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Tofranil (Imipramine)
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Tofranil

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.

Description

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.

Dosage

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.

Overdose

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.

Storage

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.

Contraindications

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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CRP experiments were performed, and the data were analyzed using a software-aided approach. This automated-evaluation approach led to (1) the detection of the CYP450 enzymes responsible for both substrate depletion and metabolite formation, (2) the identification of specific biotransformations, (3) the elucidation of metabolite structures based on MS/MS fragment analysis, and (4) the determination of the initial relative formation rates of major metabolites by CYP450 enzymes.

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These results, together with those of previously reported studies, suggest that venlafaxine has antidepressant efficacy comparable to that provided by available antidepressants.

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Treatment of urinary incontinence in children with ADHD is impaired compared to those without ADHD, and is directly affected by compliance and IQ.

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A case of significant hepatic reaction related to imipramine is presented, documented by challenge with imipramine and liver biopsy. The mechanism, while not entirely clear, is presumed to involve hypersensitivity or induction of toxic metabolites.

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Effects of CGP 36742 and CGP 51176 as well as the agonist CGP 44532 were assessed in the forced swim test in mice. Both antagonists were also investigated in an olfactory bulbectomy (OB) model of depression in rats, while CGP 51176 was also investigated in the chronic mild stress (CMS) rat model of depression. The density of GABAB receptors in the mouse hippocampus after chronic administration of CGP 51176 was also investigated.

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Experimental pain models may help to evaluate the mechanisms of analgesics and target the clinical indications for their use. This review, the second in a series of two, addresses how the efficacy of non-opioid analgesics have been assessed in human volunteers using experimental pain models.

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The computed analysis of the EEG-effects of a neuroleptic ethaperazine and an antidepressant melipramine administered in different doses was made in the experiments on cats. It was established that ethaperazine (3 mg/kg) and melipramine (6 mg/kg) increase the spectral power in the range of 1-2 Hz; the maximal effect was noted 2 hours after their oral administration Ethaperazine primarily decreases the powers of the spectra of the hypothalamus and reticulotegmental nucleus in the range of 13-14 Hz and over. Melipramine in a dose of 6 mg/kg decreases the spectral power of the hippocampus in the range of 4-12 Hz, of the mediodosal and caudal nuclei in the range of 8-12 Hz. The peak of the effects of melipramine administered in a dose of 12 mg/kg manifests itself in the decrease of the power in the range of 14-20 Hz and over both of the cortical and subcortical structures of EEG spectra.

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Dysthymic patients in this sample were significantly undertreated. Newer antidepressant agents may alter the potential for pharmacotherapy interventions in this vulnerable population.

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Studies suggest alpha2A-adrenoceptors (alpha(2A)AR) dysregulation in major depressive disorder (MDD). Platelet alpha(2A)ARs exist in high- and low-conformational states that are regulated by Gi protein. Although alpha(2A)AR coupling to Gi protein plays an important role in signal transduction and is modulated by antidepressants, it has not been previously investigated. Alpha2AR density in the high- and low-conformational states, agonist affinity and coupling efficiency were investigated in 27 healthy control subjects, 23 drug-free MDD patients and 16 patients after imipramine treatment using [3H]yohimbine saturation and norepinephrine displacement of [3H]yohimbine binding experiments. Coupling measures were derived from NE-displacement experiments. Patients had significantly higher alpha(2A)AR density, particularly in the high-conformational state, than control subjects. Coupling indices were normal in patients. High pre-treatment agonist affinity to the receptor in the high-conformational state and normal coupling predicted positive treatment outcome. Decreased coupling to Gi predicted a negative treatment outcome. Imipramine induced uncoupling (-11%) and redistribution of receptor density in treatment responders only, but had no effect on alpha(2A)AR coupling or density in treatment non-responders. Increased alpha(2A)AR density may represent a trait marker in MDD. The results provide indirect evidence for abnormal protein kinase A (PKA) and protein kinase C (PKC) in MDD which may be pursued in future investigations.

