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Tofranil (Imipramine)

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Generic Tofranil is a member of the family of drugs called tricyclic antidepressants. Generic Tofranil is used to treat depression. Generic Tofranil is also used on a short-term basis, along with behavioral therapies, to treat bed-wetting in children aged 6 and older. Sometimes Generic Tofranil is prescribed to treat bulimia, attention deficit disorder in children, obsessive-compulsive disorder and panic disorder.

Other names for this medication:

Similar Products:
Pamelor, Norpramin, Silenor, Zonalon, Aventyl, Norpress, Elavil


Also known as:  Imipramine.


Generic Tofranil is used to treat depression. Generic Tofranil is also used on a short-term basis, along with behavioral therapies, to treat bed-wetting in children aged 6 and older. Sometimes Generic Tofranil is prescribed to treat bulimia, attention deficit disorder in children, obsessive-compulsive disorder and panic disorder.

Generic Tofranil is a member of the family of drugs called tricyclic antidepressants.

Tofranil is also known as Imipramine, Antideprin, Deprenil, Deprimin, Deprinol, Depsonil, Dynaprin, Eupramin, Imipramil, Irmin, Janimine, Melipramin, Surplix, Antidep, Apo-Imipramine, Chrytemin, Daypress, Depsol, Ethipramine, Fronil, Imidol, Imimine, Imine, Imiprex, Imiprin, Impril, Medipramine, Melipramine, Mipralin, Novopramine, Primonil, Pryleugan, Sermonil, Sipramine, Talpramin, Tofnil, Tofranil-PM, Venefon.

Generic name of Generic Tofranil is Imipramine hydrochloride.

Brand names of Generic Tofranil are Tofranil, Tofranil-PM.


Take Generic Tofranil orally.

Take Generic Tofranil with or without food.

For adults

The usual starting dose is 75 mg a day. The maximum daily dose is 200 mg.

For children

Total daily dosages for children should not exceed 2.5 mg for each 2.2 pounds of the child's weight. Doses usually begin at 25 mg per day. This amount should be taken an hour before bedtime. If needed, this dose may be increased after 1 week to 50 mg (ages 6 through 11) or 75 mg (ages 12 and up), taken in one dose at bedtime or divided into 2 doses, 1 taken at mid-afternoon and 1 at bedtime.

Aged people

The usual dosage should start with 25 to 50 mg per day. The dose may be increased as necessary, but effective dosages usually do not exceed 100 mg a day.

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


If you overdose Generic Tofranil and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Tofranil overdosage: agitation, bluish skin, convulsions, difficulty breathing, dilated pupils, drowsiness, heart failure, high fever, involuntary writhing or jerky movements, irregular or rapid heartbeat, lack of coordination, low blood pressure, overactive reflexes, restlessness, rigid muscles, shock, stupor, sweating, vomiting.


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 Tofranil 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 Tofranil if you are allergic to Generic Tofranil components.

Be very careful with Generic Tofranil if you are pregnant, planning to become pregnant, or are breast-feeding.

Do not take Generic Tofranil if you are recovering from a recent heart attack or take MAO inhibitors, such as the antidepressants Nardil and Parnate.

Be very careful with Generic Tofranil if you have diabetes, hypoglycemia, a history of mental disorders.

Be very careful with Generic Tofranil if you are taking albuterol (Proventil, Ventolin), antidepressants that act on serotonin, including Prozac, Paxil and Zoloft, antipsychotic drugs such as Mellaril and chlorpromazine, barbiturates such as Nembutal and Seconal, blood pressure medications such as Catapres, Carbamazepine (Tegretol), cimetidine (Tagamet), decongestants such as Sudafed, drugs that control spasms, such as Cogentin, Epinephrine (EpiPen), Flecainide (Tambocor), Guanethidine, Methylphenidate (Ritalin), Norepinephrine, other antidepressants such as Elavil and Pamelor, Phenytoin (Dilantin), Propafenone (Rythmol), Quinidine, thyroid medications such as Synthroid, tranquilizers and sleep aids such as Halcion, Xanax, and Valium.

Avoid alcohol.

Do not participate in any activities that require full alertness if you are unsure about your ability.

Try to stay out of the sun as much as possible.

It can be dangerous to stop Generic Tofranil taking suddenly.

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These results suggest that the automated analysis system of forced swimming of mice using MicroAct can be used as a high-throughput method to examine antidepressive activity of a compound with objectivity and reliability.

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Chinese herbal products including SHs and HFs are prescribed for patients with sleep disorder and MDD. However, the efficacy and safety of CHPs for sleep disorder and MDD need to be further evaluated.

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Both preclinical and clinical evidence support the usefulness of antidepressants in chronic pain treatment. Monoamine uptake inhibitors influence the neurotransmissions of noradrenaline (NA) and/or serotonin (5-HT); their effect on nociception is thought to take place predominantly within the spinal cord. Antidepressant drugs seem to differ in their properties as analgesics and as thymoleptics. The present work is aimed at correlating the special mechanism of action of antidepressants in diminishing nocicepetion with the pharmacological profile of these drugs in clinical pain treatment. From a preclinical, experimental point of view, it can be expected, that mixed type uptake blockers should be superior to selective NA or 5-HT uptake inhibitors. The analgesic profile of antidepressants was established by a metaanalysis of clinical trials on the effect of these drugs, given alone or in combination with other analgetics, in chronic pain syndromes. 57 Clinical trials were separated into 5 groups according to their scientific quality: [1] placebo-controlled double-blind studies with high power; [2] placebo-controlled double-blind studies with low power; [3-4] open controlled studies or studies with historical controls; [5] case reports. A study was positive if the tested antidepressant was more effective than placebo or the compared drug or seemed beneficial with respect to the interval of its previous absence. The most effective antidepressants in chronic pain treatment only included unselective monoamine reuptake inhibitors in the following rank order: amitriptyline > clomipramine > or = desipramine > or = imipramine > or = doxepin. A statement about the appropriate dosage of these drugs in chronic pain treatment, however, must wait for properly conducted dose finding studies which include the measurement of plasma concentrations.

