremulousness. It is suggested that Black African patients respond to tricyclic antidepressants in much lower doses than those recommended in Western textbooks. It is also apparent that side effects of tricyclic antidepressants, which have been implicated in non-compliance to medication, could be avoided without compromising treatment outcome.

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NA concentrations in the LC perfusate were significantly higher in the tramadol and clomipramine groups compared to the morphine group. Naloxone administration did not significantly affect NA concentrations. In the morphine group, NA release in the LC was not significantly correlated with the pain threshold. In contrast, in the tramadol and clomipramine groups, NA release in the LC was significantly correlated with the pain threshold. The correlation coefficient was higher in the clomipramine group than in the tramadol group.

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The major findings of our investigation were that rats subjected to neonatal instrumental RSD demonstrated diminished sexual activity, decreased aggressive behavior, increased percentage of REM sleep, and decreased wake-REM sleep ratio compared with yoked control rats. These data are compatible with the findings from adult rats subjected to neonatal treatment with the REM-sleep suppressant, clomipramine, and supports the hypothesis that neonatal RSD results in adult depressive abnormalities.

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An electronic search of PsycInfo, Embase, Medline and Cinahl databases was conducted spanning the time period 1990 to October 2005 for primary trials. This was supplemented by hand searching and cross-referencing of relevant reviews. Strict scientific methodology requirements were formulated that the studies had to meet in order to merit inclusion in this review.

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Pisa syndrome was suspected, and then, the daily dose of clomipramine hydrochloride was decreased from 9x to 3x25 mg tablets. Approximately 2 weeks after reducing the dose, abnormal postures gradually improved, and after 1 month, flexion of the trunk resolved.

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Non-antiepileptic drugs have been buy anafranil online used in the management of trigeminal neuralgia since the 1970s.

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This study has investigated the effects of chronic treatment with amitriptyline, chlorimipramine, mianserin and metergoline on levels and ex vivo release of thyrotrophin-releasing hormone (TRH), 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in specific regions of the brain and lumbar spinal cord of the rat. All four treatments caused a significant increase in levels of TRH in the lumbar spinal cord with amitriptyline producing the most marked effect. Amitriptyline alone caused a similar marked increase in levels of TRH in the nucleus accumbens and suprachiasmatic nucleus but none of the treatments had a significant effect on the TRH content of the median eminence or septal nuclei. Potassium-induced release of TRH and 5-HT ex vivo was measured from tissue slices of the nucleus accumbens, septal nuclei and lumbar spinal cord after treatment with amitriptyline and mianserin. An increase in release of TRH was observed only from tissue slices of areas where increased levels of the peptide had occurred; namely nucleus accumbens and lumbar spinal buy anafranil online cord after administration of amitriptyline and lumbar spinal cord after mianserin. None of the drugs significantly altered the ex vivo release of 5-HT or 5-HIAA. The results are discussed in relation to a possible interaction between TRH and 5-HT receptors in the antidepressant action of these drugs.

anafranil 20 mg 2016-06-26

The case is described of a neonate who suffered from withdrawal symptoms within 24 hours after birth as a result of the use of clomipramine by the mother during pregnancy. The symptoms consisted of increased irritability, alternating hyper- en hypotonia, hyperreflexia, cyanosis and hypothermia. He was treated with clonazepam with good result. Prescription of clomipramine during pregnancy should be restricted to specific cases and the doses should be kept as low as possible. Because the symptoms are withdrawal symptoms, phenobarbital should not be used as treatment, as it increases drug metabolism by buy anafranil online the liver causing an even faster decrease of plasma concentrations of clomipramine. Clonazepam is the drug of choice.

anafranil online 2016-04-24

The effects of the buy anafranil online cumulative addition of serotonin and the SRIs clomipramine, fluoxetine and imipramine (1 nM-10 microM) on the tension induced by the alpha(1)-adrenoceptor agonist NE (10 microM) of SV strip preparations were studied using the organ bath technique. Cyclic AMP and cyclic GMP were measured by means of specific radioimmunoassays.