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We searched CENTRAL, MEDLINE, and EMBASE on 18 November 2013, as well as the reference lists of retrieved papers and other reviews. We also used our own handsearched database for older studies, and two clinical trials databases.

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This data suggests that besides neuroprotective and anti-inflammatory activities, SalB has promising therapeutic potential in treatment of depressive disorders.

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Based on placebo-controlled, double-blind, comparative trials, nefazodone demonstrates greater efficacy than placebo, and equivalent efficacy to imipramine. Somnolence, dry mouth, nausea, dizziness, and constipation are the most common adverse effects. Nefazodone appears to have a milder adverse effect profile than the tricyclic antidepressants, causes fewer sexual dysfunctions than the serotonin selective reuptake inhibitors, and may cause less dizziness than trazodone. Nefazodone at dosages of at least 300 mg/d provides another option for the treatment of depression.

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every randomised, placebo-controlled trial in which antidepressant medications were compared to placebo to reduce the symptoms of bulimia nervosa in patients of any age or gender.Quality criteria: reports were considered adequate if they were classified as A or B according to the Cochrane Manual. The Jadad scale, with a cut off of 2 points, was applied to check the validity of the above referred criterion but was not used as an inclusion criterion.

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Dopamine infused persistently (25 micrograms/24 h for 13 days) into the nucleus accumbens of rat brain caused phasic increases in spontaneous locomotor activity during the period of infusion. This phasic responding was prevented by lithium administered throughout the infusion period in divided doses (3 X daily administrations of 2.5 mg/kg IP) or as a continuous IP infusion (7.5 mg/kg/24 h), and by bupropion treatment (5-20 mg/kg 3 X daily). In contrast, imipramine, amitriptyline and nomifensine failed to prevent the phasic locomotor response to dopamine at doses which did not by themselves cause marked motor changes. Locomotor activity was measured using individual photocell cages, and rats preselected to (-)NPA were those initially showing a modest locomotor activity. Fourteen to twenty-eight days after discontinuing the dopamine infusion rats showed increased responsiveness to (-)NPA which persisted throughout the remainder of the 70-day withdrawal period. This long-term change was prevented when lithium was given continuously throughout the period of dopamine infusion, but not when lithium was given in divided doses, showing the importance of the mode of drug delivery. The long-term change caused by the dopamine infusion could also be prevented by bupropion but not by imipramine, amitriptyline or nomifensine to show again that the actions of classical antidepressant drugs may be differentiated from those of lithium and bupropion. Therefore, it is suggested that the model of phasic hyperactivity described may provide a means for more closely analysing, both behaviourally and biochemically, the site and mechanism of action of lithium (and bupropion) in the control of the short- and long-term consequences of an enhanced mesolimbic dopamine activity.

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The plasma concentration of alpha 1-acid glycoprotein, a putative endogenous inhibitor of the site labeled by tritiated imipramine, was measured by a radial immunodiffusion assay in 36 normal human volunteers and 51 drug-free patients who fulfilled DSM-III criteria for major depression. The depressed patients exhibited a significant elevation in the plasma concentration (+/- SEM) of alpha 1-acid glycoprotein (79.6 +/- 4 mg/dL) when compared with the age- and sex-matched controls (61.7 +/- 3 mg/dL). Fourteen of the 51 patients with major depression had plasma alpha 1-acid glycoprotein concentrations that were higher than the highest values of the normal controls. There was no relationship between plasma alpha 1-acid glycoprotein concentrations and sex or affinity of platelet tritiated imipramine binding of either the normal volunteers or the depressed patients. In the depressed patients, there was a significant positive correlation between plasma concentrations of alpha 1-acid glycoprotein and postdexamethasone plasma cortisol concentrations, and two measures of depression severity, the Montgomery-Asberg Rating Scale for Depression and the Center for Epidemiologic Studies-Depression Scale, and a significant negative correlation with age. These data provide the first evidence of alterations of an endogenous inhibitor of the tritiated imipramine binding site/serotonin transporter in depressed patients.