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To study the regulatory mechanisms of intracellular Mg(2+) concentration ([Mg(2+)](i)) in renal tubular cells as well as in other cell types, we established a mutant strain of mouse renal cortical tubular cells that can grow in culture media with very high extracellular Mg(2+) concentrations ([Mg(2+)](o) > 100 mM: 101Mg-tolerant cells). [Mg(2+)](i) was measured with a fluorescent indicator furaptra (mag-fura 2) in wild-type and 101Mg-tolerant cells. The average level of [Mg(2+)](i) in the 101Mg-tolerant cells was kept lower than that in the wild-type cells either at 51 mM or 1 mM [Mg(2+)](o). When [Mg(2+)](o) was lowered from 51 to 1 mM, the decrease in [Mg(2+)](i) was significantly faster in the 101Mg-tolerant cells than in the wild-type cells. These differences between the 101Mg-tolerant cells and the wild-type cells were abolished in the absence of extracellular Na(+) or in the presence of imipramine, a known inhibitor of Na(+)/Mg(2+) exchange. We conclude that Na(+)-dependent Mg(2+) transport activity is enhanced in the 101Mg-tolerant cells. The enhanced Mg(2+) extrusion may prevent [Mg(2+)](i) increase to higher levels and may be responsible for the Mg(2+) tolerance.

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There at least two reasons to believe antidepressants might help in smoking cessation. Depression may be a symptom of nicotine withdrawal, and smoking cessation sometimes precipitates depression. In some individuals, nicotine may have antidepressant effects that maintain smoking. Antidepressants may substitute for this effect.

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Among study completers, 31 (39%) had AIDS. The response rate to imipramine was 74% and the response rate to placebo was 26%. There was no difference in depression response between patients with more or less severe immunodeficiency, nor was there a difference in medication dose or side effects. Neither type nor duration of treatment influenced CD4 cell count during the course of treatment.

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The antidepressant efficacy and safety of venlafaxine was shown previously in 6-week, placebo-controlled trials. We evaluated the long-term safety and clinical acceptability of venlafaxine and imipramine in a double-blind, parallel-group, comparative study. Two hundred ninety depressed outpatients were treated with venlafaxine, and an additional 91 received imipramine for as long as clinically necessary, up to 1 year. The total daily dose of each drug could vary from 75 to 225 mg. The Clinical Global Impressions Scale and a therapeutic response rate that was based on Clinical Global Impressions Scale-Improvement and incorporated discontinuation information were used to evaluate efficacy. Safety determinations and patient subjective ratings were used to evaluate safety and clinical acceptability. During the study, the adverse events were generally mild to moderate and most subsided with continued treatment; the most frequent were nausea for venlafaxine and dry mouth for imipramine. The anticholinergic side effect burden was significantly higher in the imipramine group than in the venlafaxine group. Venlafaxine was judged significantly more acceptable than imipramine, on the basis of the subjective ratings by patients. Fewer venlafaxine-treated patients than imipramine-treated patients withdrew because of adverse events and unsatisfactory response. There was a consistent trend in the therapeutic response rates in favor of venlafaxine that reached statistical significance at months 2, 6, and 12. In this long-term study, patient acceptability was greater for venlafaxine than for imipramine, suggesting therapeutic advantages for venlafaxine in the long-term treatment of depression. Additional studies with other active comparators are underway to confirm and extend these encouraging results.

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This report deals with a series of experimental approaches carried out in clinical studies to attempt to examine the role of amines in relationship to affective state and the mode of action of thymoleptic agents. Attempts have been made to examine enzymes, amines and other metabolites in biological fluids to assess the role of catecholamines and indoleamines in these disorders. Synthesis inhibitors were employed in studies where antidepressant drug-induced remission was initiated and the effect of two inhibitors was assessed on the clinical state. The results are presented and discussed in regard to the significance of the role of serotonin in depressive states and the action of thymoleptic agents.

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This article reviews the available data on social functioning in depression and provides clinical guidelines and opinion on this important and expanding field.

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We found 19 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.

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One patient died of a massive pulmonary embolism postoperatively. Followup ranged from 6 to 36 months (mean 19.2 +/- 7.0). During the observation period 6 patients died of local recurrence and/or distant metastasis within 8 months. Of the patients 57 are currently evaluable. All patients are continent during the day with an emptying frequency of 2 to 4 times. Nocturnal enuresis was observed in 4 children who responded favorably to imipramine hydrochloride therapy. Upper urinary tract function was maintained or improved in 95% of the patients. No clinical evidence of acidosis was observed, since all patients were kept on prophylactic oral alkalization.