anafranil 30 mg 2016-12-05

Exercise exerts antidepressant effects in humans and rodent models of affective disorders. These effects may be mediated by the upregulation of endogenous factors that exert antidepressant actions. The physiological functions and behavioral actions of the neuropeptide galanin (GAL) suggest antidepressant activity. Previous studies have shown that various modes of exercise elevate GAL gene expression in the locus coeruleus (LC) in rats. The present experiments examined the interaction between voluntary exercise and antidepressant pharmacotherapy. Male Sprague-Dawley rats were provided access to buy anafranil online activity wheels (exercise condition) or inoperative wheels (sedentary condition) for 28 days. Rats in each group were injected with clomipramine (10mg/kg/day) or vehicle throughout this period (for 3 weeks). Prepro-GAL mRNA in the LC was measured by in situ hybridization histochemistry. Exercise and clomipramine treatment significantly elevated GAL gene expression, though prepro-GAL mRNA levels in rats receiving both interventions did not differ from sedentary controls that received vehicle. Prepro-GAL mRNA levels were significantly correlated with running distance. The results further implicate a role for GAL in the antidepressant effects of exercise and pharmacotherapy, though the mechanisms through which these treatments influence GAL gene expression appear to differ significantly.

anafranil drug class 2017-11-16

The recommended starting buy anafranil online dosage of mirtazapine is 15 mg/day for 4 days, then 30 mg/day for 10 days. If effective, the drug should be continued unchanged at this dosage or, in patients assessed as insufficiently improved, the daily dosage may be further increased to 45 mg/day. In patients with hepatic or renal insufficiency, careful dosage titration as well as regular and close monitoring for adverse events is recommended. Concomitant use of mirtazapine and diazepam or alcohol (ethanol) may also impair cognitive and/or motor performance.

anafranil medication 2017-04-21

Paroxetine is a potent and selective inhibitor of the neuronal reuptake of serotonin, thereby facilitating serotoninergic transmission; this action appears to account for the antidepressant activity observed with this drug. A mean terminal elimination half-life of approximately 24 hours permits once daily administration. Results of short term clinical trials have shown paroxetine to be significantly superior to placebo, and comparable to amitriptyline, clomipramine, imipramine, dothiepin and mianserin in relieving symptoms associated with major depressive disorders. Paroxetine has shown some preliminary promise in the treatment of depressive illness resistant to tricyclic antidepressant therapy but further studies are required before any conclusions can be drawn. Paroxetine in therapeutic doses has been very well tolerated, and the favourable tolerability profile of this agent appears to be its primary advantage over traditional antidepressant agents. Paroxetine causes minimal anticholinergic-type adverse effects, and unlike tricyclic antidepressants, it does not precipitate cardiovascular effects or provoke cardiac conduction disturbances. Nausea has been the most frequently reported adverse event during short term use of paroxetine, but it is generally mild and transient and subsides with continued use. With longer term use headache, sweating and constipation were the most frequently reported side effects but the incidence rate was not significantly different from that noted for comparator antidepressants. Furthermore, the frequency of withdrawal due to adverse effects is less with buy anafranil online paroxetine than with tricyclic antidepressant agents. Overall, available data appear to indicate that while the efficacy of paroxetine is similar to that of traditional antidepressant drugs, the newer agent possesses much improved tolerability. In addition, the wide therapeutic index of paroxetine may be beneficial when treating patients with an increased risk of suicide. Thus, paroxetine clearly looks to become a valuable addition to the range of drugs currently available to treat depressive illness. Future research may help to further define the relative place of this newer agent in antidepressant therapy and determine how its overall therapeutic efficacy compares with that of other related antidepressant agents such as fluoxetine.

anafranil 225 mg 2017-11-24

The Roman low- (RLA) and high-avoidance (RHA) rats were selectively bred for, respectively, poor versus rapid acquisition of active avoidance in a shuttle box and, under aversive conditions, display reactive (RLA) versus proactive (RHA) coping behaviors. In the forced swim test (FST), RLA rats exhibit a depression-like behavior characterized by greater immobility and fewer climbing counts when compared with their RHA counterparts. Furthermore, subacute buy anafranil online treatments with clinically effective antidepressant drugs decrease immobility and increase climbing or swimming in RLA rats but do not modify the performance of RHA rats.