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Tricyclic antidepressants and carbamazepine have become the mainstay in the treatment of neuropathic pain. Within the last decade, controlled trials have shown that numerous other drugs relieve such pain. We identified all placebo-controlled trials and calculated numbers needed to treat (NNT) to obtain one patient with more than 50% pain relief in order to compare the efficacy with the current treatments, and to search for relations between mechanism of pain and drug action. In diabetic neuropathy, NNT was 1.4 in a study with optimal doses of the tricyclic antidepressant imipramine as compared to 2.4 in other studies on tricyclics. The NNT was 6.7 for selective serotonin reuptake inhibitors, 3.3 for carbamazepine, 10.0 for mexiletine, 3.7 for gabapentin, 1.9 for dextromethorphan, 3.4 for tramadol and levodopa and 5.9 for capsaicin. In postherpetic neuralgia, the NNT was 2.3 for tricyclics, 3.2 for gabapentin, 2.5 for oxycodone and 5.3 for capsaicin, whereas dextromethorphan was inactive. In peripheral nerve injury, NNT was 2.5 for tricyclics and 3.5 for capsaicin. In central pain, NNT was 2.5 for tricyclics and 3. 4 for carbamazepine, whereas selective serotonin reuptake inhibitors, mexiletine and dextromethorphan were inactive. There were no clear relations between mechanism of action of the drugs and the effect in distinct pain conditions or for single drug classes and different pain conditions. It is concluded that tricyclic antidepressants in optimal doses appear to be the most efficient treatment of neuropathic pain, but some of the other treatments may be important due to their better tolerability. Relations between drug and pain mechanisms may be elucidated by studies focusing on specific neuropathic pain phenomena such as pain paroxysms and touch-evoked pain.

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WAY 100635 blocked the antidepressant-like effect of linalool and β-pinene. In contrast, pretreatment of mice with PCPA did not modify reductions in the immobility time elicited by the two monoterpenes. The yohimbine modified the effect of linalool on immobility time. Propranolol and neurotoxin DSP-4 reversed the anti-immobility effect of β-pinene; also, SCH23390 blocked the antidepressant-like effect of β-pinene.

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The effects of chronic imipramine and electroconvulsive shock alone or combined were assessed on rat brain beta-adrenoceptors and serotonin2 (5-HT2) receptors and on dynorphin and thyrotropin releasing hormone (TRH) levels. These treatments resulted in regionally discrete and treatment-specific patterns of change in beta-adrenoceptor and 5-HT2 receptor density and in TRH and dynorphin levels. Electroconvulsive shock eliminated the serotonergic component of hippocampal DHA binding, suggesting an effect of this treatment on 5-HT1 receptors. The effects of combined electroconvulsive shock and imipramine treatments on cortical 5-HT2 and beta-adrenoceptor density appeared to be the additive sum of the individual treatment effects. No treatment interaction was observed on hippocampal 5-HT2 and beta-adrenoceptors, except after day 2. No treatment interaction on peptide content was observed at any time. These results demonstrate independent anatomical specificity for the effects of electroconvulsive shock and imipramine and provide evidence that the mechanisms responsible for their antidepressant actions differ.

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A chronic mild stress (CMS) model of depression was used to study an antidepressant-like activity of alnespirone (S 20499), a selective agonist of 5-HT1A receptors. In this model, a substantial decrease in consumption of a palatable sucrose solution over time is observed in rats subjected to a variety of mild stressors. This effect can be reversed by chronic administration of various classes of antidepressant drugs. Chronic (5 weeks) treatment with alnespirone, in a dose range between 1-5 mg/kg/day, gradually and dose dependently reversed the CMS-induced reductions in sucrose consumption without any significant effects in the non-stressed control animals. The onset of action of the most active doses (2.5 and 5 mg/kg/day) and the overall efficacy of alnespirone in the CMS model were comparable to those observed following similar administration of imipramine (10 mg/kg/ day). At the lower (0.5 mg/kg/day) and higher (10 and 20 mg/kg/day) doses, alnespirone was ineffective against the CMS-induced deficit in sucrose consumption. These data provide further support for previous suggestions, based on both the clinical observations and animal data, that agonism at 5-HT1A receptors may result in antidepressant action.