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In this study, the effect of imipramine on morphine antinociception in tolerant and non-tolerant mice in the formalin test, was investigated. Subcutaneous administration of different test doses of morphine (3, 6 and 9 mg/kg) and intraperitoneal injection of test doses of imipramine (10, 20 and 40 mg/kg) induced a dose-dependent antinociception in non-tolerant mice, both in the first and second phases of the formalin test. The combination of morphine (1 mg/kg) with imipramine (10 mg/kg) showed a potentiated response in the second phase of the test. Combination of a single dose of morphine (1.5 mg/kg) with lower doses of imipramine (2, 4 and 8 mg/kg) did not show potentiation. The antinociceptive response of either morphine or morphine plus imipramine was reduced by the opioid receptor antagonist naloxone (2 mg/ kg). In order to induce tolerance, mice were treated subcutaneously with morphine (50 mg/kg) once daily for 3 days. On day 4, the antinociceptive effect of test doses of morphine or imipramine were assessed. Tolerance to the responses of test doses of morphine (3, 6 and 9 mg/kg), but not imipramine (10, 20 and 40 mg/kg) in both phases of the test was observed. Administration of lower dose of imipramine (4 mg/kg) before the test doses of morphine (3, 6 and 9 mg/kg) was not able to alter the expression of morphine tolerance. When imipramine was used during development of tolerance, either on days 1 and 2 or on days 2 and 3, the morphine tolerance in the second phase of the test was reduced. It is concluded that opioid receptor mechanism(s) may mediate the antidepressant-induced antinociception, however, imipramine may be useful in inhibiting morphine tolerance.

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Moclobemide is an effective antidepressant and is better tolerated than imipramine.

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[3H]Imipramine binding sites are located on serotonergic nerve terminals and on blood platelets. Previous studies on our laboratories have indicated temperature-sensitive conformational changes in [3H]imipramine binding sites in hippocampal and cerebral cortex membranes. We now report that similar changes are observed in both membrane-bound and digitonin-solubilized [3H]imipramine binding sites of human blood platelets. This may indicate integrity of the solubilized binding site.

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In a double blind trial in 88 patients, 71 of whom were included in the fin al evaluation, viloxazine (Vivalan ICI) showed an effectiveness corresponding to imipramine. Both antidepressives show properties for lysis of depression and improvement of mood, the target symptom is vitally depressive disturbance of mood. There was clear improvement of depression, anxieties, restlessness, loss of initiative and activity as well as pain syndromes in psychosomatic disorders. In cases of psychomotor inhibition viloxazine was superior to the older drug. Effectiveness of viloxazine commenced rapidly as demonstrated by control assessment after 10-14 days. Results improved further in a second equally long treatment period. Tolerance of viloxazine was superior to imipramine.

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The literature dealing with the convulsant effects of the antidepressant drugs of the non-monoamine oxidase inhibitor variety is reviews. It is concluded that most of these drugs do lower the seizure threshold and may precipitate seizures even at normal therapeutic doses. The pathophysiology of antidepressant-induced seizures is discussed, and attention is drawn to biochemical differences in those antideprssants that have the least epileptogenic potential or may even be anticonvulsant. The clinical difficulties regarding administration of antidepressant drugs to epileptic patients are mentioned, and some practical advice is offered.

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The electroencephalographic (EEG) and cardiovascular effects of milnaciplan hydrochloride (TN-912) were compared with those of imipramine (IMP) and maprotiline (MPT) in rats, guinea pigs and dogs. In conscious rats with chronic electrode implants, TN-912 (10-100 mg/kg, p.o.) had little effect on either the EEG activity or the EEG arousal response to auditory stimulation (2000 Hz). Both IMP (10-100 mg/kg, p.o.) and MPT (10-100 mg/kg, p.o.) tended to increase the drowsy EEG pattern period in the cortical and hippocampal EEG and inhibited the EEG arousal response to auditory stimulation. In conscious rats with a chronic arterial catheter, TN-912 (100 mg/kg, p.o.) slightly elevated the mean blood pressure (MBP) and decreased the heart rate (HR), while both IMP (10-100 mg/kg, p.o.) and MPT (10-100 mg/kg, p.o.) dose-dependently increased MBP and HR. In anesthetized dogs, i.v. injection of TN-912 (1-10 mg/kg), IMP (0.3-10 mg/kg) and MPT (1-20 mg/kg) produced a dose-dependent fall in MBP. IMP and MPT but not TN-912 dose-dependently increased HR. TN-912 did not show typical effects on femoral blood flow. TN-912 (30 mg/kg) had little effect on lead II electrocardiogram (ECG), while IMP and MPT markedly increased height of the T-wave on ECG. In the in vitro study with the isolated guinea pig atrium, TN-912 caused a slight positive inotropic and negative chronotropic effect, while both IMP and MPT showed marked negative inotropic and chronotropic actions. These results suggest that TN-912 has less EEG effect and cardiac toxicity, indicating that TN-912 may be safe in clinical use.

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After a 7- to 14-day screening period, 275 adolescents with major depression began 8 weeks of double-blind paroxetine (20-40 mg), imipramine (gradual upward titration to 200-300 mg), or placebo. The two primary outcome measures were endpoint response (Hamilton Rating Scale for Depression [HAM-D] score < or = 8 or > or = 50% reduction in baseline HAM-D) and change from baseline HAM-D score. Other depression-related variables were (1) HAM-D depressed mood item; (2) depression item of the Schedule for Affective Disorders and Schizophrenia for Adolescents-Lifetime version (K-SADS-L); (3) Clinical Global Impression (CGI) improvement scores of 1 or 2; (4) nine-item depression subscale of K-SADS-L; and (5) mean CGI improvement scores.