anafranil 25mg tablets 2016-01-24

Despite the effectiveness of clomipramine and selective serotonin reuptake inhibitors (SSRIs) in the treatment of obsessive-compulsive disorder (OCD), 40% to 60% of patients who receive an adequate treatment with these agents have significant persisting symptoms. Newer atypical antipsychotic drugs showed efficacy as augmenting agents in patients with OCD resistant to serotonin reuptake inhibitors (SRIs). The objective of this study was to evaluate the efficacy and safety of amisulpiride augmentation in treatment resistant OCD. A total of 20 patients diagnosed with OCD according to DSM-IV criteria and having a history of resistance to buy anafranil online treatment with SRIs were included in the study. Amisulpiride 200 mg/day was added to ongoing SRI treatment and titrated up to 600 mg/day in flexible doses. The mean amisulpiride dose was 325 +/- 106 mg/day. The patients were assessed with the Yale-Brown obsessive-compulsive scale (Y-BOCS) at baseline and at week 12 of amisulpiride treatment. Side effects were monitored by the UKU side effect rating scale. The reduction in Y-BOCS scores between the baseline (26.7 +/- 6.3) and the end of the treatment (12.5 +/- 2.8) was statistically significant (p=0.0001). The most commonly observed side effects included weight gain (14 patients, 70%), mild sedation (13 patients, 65%) and asthenia (7 patients, 35%). This study has several limitations and, hence, the results are preliminary and require confirmation in a randomized controlled trial. In conclusion, this study suggests that amisulpiride may be a promising option as an augmentation strategy in treatment resistant OCD.

anafranil ocd dosage 2017-09-19

A 29-year-old man was admitted to hospital, unconscious and with extensive bleedings in skin and muscles. For many weeks he had been practically starving himself with suicidal intent. Physical examination revealed signs of anaemia and gingivitis with hypertrophy of the tooth borders and bleeding gums, as well as bright blood on rectal examination. There were extensive ecchymoses and petechiae, especially in the legs. Some of the body hair was corkscrew-curly. Haemoglobin level was 7.2 g/dl, mean corpuscular volume 93 fl, reticulocyte count 29/1000. The Rumpel-Leede test was abnormal (60 petechiae/4 cm2), as were the vitamin C level (0.026 mg/dl whole blood) and the ascorbic acid tolerance test. As these findings indicated scurvy, vitamin C was administered, 1 g daily intravenously for 5 days, followed by 500 mg daily by mouth. Remarkable improvement was apparent as early as 72 hours after onset of treatment. The endogenous depression, the underlying cause of the suicide attempt, was treated with clomipramine. When the patient was discharged after 13 days his physical and mental state was buy anafranil online much improved.

anafranil brand names 2017-03-13

These findings buy anafranil online suggest that in addition to tricyclics, some relatively novel antidepressants such as mirtazapine can induce voiding impairment, attributed to diminished UBSM contractility from the inhibition of muscarinic receptors in the UBSM.