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In order to evaluate the enzymes CPK and LDH as potential biochemical markers of tricyclic antidepressant (TCA) cardiotoxicity, we prospectively followed 29 patients with TCA overdose. Serum CPK and LDH were obtained on all patients at admission. Population characteristics included a mean age of 33 y, a mean peak serum TCA concentration of 1190 ng/ml and mean maximal QRS interval of 0.10 sec. Seven patients (23%) had admission hypotension, 7 (23%) had severe respiratory depression, 6 (20%) had seizures and 4 (13%) had cardiac arrhythmias. One patient died. Mean admission CPK was 301 IU/L (nl less than 230 IU/L) while mean LDH was 221 IU/L (nl less than 250 IU/L). In 17 patients (57%), CPK remained in the normal range. There was no correlation between blood pressure, maximal QRS interval, serum TCA concentration, arrhythmias or seizures and CPK or LDH by regression analysis. CPK isoenzymes were obtained in 6 patients (both with and without severe myocardial dysfunction). One patient had an MB fraction of 10%; the remaining 5 had no measurable enzymes of myocardial origin. We conclude that modest elevations in CPK or LDH may occur after TCA overdose. These enzymes do not appear to originate from the myocardium and are of no utility in the assessment of antidepressant cardiotoxicity or prediction of clinical course.

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The diagnostic concept of posttraumatic stress disorder (PTSD) has long been recognized but usually applied in postwar circumstances. Recently developed criteria have allowed the disorder to be recognized in civilian patients having stress from such common insults as trauma, burns, or rape. Because PTSD may become chronic and difficult to treat if unrecognized, early intervention is desirable. In this report I describe three patients with acute PTSD who had favorable therapeutic response to tricyclic antidepressants. Although the use of the tricyclic agents in PTSD is rational because of their antianxiety and antidepressant properties, little has previously been said of their effectiveness in this disorder. These agents may provide an effective means of diminishing or preventing chronic PTSD.

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Exposure of rodents to an open elevated plus-maze (oEPM) elicits antinociception and increases plasma corticosterone levels. However, no studies have yet assessed the defensive behaviour repertoire of animals in this modified test. In Experiment 1, factor analysis was employed to characterise the behavioural profile of mice exposed to the oEPM. Experiments 2 and 3 assessed the effects of acute alprazolam (0.5-1.5mg/kg; diazepam 0.5-1.5mg/kg), pentylenetetrazole (10.0-30.0mg/kg), yohimbine (2.0-6.0mg/kg), mCPP (0.3-3.0mg/kg), and acute and chronic fluoxetine (10.0-30.0mg/kg) and imipramine (1.0-15.0mg/kg) on behaviours identified in Experiment 1. The factor analyses revealed that behaviour in the oEPM can largely (77% total variance) be accounted for in terms of 3 factors: factor 1 ('depth exploration'; e.g. head-dipping on the arms), factor 2 ('cautious exploration of arms'; e.g. flatback approach), and factor 3 ('risk assessment'; stretched attend postures - SAP). Experiments 2 and 3 showed that, over the dose range used, alprazolam selectively attenuated all measures of defensiveness. Similar, though more modest, effects were seen with diazepam. Confirming the intensity of the emotional response to the oEPM (nociceptive, endocrine and behavioural), relatively few significant behavioural changes were seen in response to the anxiogenic compounds tested. Although acute fluoxetine or imipramine treatment failed to modify behaviour in the oEPM, chronic fluoxetine (but not chronic imipramine) attenuated total flat back approach and increased head dipping outside the central square. Together, the results indicate that the oEPM induces behavioural defensive responses that are sensitive to alprazolam and chronic fluoxetine.