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A dynamic 23Na nuclear magnetic resonance (NMR) technique was applied to the exchange system of Na+ ions present inside and outside large unilamellar vesicles at an equivalent concentration. Addition of melittin to phosphatidylcholine vesicles did not induce any detectable Na+ transport across the membrane but subsequent addition of a trace of chlorpromazine or imipramine did induce Na+ transport. Because the formation of a drug-melittin adduct in a solution was detected by 1H NMR, the activation of melittin channels was assumed to originate from the direct interaction of the drug and melittin.

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Primary care physicians must initiate a discussion of overactive bladder and urinary incontinence with their patients who are at risk. A stepwise approach to evaluation and diagnosis and the use of systematic evaluation and treatment algorithms suitable to the primary care setting will improve identification and effective management of the incontinent patient.

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Depression is associated with vascular disease, such as myocardial infarction and stroke. Pharmacological treatments may contribute to this association. On the other hand, Mg(2+) deficiency is also known to be a risk factor for the same category of diseases. In the present study, we examined the effect of imipramine on Mg(2+) homeostasis in vascular smooth muscle, especially via melastatin-type transient receptor potential (TRPM)-like Mg(2+) -permeable channels. The intracellular free Mg(2+) concentration ([Mg(2+) ](i) ) was measured using (31) P-nuclear magnetic resonance (NMR) in porcine carotid arteries that express both TRPM6 and TRPM7, the latter being predominant. pH(i) and intracellular phosphorus compounds were simultaneously monitored. To rule out Na(+) -dependent Mg(2+) transport, and to facilitate the activity of Mg(2+) -permeable channels, experiments were carried out in the absence of Na(+) and Ca(2+) . Changing the extracellular Mg(2+) concentration to 0 and 6 mM significantly decreased and increased [Mg(2+) ](i) , respectively, in a time-dependent manner. Imipramine statistically significantly attenuated both of the bi-directional [Mg(2+) ](i) changes under the Na(+) - and Ca(2+) -free conditions. This inhibitory effect was comparable in influx, and much more potent in efflux to that of 2-aminoethoxydiphenyl borate, a well-known blocker of TRPM7, a channel that plays a major role in cellular Mg(2+) homeostasis. Neither [ATP](i) nor pH(i) correlated with changes in [Mg(2+) ](i) . The results indicate that imipramine suppresses Mg(2+) -permeable channels presumably through a direct effect on the channel domain. This inhibitory effect appears to contribute, at least partially, to the link between antidepressants and the risk of vascular diseases.

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The present study was designed to get further insight into the mode of antidepressant action of extracts prepared from St. John's wort (SJW) and relevant active constituents. Down-regulation of central beta-adrenergic receptors (beta-AR's) has been widely considered a common biochemical marker of antidepressant efficacy. Although previous studies have reported a beta-AR down-regulation for SJW extracts, in vivo studies that compare the effects of SJW extracts with those of relevant active constituents on beta-AR density have not been done yet. We used quantitative radioligand receptor-binding-studies to examine in rats the effects of short-term (2 wks) and long-term (8 wks) administration of different SJW extracts and constituents on beta-AR binding in rat frontal cortex. The effects were compared to those of the standard antidepressants imipramine and fluoxetine. [125I]CYP binding to beta-AR was found to be decreased after short as well as after long-term treatment with imipramine (36%, 40%). Short-term treatment with fluoxetine decreased the number of beta-adrenergic receptors (17%) while long-term treatment with fluoxetine elicited an increase (14%) in beta-AR-binding. This effect was comparable to that of the lipophilic CO2 extract which decreased beta-AR-binding (13%) after two weeks and slightly increased the number of beta-AR's after 8 weeks (9%). Short-term treatment with the methanolic SJW extract decreased beta-AR-binding (14%), no effects for this extract were observed after 8 weeks. Treatment with hypericin led to a significant down-regulation (13%) of beta-AR's in the frontal cortex after 8-weeks, but not after 2 weeks, while hyperforin (used as trimethoxybenzoate, TMB), and hyperoside were ineffective in both treatment paradigms. Compared to the SJW extracts and single compounds the effect of imipramine on beta-AR-binding was more pronounced in both treatment paradigms.

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We reviewed literature regarding the use of TCAs and SSRIs in depressed patients with comorbid anxiety.

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Unsatisfactory clinical efficacy and a variety of adverse effects of current antidepressant drugs have incited search for better therapy. Zinc, an antagonist of the glutamate/N-methyl-D-aspartate (NMDA) receptor, exhibits antidepressant-like activity in rodent tests/models of depression. Similarly to antidepressants, zinc induces brain derived neurotrophic factor (BDNF) gene expression and increases level of synaptic pool of zinc in the hippocampus. Clinical observations demonstrated serum hypozincemia in depression, which was normalized by effective antidepressant treatment. Moreover, our preliminary clinical study demonstrated the benefit of zinc supplementation in antidepressant therapy. All the data indicate the important role of zinc homeostasis in psychopathology and therapy of depression and potential clinical antidepressant activity of this ion.

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The authors review the main pharmacological factors playing a role in the kinetics of tricyclic antidepressant plasma levels. The current data concerning the relationship between tricyclic plasma levels and their clinical responses indicate that there is a therapeutic window at 50-150 ng/ml for the secondary derivatives (nortriptyline and desipramine). The lower limit of efficiency for the primary derivatives (imipramine and amitriptyline) is estimated at 200 ng/ml. The boundaries and prospects of the clinical use of antidepressant plasma levels are discussed in their various methodological aspects.