anafranil dosage 2015-07-23

The effect of the i.c.v. administration of pertussis toxin (PTX) and antisense oligodeoxynucleotides directed against the alpha subunit of different Gi-proteins (anti-Gi alpha(1), anti-Gi alpha(2), anti-Gi alpha(3), anti-Go alpha(1), anti-Go alpha(2)) on the antidepressant-like effect induced by amitriptyline and clomipramine, was evaluated in the mouse forced swimming test, an animal model of depression. The administration of amitriptyline (15 mg kg(-1) s.c.) and clomipramine (25 mg kg(-1) s.c.) produced an increase in the mobility time that was prevented by PTX (0.25 micro g per mouse i.c.v.), administered 11 days before the mouse forced swimming test. Anti-Gi alpha(1) (12.5 micro g per mouse i.c.v.), anti-Gi alpha(2) (12.5 micro g per mouse i.c.v.), anti-Gi alpha(3) (6.25 micro g per mouse i.c.v.), and anti-Go alpha(1) (6.25 micro g per mouse i.c.v.), administered 24 and 18 h before the training session, prevented the amitriptyline and clomipramine increase of the mobility time. By contrast, pretreatment with anti-Go alpha(2) (1.56- buy anafranil online 12.5 micro g per mouse i.c.v.) never modified the antidepressant-like effect induced by the two investigated compounds. At the highest effective doses, none of the compounds used impaired motor coordination, as revealed by the rota-rod test, nor modified spontaneous motility and inspection activity, as revealed by the hole-board test. These results suggest the important role played by Gi(1), Gi(2), Gi(3), and Go(1) protein subtypes and the lack of involvement by Go(2) protein subtype in the transduction mechanism responsible for the antidepressant-like effect produced by amitriptyline and clomipramine.

anafranil 35 mg 2016-09-15

The aim of this study was to evaluate the effectiveness of the addition of manual-based cognitive-behavioral therapy to a medication regimen of clomipramine and fluoxetine and the withdrawal of medication during cognitive-behavioral therapy. The participant was an 11-year-old girl with symptoms of obsessive thoughts about germs and illness and buy anafranil online handwashing compulsions. The addition of cognitive-behavioral therapy reduced the participant's daily number of obsessions and avoidance behaviors after three sessions. When medication was tapered during the cognitive-behavioral therapy program, the participant's symptoms continued to decline, and after treatment, she no longer met diagnostic criteria for obsessive-compulsive disorder. Impressively, the participant remained medication free and treatment gains were maintained at 4 months' follow-up.

anafranil 25 mg 2016-09-19

A significant diurnal rhythm in heart rate Norvasc Starting Dose was detected; minimum values were recorded at night. Administration of 20 mg of clomipramine/kg induced a significant reduction in heart rate, with peak effect achieved approximately 12 hours after dosing. Administration of 4 or 12 mg of clomipramine/kg did not result in significant changes in heart rate. Sinoatrial and second-degree atrioventricular block and ventricular escape beats were observed during periods of slow heart rate in more dogs that received clomipramine (3 to 4 of 8 dogs), compared with dogs that received placebo (1 to 2 of 8 dogs), but this difference was not significant.

anafranil drug 2016-05-17

Tricyclic antidepressants (TCAs) are widely used in treating depressive disorders. It has been demonstrated that, for instance, IL-1 beta and IL-6 inhibit the HPA axis, which plays a role in the development of depressions. Therefore. we were interested in investigating how TCAs influence cytokine release by T lymphocytes and monocytes respectively. Cells were incubated with either 5 microM clomipramine, 15 microM imipramine or 20 microM citalopram. IL-2 release was suppressed to 60% of the control values by clomipramine and imipramine (p = 0.001; p = 0.000), but citalopram was found to cause a much weaker inhibition (only 18%) (p = 0.16). INF-gamma release was affected to a lower degree than IL Combivir Drug -2 release, and imipramine (34%) (p = 0.054) was more potent than clomipramine (24%) (p = 0.16) and citalopram (12%) (p = 0.059) in this case. Monocytes incubated with TCA for 4 h exhibited only limited inhibition of IL-1 beta and IL-6 release, i.e., 6-25% for all three compounds. The corresponding value for TNF-alpha release was 20-45% inhibition, with citalopram being the weakest inhibitor. After 10 h of monocytes to LPS exposure, all three compounds exerted a strong inhibition of IL-1 beta and TNF-alpha release, i.e., 60-70% with p-values below 0.012 for all of them. However the inhibition of IL-6 release was less than 35%. Citalopram was equality as potent as imipramine and clomipramine in inhibiting IL-6 release after long-term exposure of monocytes to LPS. All three TCAs elevated intracellular cAMP concentrations significantly in T lymphocytes and monocytes (p < 0.001).