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Twelve pigeons key-pecked under a multiple variable interval 15-s, 150-s schedule of food reinforcement. The effects of methadone were studied alone and in combination with chronic daily administration of either imipramine (IMI) or desipramine (DMI). Chronic IMI was also given following reductions in response rates by unsignaled delay-to-reinforcement (UDR). Acute administration of methadone produced dose-dependent reductions in response rates under both schedules of reinforcement. Chronic daily administration of IMI or DMI alone did not result in lasting changes in baseline responding. When administered in combination, chronic daily IMI significantly attenuated the rate-reducing effects of methadone, whereas neither a low nor a high dose of chronic daily DMI was effective. The same dose of chronic daily IMI failed to ameliorate response rate reductions under delayed reinforcement. The behavioral and neurochemical specificity of the antidepressant effect is discussed.

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Serotonin (5-HT) uptake in synaptosomes was studied at 0 degree C (1), at 37 degrees C in the presence of 100 microM imipramine (IIa) or 100 microM zimelidine (IIb), in the absence of Na+ ions (III) in the incubation medium. A significant decrease (P less than 0.01) of the uptake rate has been found (III greater than IIa, b greater than I). Nonspecific uptake inhibition was thought to be the cause of these differences. Determination of specific uptake, using control III, has shown Na+-dependent transport of 5-HT only on the one type of carrier (Km = 174 + 24 nM). It is concluded that determination of 5-HT nonspecific uptake, using control III, has permitted a more exact evaluation of specific uptake parameters, than determination, using controls I and IIa, b.

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The alpha-adrenergic mechanisms exert a stimulatory influence on the secretion of growth hormone (GH) in the rat. In the present study the alpha receptors involved in GH regulation were characterized with respect to subtype. It was also investigated whether the GH response to alpha receptor agonists can be utilized to assess change in the responsiveness of central alpha receptors. The experiments were performed on rats with implanted intra-aortic cannulae allowing frequent blood sampling from freely moving animals. Plasma GH was determined by radioimmunoassay. Reserpine (10 mg/kg) caused a suppression of the normal pulsatile secretory pattern of GH. The alpha receptor agonist clonidine (CLON) given to reserpine-pretreated animals induced a dose-dependent increase in plasma GH. The effect of CLON (0.2 mg/kg) was prevented by pretreatment with the alpha 2 receptor antagonist yohimbine (3 mg/kg), but not by the alpha 1 receptor antagonist phenoxybenzamine (10 mg/kg). Chronic pretreatment with CLON or imipramine, either of which can be expected to produce a reduced sensitivity of central alpha 2 receptors, resulted in reduced GH responses to CLON. On the other hand, chronic treatment with yohimbine, which should cause denervation supersensitivity of alpha 2 receptors, led to enhanced GH responses to CLON. The results indicate that GH release in the rat is stimulated by postsynaptic alpha 2 receptors. They also suggest that the GH response to CLON can be used as a valid in vivo model reflecting decreased, as well as increased responsiveness of this type of receptor.

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In summary, on the basis of our inpatient and outpatient double-blind control trials and open-label experience with trazodone, we find it to be an effective broad-spectrum antidepressant generally well tolerated by most patients. When atropine side effects of the standard tricyclic antidepressants and bridged tricyclic antidepressants are undesirable and medically contraindicated, trazodone should be one of the drugs of choice in major depressive disorders.

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tofranil drug information 2017-04-21

Stress urinary incontinence (SUI) is a symptom appearing in both males and females. Pharmacological treatment has demonstrated to be effective for female buy tofranil SUI, but its role for treatment in males is controversial. This review evaluates the various types of drugs, their effects, and levels of efficacy in the studies.