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Congenic mouse strain AKR.CBA-D13Mit76 carries the 59-70 cM fragment of chromosome 13 transferred from genome of cataleptic CBA/Lac strain to genome of AKR/J none-cataleptic strain. This fragment contains the major gene of predisposition to pinch-induced catalepsy. We investigated contribution of the fragment to regulation of sensitivity of catalepsy, sexual motivation and social investigation to classical tricyclic antidepressant imipramine. The sexual motivation was higher in AKR.CBA-D13Mit76 than in AKR mice. Chronic imipramine treatment (25 mg/kg) reduced it in AKR.CBA-D13Mit76 mice and had no effect on weakly expressed sexual motivation of AKR males. No significant effects of genotype or chronic imipramine treatment on characteristics of social interest were observed. Imipramine failed to alter catalepsy expression in AKR.CBA-DI3Mit76 mice. Possible molecular genetic mechanisms underlying difference in behavioral responses to antidepressant administration are discussed.

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Central insulin receptor-mediated signaling is attracting the growing attention of researchers because of rapidly accumulating evidence implicating it in the mechanisms of plasticity, stress response, and neuropsychiatric disorders including depression. Dicholine succinate (DS), a mitochondrial complex II substrate, was shown to enhance insulin-receptor mediated signaling in neurons and is regarded as a sensitizer of the neuronal insulin receptor. Compounds enhancing neuronal insulin receptor-mediated transmission exert an antidepressant-like effect in several pre-clinical paradigms of depression; similarly, such properties for DS were found with a stress-induced anhedonia model. Here, we additionally studied the effects of DS on several variables which were ameliorated by other insulin receptor sensitizers in mice. Pre-treatment with DS of chronically stressed C57BL6 mice rescued normal contextual fear conditioning, hippocampal gene expression of NMDA receptor subunit NR2A, the NR2A/NR2B ratio and increased REM sleep rebound after acute predation. In 18-month-old C57BL6 mice, a model of elderly depression, DS restored normal sucrose preference and activated the expression of neural plasticity factors in the hippocampus as shown by Illumina microarray. Finally, young naïve DS-treated C57BL6 mice had reduced depressive- and anxiety-like behaviors and, similarly to imipramine-treated mice, preserved hippocampal levels of the phosphorylated (inactive) form of GSK3 beta that was lowered by forced swimming in pharmacologically naïve animals. Thus, DS can ameliorate behavioral and molecular outcomes under a variety of stress- and depression-related conditions. This further highlights neuronal insulin signaling as a new factor of pathogenesis and a potential pharmacotherapy of affective pathologies.

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1. The carrier-mediated uptake of labelled 5-hydroxytryptamine (3H-5-HT) in rabbit platelets (defined as the difference between uptake observed in the absence and presence of 10 mumol l-1 imipramine) was studied after inhibition of monoamine oxidase and after a 1:13 dilution of the platelet-rich plasma (PRP) with Tris-containing buffer. 2. Irrespective of whether the rabbits were pretreated with reserpine or not, initial rates of 3H-5-HT uptake were maintained for at least 15 s. 3. Analysis of the saturation kinetics of 3H-5-HT uptake using Hill's equation yielded Km, Vmax and nH values of 130 nmol l-1, 116 pmol 10(8) platelets-1 min-1 and 1.40, respectively. Pretreatment of the animals with reserpine did not affect any of these kinetic parameters, but depleted more than 99% of the platelets' 5-HT stores. 4. The nH value remained greater than unity when the duration of incubation with 3H-5-HT was extended from 15 to 30 s and when the uptake of 3H-5-HT was inhibited by the presence of imipramine (10-40 nmol l-1). However, it was reduced to unity (with a consequential increase in Km) when 300 nmol l-1 ketanserin was present. This concentration of ketanserin did not affect 3H-5-HT uptake at substrate concentrations far below Km. 5. Imipramine inhibited 3H-5-HT uptake by increasing the Km for 3H-5-HT without changing Vmax. The Ki for this interaction was 18 nmol l-1.(ABSTRACT TRUNCATED AT 250 WORDS)

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tofranil dosage information 2017-04-29

In a multicenter series of trials, viloxazine was compared with imipramine, amitriptyline, doxepin and placebo in 123 neurotic and endogenous depressive buy tofranil inpatients and outpatients. While significant period effects reflecting improvement were obtained on the majority of efficacy variables, no significant differences were obtained among the treatment groups or depressive types. Imipramine and amitriptyline exhibited more anticholinergic adverse reactions; while, viloxazine exhibited greater CNS effects. Dizziness and nausea were much more frequent in neurotic depressives which may be related to their psychopathology.