anafranil drug insert 2017-04-29

As of 1989, the psychotropic drugs that Anafranil Dosage Range have been reported to inhibit female orgasm include antipsychotic agents (thioridazine, trifluoperazine and fluphenazine), the combination drug perphenazine/amitriptyline, antidepressants (phenelzine, isocarboxazid, tranylcypromine, amoxapine, clomipramine, imipramine, nortriptyline and desipramine) and anxiolytic agents (diazepam, flurazepam and alprazolam). The management of psychotropic-drug-induced female anorgasmia includes discontinuation of the offending drug, reduction of the dosage level, a wait for spontaneous remission while the patient remains on the agent and substitution of another medication. The use of bethanechol chloride and cyproheptadine has been successful in resolving anorgasmia while patients continue to receive antidepressants.

anafranil 10mg dosage 2016-02-02

We have reviewed literatures about neurobiological aspect of mood disorders in the light of abnormalities of REM sleep. A shortened REM latency is a consistent finding in depressed patients and may be considered a biological marker for depression. Most depressed patients with shortened REM latency also show non-suppression on dexamethasone-suppression test (DST). The commonly used antidepressant drugs cause a significant reduction in REM sleep. Patients with abnormal DST show a better response to sleep deprivation than those with normal DST. Recent studies indicated that borderline patients, primary dysthymic patients and obsessive-compulsive Geodon User Reviews patients (OCD) have shortened REM latency. Farthermore, patients with OCD have a fairly good response to antidepressant clomipramine. Diagnostic and therapeutic strategies can conceivably be related on the examination of sleep patterns of psychiatric patients.

anafranil user review 2016-06-07

Clomipramine, by acutely elevating synaptic monoamine levels, could exacerbate Omnicef Dosage Chart absence seizures.

anafranil dosage information 2017-09-18

Overweight and obesity are common in patients with bipolar disorder. Rates of up to 70% are described in scientific publications. There is sufficient evidence that these conditions are Reglan Dosage associated with a worse course of the disease (more episodes, higher suicide and hospitality rates, worse response to lithium, somatic comorbidities). Most of the mood stabilisers lead to weight gain. This is also true for clozapine, which can be effective in therapy-refractory courses of bipolar disorder. This case report demonstrates the complexity of the treatment of bipolar disorder. A young patient in depressive stupor following a severe suicide attempt after 5 months of hospital treatment was sent to our department to perform ECT. This was not possible because of the severity of his injuries. We were able to cure the acute condition and interrupt the course of rapid cycling with a combination of clomipramine, lithium and clozapine. A stable course of four years under this medication and psychoeducation has been achieved. In this period the patient was able to lower his body mass index from 38 to 26 because of a consequent lifestyle modification.

anafranil pill 2016-10-23

Mazindol, a new anorexiant, was administered at a daily dose of 0.5-4 mg to 10 narcoleptic subjects aged 21-63 years. All the patients suffered from sleep attacks and one or more of the REM-related symptoms. Eight patients received only mazindol, and two patients received mazindol simultaneously with clomipramine or flurazepam. Sleep attacks were reduced in nine patients, and cataplexy was also markedly reduced in four patients. Mild adverse reactions were reported in six Flagyl Buy patients: two patients complained of headache, four of nocturnal sleep disturbance, and two of reduced appetite. Most side effects disappeared spontaneously or after dose reduction, and none of the patients had to stop medication. The results suggest that mazindol is effective not only for sleep attacks but also for cataplexy. It is recommended as a treatment for mild cases of narcolepsy.

anafranil 45 mg 2017-06-28

A case of narcolepsy with marked cataplexy is described Protonix Neonatal Dosing in detail. Clomipramine hydrochloride effectively controlled the cataplexy and partially alleviated the daytime sleep attacks. However, clomipramine treatment resulted in episodes of severe motor hyperactivity during sleep, which were most intense during rapid eye movement sleep.