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Acamprosate is a new psychotropic drug used in the treatment of alcohol (ethanol)-dependence. Recent studies suggest that acamprosate inhibits neuronal hyperexcitability by antagonising excitatory amino acids. It is available as a 333 mg enteric-coated tablet, with a recommended dosage of 1.3 g/day for patients with a bodyweight < 60 kg and 2 g/day for patients with a bodyweight > or = 60 kg. Treatment with higher dose strength tablets 2 x 500 mg twice daily is bioequivalent to treatment with the 2 x 333 mg 3 times daily dosage regimen. Acamprosate is absorbed via the paracellular route in the gastrointestinal tract. Absorption is rapid but limited after oral administration. At steady- buy tofranil state, acamprosate has a moderate distribution volume of about 20L. Acamprosate is not protein bound or metabolised. Half of the elimination of acamprosate occurs as unchanged acetyl-homotaurine in urine, the other half might be eliminated by biliary excretion. The administration of the enteric-coated tablets showed a flip-flop mechanism with a terminal elimination half-life 10-fold higher than the 3-hour half-life reported after intravenous infusion. During repeated oral administration of 666 mg 3 times daily, steady-state is reached after 5 to 7 days and leads to plasma concentrations ranging from 370 to 650 micrograms/L. The pharmacokinetics of acamprosate administered as an enteric-coated tablets are time- and dose-independent, and its accumulation ratio is about 2.4 at steady-state. Acamprosate disposition does not differ between males and females. The pharmacokinetics of acamprosate are not modified in patients with hepatic insufficiency or chronic alcoholism. In contrast, renal insufficiency influences the elimination of acamprosate and it is, therefore, contraindicated under such circumstances. Interaction studies have confirmed that when acamprosate is concomitantly administered with food, the amount absorbed is decreased. When combined with diazepam, disulfiram or alcohol, the pharmacokinetic disposition of acamprosate is not modified. Acamprosate does not influence the kinetics of diazepam, alcohol or imipramine and its metabolite desipramine.

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A boy aged 7 years 10 months was admitted to hospital on several occasions in an unconscius state with twitching and apnoeic episodes. Initial investigations failed to show a buy tofranil specific cause. During his time in hospital he had recurrent episodes of loss of consciousness and, on the last occasion, hypotension and ventricular tachycardia. A diagnosis of imipramine poisoning was established by the presence of imipramine in stomach washings and blood. The drug was being given to the child, both at home and in hospital, by his mother. The possibility of nonaccidental poisoning must be considered if there is no obvious cause for a child's illness. In this case the mother responded to psychiatric treatment.

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Clomipramine and imipramine treatments were compared in a sample of 152 panic disorders. Diagnosis was according to the positive criteria of DSM-III-R, but without exclusion of comorbid affective or personality disorders. The 2-year design provides non-blind treatment under typical clinical practice conditions, and it includes random assignment, periodic assessment with standardized measures, and comparable, flexible drug dosages. Findings on six outcome measures in the first 59 cases to complete 10 weeks showed both tricyclics to be markedly and equally effective for blocking panic attacks, alleviating phobic buy tofranil avoidance, and reducing nonspecific aspects of anxiety. Clomipramine's predominantly serotonergic action seemed not to determine a different action spectrum. During the first 2 weeks, clomipramine was significantly and unexpectedly superior to imipramine in both antipanic and antiphobic actions. These results require replication under double-blind conditions.

tofranil low dose 2016-09-27

The pharmacological properties of MO-8282 (1,2,3,4-tetrahydro-2-methyl-9H-dibenzo [3,4: 6,7]cyclohepta [1,2-c]pyridine maleate) as an antidepressant were investigated. At doses 10 times less than those of amitriptyline, MO-8282 showed similar potencies in reducing the duration of immobility during forced swimming in rats and in potentiating stereotype induced by L-DOPA. Intermediate doses of MO-8282 reduced the duration of immobility during forced swimming, in mice as well, suppressed muricide behavior of olfactory-bulbectomized rats and antagonized clonidine-induced suppression of exploratory activity in mice. MO-8282 moderately antagonized the ptosis but not the hypothermia induced by reserpine in mice. MO-8282 exhibited weak antagonism against the tremor, lacrimation and diarrhea induced by tremorine, but its activity was milder than that of amitriptyline. The uptake of noradrenaline into rat hypothalamic synaptosomes was inhibited by MO-8282 at concentrations 20 times less than equally effective doses of amitriptyline, but the uptake of dopamine or serotonin was unaffected by MO-8282. A single oral administration of MO-8282 at a dose of 30 mg/kg accelerated noradrenaline turnover, but did not affect dopamine and serotonin turnover in the rat brain. MO-8282 strongly inhibited noradrenaline-, histamine- or adenosine-sensitive adenylate cyclase activity of guinea buy tofranil pig brain. Its mode of action differed from that of imipramine, rather resembling that of mianserin. MO-8282 did not affect monoamine oxidase activity of rat liver. These results suggest that the pharmacological characteristics of MO-8282 are different from those of tricyclic antidepressants and rather similar to those of mianserin, but more potent. The results, therefore, indicate that MO-8282 is possibly a novel antidepressant.