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We found that ADs fail to induce TrkB signalling before postnatal day 12 (P12) after which an adult response of TrkB to ADs was observed. Interestingly, there was a temporally inverse correlation between the appearance of the responsiveness of TrkB to systemic ADs and the marked developmental reduction of BDNF-induced TrkB in brain microslices ex vivo. Basal p-TrkB status in the brain of BDNF deficient mice was significantly reduced only during early postnatal period. Enhancing cAMP (cyclic adenosine monophosphate) signalling failed to facilitate TrkB responsiveness to BDNF. Reduced responsiveness of TrkB to BDNF was not produced by the developmental increase in the expression of dominant-negative truncated TrkB.T1 because this reduction was similarly observed in the brain microslices of trkB.T1(-/-) buy tofranil mice. Moreover, postnatal AD administration produced long-lasting behavioural alterations observable in adult mice, but the responses were different when mice were treated during the time when ADs did not (P4-9) or did (P16-21) activate TrkB.

tofranil bedwetting reviews 2015-11-02

Ketoconazole is no longer available for clinical determination of worst-case victim drug-drug interaction (DDI) potential for cytochrome P450 3A (CYP3A)-substrate drugs; clarithromycin and itraconazole are the proposed replacements. Ketoconazole DDIs are described by unbound systemic exposures due to absence of carrier-facilitated hepatic uptake, but this aspect of clarithromycin and itraconazole disposition has not been investigated. At present, transport of buy tofranil clarithromycin, itraconazole, and hydroxyitraconazole by hepatic organic anion transporting polypeptides (OATPs) and organic cation transporter 1 (OCT1) was examined in vitro and in vivo. As for ketoconazole, uptake of clarithromycin, itraconazole, and hydroxyitraconazole into OATP1B1, OATP1B3, OATP2B1, and OCT1 expressing human embryonic kidney 293 (HEK293) cells was not greater than in vector controls. Uptake into these HEK293 cells and human hepatocytes was not impaired by the prototypical OATP, OCT, and sodium/taurocholate cotransporting polypeptide inhibitors bromosulfophthalein, imipramine, and taurocholate, respectively. In contrast, uptake of the positive controls, atorvastatin for OATPs and metformin for OCT1, was significantly enhanced by relevant transporter expression, and uptake into both these HEK293 cells and human hepatocytes was significantly impaired by prototypical inhibitors. In Oatp1a/1b gene cluster knockout mice, which lack the major hepatic Oatps, and in Oct1/2 knockout mice, ketoconazole, clarithromycin, itraconazole, and hydroxyitraconazole oral exposure was not increased, and the liver-to-blood partition coefficient (Kp) was not decreased. By contrast relative to wild-type mice, in Oatp1a/1b- and Oct1/2-knockout mice, atorvastatin and metformin oral exposure was significantly increased, and liver Kp was significantly decreased. The present studies provide in vitro and in vivo evidence that, like ketoconazole, clarithromycin, itraconazole, and hydroxyitraconazole are not transported into the liver by hepatic uptake transporters, including OATPs and OCT1.

tofranil 35 mg 2016-06-19

Beta-arrestin-1 measurements were carried out in cortical, hippocampal, and striatal brain regions of rats chronically intragastrically treated with either imipramine, desipramine, or fluvoxamine. Similar measurements were conducted in mononuclear leukocytes of 36 untreated buy tofranil patients with major depression and 32 healthy volunteer subjects. Beta-arrestin-1 levels were evaluated through immunoblot analyses using monoclonal antibodies to beta-arrestin-1.

tofranil drug information 2016-02-29

Binding of four tricyclic antidepressants (TCAs)--imipramine, desipramine, didesmethylimipramine and amitriptyline--on the lipid part of biological membranes was studied. Heterogeneity in partitioning of these drugs in artificial lipid bilayers (liposomes) was quantified using a radioligand binding method. High-affinity binding sites on the buy tofranil liposomes were found and characterized by apparent dissociation constant (Kd) and by binding capacity (Bmax). Change in the membrane lipid composition affected the binding parameters of the high-affinity binding, while the ligand modification affected non-specific binding (low-affinity adsorption) of TCAs. The possible role and methodological importance of high-affinity binding to the lipid part of biological membranes are both discussed. Determination of radioligand binding on model lipid membranes is recommended to avoid certain problems in interpretation of receptor binding studies.

tofranil brand 2015-03-20

Six women and 6 men who were treated in double-blind fashion major depressive illness did not respond to imipramine or buy tofranil amitriptyline, 150-300 mg/day, during periods of 26-112 days. After the addition of 25 micrograms/day (10 patients) or 50 micrograms/day (2 patients) of L-triiodothyronine (T3), 9 patients showed statistically significant improvement in depression scores; in 8 patients the response was marked. Improvement generally began within 1-3 days and was noted in all aspects of the depressive syndrome; side effects were minimal. T3 did not change plasma levels of imipramine or desipramine or their ratio but did suppress serum thyroxine.

tofranil with alcohol 2016-07-05

Tianeptine is a tricyclic agent provided with antidepressant activity in experimental models and in clinical trials. In vitro tianeptine and its two principal metabolites have no effects on monoamine uptake, release or neurotransmitter receptor binding. The biochemical effect of tianeptine in vivo after acute or repeated treatment indicates an enhanced serotonin uptake in cortex and hippocampus but not in mesencephalon, with no effect on noradrenaline or dopamine uptake. This enhanced serotonin uptake is not due to decrease in serotonin release, but is related to increase in the Vmax of the uptake carrier for serotonin. The fact that enhancers as well as inhibitors of serotonin uptake are provided with antidepressant activity challenge simple conclusion as to their mechanism of action. The possibility that increased serotonin uptake after repeated treatment may be related to the antidepressant activity exerted by these drugs, and drugs enhancing serotonin uptake might have antidepressant buy tofranil activity, with an earlier onset, is proposed.