anafranil 60 mg 2016-10-26

Improvement Prandin Generic Form in depression after total sleep deprivation (TSD) is, as a rule, followed by relapse after subsequent ad libitum sleep. This study is addressed to the question of how nocturnal partial sleep following TSD affects this relapse. Thirty endogenously depressed patients participated in the study. During the night after TSD, subjects were allowed sleep during one of three periods, i.e., unlimited sleep (11:00 p.m.-8:00 a.m.), early partial sleep (11:00 p.m.-3:00 a.m.), or late partial sleep (4:00 a.m.-8:00 a.m.). The hypothesis that partial sleep deprivation on the night following TSD prevents relapse has to be rejected. Relapse was inversely related to a drop in minimum rectal temperature during the night with unlimited or partial sleep, compared with minimum rectal temperature on the previous night.

anafranil generic name 2015-11-07

The goal of the study was to provide a quantitative analysis of the relative efficacy of all five currently available serotonin reuptake inhibitors (SRIs) and behavior therapy [exposure and response prevention (ERP)] for obsessive compulsive disorder. The relationship between effect size and methodological characteristics was also empirically examined. A search was conducted of several computerized databases covering the dates from 1973 to 1997. Seventy-seven studies were identified, yielding 106 treatment comparisons involving 4641 patients. Effect sizes were analyzed between individual interventions and between intervention class [SRI, ERP or the combined treatment of an SRI with ERP(ERP/SRI)]. Data were analyzed both before and after controlling for methodological variables. The effect size for clomipramine (CMI) was significantly greater than the other SRIs, with the exception of fluoxetine (FLX). CMI was not significantly greater than ERP or ERP/SRI. As a class, ERP was significantly greater than SRIs as a whole. Effect sizes were larger for studies without a control group or random assignment, for self-reported outcome measures, and varied significantly by method of effect size calculation. Year of publication was significantly related to effect size. When controlling for these methodological variables, CMI was not significantly greater than FLX or fluvoxamine (FLV), and ERP was no longer significantly greater than the SRIs as a whole. No significant difference was found between CMI and the other SRIs as a group in head to head trials. Imitrex Dosage Oral No differences in drop-out rates were found. CMI stands out from the other SRIs. This difference is probably not clinically significant enough to warrant first choice treatment, given CMI's greater lethality in overdose. The choice between an SRI or ERP is dominated primarily by the infrequent availability of ERP and to a lesser degree by personal preference. Methodological differences significantly impact effect size.

anafranil pills 2017-06-25

In this systematic review and network meta-analysis, we searched the two controlled trials registers maintained by the Cochrane Collaboration Common Mental Disorders group for trials published up to Feb 16, 2016. We selected randomised controlled trials in which an active psychotherapeutic or pharmacological intervention had been used in adults with obsessive-compulsive disorder. We allowed all comorbidities except for schizophrenia or bipolar disorder. We excluded studies that focused exclusively on treatment-resistant patient populations defined within the same study. We extracted Buy Cleocin Cream data from published reports. The primary outcome was symptom severity as measured by the Yale-Brown Obsessive Compulsive Scale. We report mean differences with 95% credible intervals compared with placebo. This study is registered with PROSPERO, number CRD42012002441.

anafranil patient reviews 2015-10-12

The antinociceptive activities of clomipramine and pethidine alone and in combination were investigated in Swiss albino mice using the formalin test. Normal saline was employed as the control. Ten animals were used in each experiment.

anafranil drug classification 2015-03-21

Demonstration of the efficacy of serotonin (5-hydroxytryptamine; 5-HT) reuptake inhibitors such as clomipramine in the treatment of obsessive compulsive disorder has fueled interest in the neurobiological basis of this illness. Results of treatment studies, investigations of biological markers, and pharmacologic challenges are reviewed and implications for a 5-HT theory of obsessive compulsive disorder discussed. While the nature of the dysregulation in serotonin transmission that may attend obsessive compulsive disorder has yet to be fully elucidated, evidence accumulates that 5-HT function in part modulates obsessive compulsive symptoms. Development of more specific probes and new brain imaging techniques will further enhance understanding of the pathophysiology of obsessive compulsive disorder.