tofranil and alcohol 2017-08-26

The purpose of this study was twofold: to measure the overall direct costs of depression for 1990 in the UK, and to develop a model to illustrate issues in the evaluation of the relative cost-effectiveness of the pharmacological treatment of depression. We compared a tricyclic antidepressant, imipramine, with paroxetine, a newer antidepressant. For assessing the cost of illness, we used a top-down approach. We calculated direct but not indirect costs. Cost-effectiveness was evaluated by developing a simulation model based on the theory of clinical decision analysis to compare the costs and outcome of each treatment. From this we estimated buy tofranil the expected cost per patient and the cost per successfully treated patient. The total cost to the nation of depressive illness was estimated to be 222 pounds million. The expected costs per patient were found to be similar for paroxetine and imipramine (430 pounds v. 424 pounds). The costs per successfully treated patient were found to be lower for paroxetine (824 pounds) than for imipramine (1024 pounds). The results were stable when a sensitivity analysis was applied to the variables employed in the model. The most sensitive variable was the cost of treatment failure. Our model thus reveals that medication that appears expensive in terms of cost per day may not be so when patient compliance and the total costs of treatment are taken into account.

tofranil generic name 2015-03-16

Previous studies suggest that the responsiveness of TrkB receptor to BDNF is developmentally regulated in rats. Antidepressant drugs (AD) have been shown to increase TrkB signalling in the adult rodent brain, buy tofranil and recent findings implicate a BDNF-independent mechanism behind this phenomenon. When administered during early postnatal life, ADs produce long-lasting biochemical and behavioural alterations that are observed in adult animals.

tofranil reviews 2016-09-27

The available evidence suggests that antidepressants are superior to placebo in treating GAD. There is evidence from one trial suggesting that paroxetine and imipramine have a similar efficacy and tolerability. There is also evidence from placebo-controlled trials suggesting that these drugs buy tofranil are well tolerated by GAD patients. Further trials of antidepressants for GAD will help to demonstrate which antidepressants should be used for which patients.

tofranil medication 2016-01-13

MSP may potentially represent a good adjunct or alternative to existing antidepressant therapeutics. Further studies are necessary to confirm the mechanism of action of MSP and its buy tofranil modulation of brain functioning.

tofranil tablets 10mg 2017-10-07

The first day test dose versus steady-state relationship for predicting drug doses was evaluated for the situation where metabolites are produced. An organ clearance model incorporated into a digital computer program simulated drug and metabolite disposition. When the terminal elimination rate for metabolite was similar to that of its precursor, the drug and metabolite concentrations could be summed for use in test dose predictions as the resulting accumulation ratios were similar. However, if an active metabolite is eliminated more slowly than its precursor, future buy tofranil studies should consider these concentrations separately for predictive purposes. The theoretical results agreed with concentration data obtained from a study of patients who took imipramine.

tofranil y alcohol 2015-01-17

Glycogen synthase kinase-3 (GSK3), which is primarily regulated by an inhibitory phosphorylation of an N-terminal serine, has been implicated as contributing to mood disorders by the finding that it is inhibited by the mood buy tofranil stabilizer lithium.

tofranil drug interactions 2015-12-07

Adult fowl of both sexes injected with the monoamine oxidase inhibitor pargyline showed elevated circulating prolactin concentrations and reduced growth hormone concentrations. Young cockerels injected with the serotonin agonist quipazine and the antagonist methysergide showed responses consistent with a buy tofranil serotoninergic stimulatory control of prolactin. Injection of the serotonin precursor tryptophan and the serotonin re-uptake blocker imipramine resulted in elevated prolactin and reduced growth hormone levels. The similarities and differences in the control of prolactin and growth hormone in birds and mammals were discussed.