tofranil tablets 10mg 2015-06-07

Models of long-term treatment in recurrent unipolar illness ideally should integrate both psychological and biological factors. In earlier reports we noted that high treatment specificity (i.e. good-quality maintenance interpersonal psychotherapy) and high delta sleep ratio were each associated with significantly increased wellness intervals in the absence of pharmacotherapy among patients with recurrent unipolar depression. To determine how these specific factors when taken together are related to length of survival time, we examined the concurrent effects of treatment specificity and delta sleep ratio on wellness intervals using survival analysis. We found significant effects of both treatment specificity and delta ratio on survival time. Seventy-three per cent of the patients in the high treatment specificity/high delta ratio group survived the 3-year trial, while 44% of the patients in the low delta ratio but high treatment specificity group survived. None of those rated low on both variables survived. We also found an effect for individual clinicians on treatment specificity and survival time and noted that the prophylactic effect of treatment specificity was buy tofranil maintained even within subsets of therapists grouped by their patients' survival times. Secondary analyses revealed an effect of patient attitudes on treatment specificity and survival time, although, when taken together, treatment specificity was the only variable remaining significantly associated with outcome. We conclude that patients remain well the longest when pre-treatment delta sleep parameters more closely approximate those of non-depressed individuals and when monthly psychotherapy is of higher quality. The key finding is that high specificity is of significant prophylactic benefit even for patients with a biological vulnerability for recurrence. We also conclude that in addition to therapists, patient expectancies contribute to treatment specificity, and high treatment specificity is, in turn, reflected in longer times to recurrence.

tofranil overdose symptoms 2015-10-25

Relative apparent molar enthalpies have been determined as a function of concentration (0.0001 to 0.2 mol kg(-1)) by heat conduction calorimetry for aqueous solutions of the structurally related antidepressant drugs imipramine and clomipramine in water over the temperature range 288 to 308 K. Critical concentrations determined from inflections in these plots for both drugs had minimum values at 298 K. The concentration dependence of the relative apparent molar enthalpy could be quantitatively described using a mass action model of association based on the Guggenheim equations for the activity coefficients of mixed electrolytes. Derived values of the monomer-counterion interaction coefficient for imipramine became increasingly negative with an increase in temperature over the temperature range 293 buy tofranil to 303 K, indicative of an increasing degree of premicellar association. In contrast, negative monomer-counterion interaction coefficients were obtained for clomipramine at only 303 and 308 K, suggesting an absence of premicellar association at lower temperatures. Values derived for the molar enthalpy of micellization of both drugs from the mass action model indicate an increasingly exothermic process with increase in temperature; positive values at 288 and 293 K arise from hydrophobic interactions while the negative values at higher temperatures suggest the importance of London dispersion interactions as the major driving force for aggregation. Copyright 2000 Academic Press.

tofranil tabs 2015-11-20

Platelets of patients with myeloproliferative disorders (MD) such as polycythaemia vera (PV), chronic myelogenous leukaemia (CML), idiopathic myelofibrosis (IM) and essential thrombocythaemia (ET) have been found to have low 5HT levels measured both by a fluorimetric and a liquid chromatographic assay. Km and Vmax for platelet active uptake of 3H-5HT were not significantly different in controls and patients. Inhibition of 5HT reuptake by imipramine or induction of moderate release by fenfluramine were not sufficient to distinguish the group of MD platelets from controls, although some patients had less of a tendency to retain intraplatelet amine. The low platelet 5HT content found in our patients seems not to be the consequence of disturbed active transport of 5HT across platelet membrane. Although defective storage of this amine within the cell is probable, the results of the present study do not rule out the possibility that platelets from MD patients undergo in vivo activation by endogenous stimuli not inhibited by aspirin. 10 d buy tofranil treatment with aspirin did not result in any significant rise in intraplatelet 5HT concentration.

tofranil medicine 2017-05-30

The buy tofranil medication status of the patient was heterogeneous.

tofranil reviews 2016-01-23

Our aim was to determine the cost-effectiveness of newer antidepressants compared with tricyclic antidepressants in managed care organization settings. buy tofranil

tofranil drug category 2015-07-29

Lead II EKG and His bundle electrograms were recorded in closed-chest pentobarbital-anesthetized dogs. Trazodone, a structurally distinct, new antidepressant agent, had no effect on His--Purkinje (HV interval) or intraventricular (HS interval) conduction following intravenous injection at graded doses between 1 and 30 mg/kg. In contrast, the tricyclic psychotropic agent imipramine (0.5--5 mg/kg) significantly slowed impulse conduction as indicated by increases in both the HV and HS intervals. Imipramine (5 mg/kg) also slowed impulse transmission across the atrium (PA interval). These responses to imipramine were associated with a concurrent prolongation of both the PR interval and QRS duration. In the anesthetized dog, trazodone administration promoted no evidence of heart block or sign buy tofranil of rhythm disturbances other than slowing in normal sinus rhythm.

tofranil 75 mg 2016-06-14

Lithium powerfully augments the effects of imipramine in resistant depression. We treated four groups of rats for five weeks with (1) saline alone, (2) saline followed by lithium, (3) imipramine alone, and (4) imipramine followed by lithium. There was no augmentation of activity by lithium. Normal human volunteers took imipramine 75 mg daily for three weeks, followed by imipramine 75 mg daily together with lithium 900 mg daily for another ten days. There was no elevation of mood after the addition of lithium. Lithium augmentation of antidepressants apparently requires a pre Trandate Iv Dose -existing neurochemical-behavioral disturbance.

tofranil overdose death 2016-06-06

Serotonergic, nitrergic pathway, and sigma receptors are possibly involved in mediating antidepressant action of T Cheap Pill Viagra . erecta in mouse forced swim test.

tofranil and alcohol 2017-07-02

The intracerebroventricular (i.c.v.) administration of increasing doses of 6-hydroxydopamine (6OHDA) (12.5-50 micrograms) induces in mice a dose-dependent hypothermic effect. This hypothermic effect is not affected either by serotonin uptake inhibitors (indalpine, clomipramine, trazodone, fluoxetine) or by dopamine uptake inhibitors (GBR 12783, amineptine). On the contrary, the hypothermia Ventolin 4mg Tablets is partly antagonized by norepinephrine uptake inhibitors (desipramine, nomifensine, viloxazine, maprotiline, protryptiline), as well as amfonelic acid. The antagonism elicited by desipramine is observed when the drug is administered intraperitoneally (from 5 mg/kg) or intracerebroventricularly (from 5 microgram per mouse). 6-hydroxydopamine-induced hypothermia is antagonized by imipramine after a time lag of 1 hour; this antagonism lasts 6-11 hours after intraperitoneal administration of the drug (20 mg/kg). The hypothermic effect of 6-hydroxydopamine is diminished by a previous 6-hydroxydopamine i.c.v. administration (50 micrograms, 7 days before), except in mice pretreated with desipramine at the time of the first 6-hydroxydopamine injection. The hypothermic effect is completely abolished by two previous 6-hydroxydopamine i.c.v. administrations (50 micrograms, 7 days interval). It is also decreased in mice receiving DSP4 15 days before testing (50 mg/kg, i.p.). Finally, neither haloperidol (0.5 mg/kg i.p.) nor SCH23390 (100 micrograms/kg s.c.) antagonize 6-hydroxydopamine-induced hypothermia. It is concluded that this effect is largely depending on central norepinephrine neurons.

tofranil pm dosage 2016-01-27

The use of a single antidepressant agent was clinically effective for the treatment of bulimia nervosa when compared to placebo, with an overall greater remission rate but a higher rate of dropouts. No differential effect regarding efficacy and tolerability among the various classes of antidepressants could be demonstrated. Elavil Starting Dose

tofranil mg 2015-01-12

We examined the effects of chronic administration of BME Glucophage Tablets on CUS exposed rats for 28 days. Behavioural changes were assessed by sucrose consumption and open field test to assess the effect of BME on CUS-induced depression. The mechanisms underlying antidepressant like action of BME was further evaluated by measuring levels of BDNF, Akt, and CREB in the hippocampus of rat brain and compared with the standard tricyclic antidepressant drug imipramine (20 mg/kg body weight).

tofranil 25mg tab 2017-09-17

Surgical complications included 2 (3%) rectal injuries, 3 (5%) repeat strictures that required reoperation and 20 (32%) repeat strictures that required dilation or visual internal urethrotomy. By 1 year after surgery all patients had a patent urethra and did not require further treatment. At 1 year 43 (72%) patients voided normally, 5 (8.3%) were areflexic and performed self-catheterization, 5 (8.3%) had urge incontinence and 5 (8.3%) had mild stress incontinence requiring no treatment. Moderate stress incontinence responded to imipramine in 1 case and collagen injection in 1. Of the patients who were potent preoperatively 31 (52%) remained potent postoperatively. Of the 29 ( Avapro Tablets 48%) patients who were impotent preoperatively and immediately postoperatively 9 regained potency at 1 year. However, at 1 year, the quality of erections of the 40 potent men was normal in only 22 (37%) and fair to poor in 18 (30%).

tofranil overdose 2015-03-12

1. Repeated administrations of trazodone as well as imipramine or mianserin (10 mg/kg i.p. twice daily for 3 weeks) attenuated the norepinephrine (NE) stimulation of adenylate cyclase studied in brain minces. Therefore trazodone shares with "tricyclic" (imipramine) and "atypic" (mianserin) antidepressants the capability to modulate the beta-adrenergic function. 2. Daily treatments with imipramine or trazodone enhanced the Vmax of neural uptake of serotonin (5HT) in minces prepared from rat frontal cortex; in contrast mianserin failed to modify the [3H]-5HT uptake. 3. Repeated administrations of imipramine but not of trazodone or mianserin reduced the maximum number of [3H]-imipramine recognition sites which are located on serotonergic axon terminals. 4. Differently, only repeated administration of trazodone decreased Bmax values of [3H]-mianserin binding sites which are located on membranes innervated by serotonergic neurons. Moreover trazodone did not change the number or affinity of 5HT2 receptors either after single or repeated administrations; in contrast even a single administration Tablet Urispas D with mianserin or repeated administrations with imipramine down-regulated [3H]-ketanserin specific binding in membranes prepared from the frontal cortex. 5. Our observations therefore suggest that trazodone, imipramine or mianserin exerts similar effects on the adenylate cyclase system, by acting on a interneuronal loop which links serotonergic and noradrenergic transmission function. However, its exact mechanism of action, in part resembling both tricyclic and atypic depressants, requires further examination.

tofranil pm generic 2016-04-25

Axis I and II diagnoses were made by using the Structured Clinical Interviews for DSM-III-R, Patient Version (SCID-P) and SCID II for Personality Disorders. The Hamilton Rating Scale for Depression and the Clinical Global Impressions scale were also completed. Prior treatment was assessed, with special attention paid to previous antidepressant drug therapy and psychotherapy.