tofranil reviews anxiety 2016-08-28

Our study sought to evaluate the anxiolytic and antidepressant activities of oleanolic acid as well as the neural mechanisms involved. Animal models such as barbiturate sleep-induction, light-dark box, elevated plus maze, forced swimming test, tail suspension test and open field test were conducted. Male Albino Swiss mice were treated orally with vehicle 10 mL/kg, fluoxetine 20 mg/kg, imipramine 15 mg/kg, diazepam 1 mg/kg or oleanolic acid 5-40 mg/kg. Pretreatment (intraperitoneal) of animals with pentylenetetrazole (PTZ) 20 mg/kg, 1-(2-methoxyphenyl)-4-[4- (2-phthalimido) butyl]piperazine hydrobromide (NAN-190) 0.5 mg/kg, p-chlorophenylalanine methyl ester (PCPA) 100 mg/kg or α-methyl-p-tyrosine (AMPT) 100 mg/kg, WAY100635 (WAY) 0.3 mg/kg, prazosin (PRAZ) 1 mg/kg, yohimbine 2 mg/kg as well as monoamine oxidase assay and hippocampal brain-derived neurotrophic factor (BDNF) quantification were carried out. Oleanolic acid potentiated the hypnotic effect of barbiturate and demonstrated an anxiolytic effect in both the light-dark box and elevated plus maze. This effect was not reversed by PTZ. Acute and/or chronic oral treatment of mice with oleanolic acid (5-20 mg/kg) elicited an antidepressant effect in the forced swimming test and the tail suspension test without interfering with the locomotor activity. The antidepressant effect of oleanolic acid was attenuated by NAN-190, AMPT, PCPA, WAY and buy tofranil PRAZ. Although monoamine oxidase activity remained unaltered by oleanolic acid, chronic administration of oleanolic acid augmented hippocampal BDNF level. These findings demonstrate multiple mechanisms of the anxiolytic and antidepressant effect of oleanolic acid.

tofranil medicine 2016-10-09

Our results verify inhibition of Pgp as a potential mechanism of action for verapamil buy tofranil during treatment resistant depression. The implications of these findings are discussed in the context of novel treatment strategies in depression.

tofranil 50 mg 2016-05-19

The study of Chloromycetin Suspension Mufel binding is not an easy task especially because of the difficulty of interpreting the results in terms of binding on specific receptor sites. The problem is not new; what is new is the increasing amount of fanciful interpretation that such a technique has generated. The tendency to interpret anomalous or intriguing results in terms of new receptor subtypes seems to have reached its peak. The need to apply severe criteria becomes imperative before concluding that a binding site may be called a receptor site. Some pitfalls in binding studies will be discussed.

tofranil pm reviews 2015-06-22

Tianeptine is a new antidepressant effective against anxiety accompanying mood disturbances. Its clinical properties have been assessed by double-blind controlled studies (versus imipramine, amitriptyline, nomifensine, viloxazine) in depressed patients fulfilling the diagnostic criteria of the DSM III: single recurrent major depressive episodes without melancholia Crestor 60 Mg or psychotic features, and dysthymic disorders. The authors have concluded that tianeptine is effective in depressive disorders as shown both by depression rating scales and subjective impressions of treated patients. This improvement increases regularly with time. Seventy-eight percent of patients were considered to be "responders" at the end of the treatment with tianeptine. Antidepressant activity of tianeptine is equally present in depressive states appearing after withdrawal from alcohol. In depressed patients with anxiety, the results also reveal the efficacy of tianeptine on anxiety symptoms. Tianeptine, in addition, shows a marked action on somatic complaints. These results have been confirmed by open long-term trials, particularly in the elderly. Tianeptine can be placed in a middle position in the bipolar classification, between the sedative and stimulant antidepressants. Its antidepressant and anxiolytic properties and its action on somatic complaints make the drug particularly suitable for the treatment of the entire range of depressive symptomatology.

recommended tofranil dosage 2015-10-03

Mitochondrial dysfunctions, impaired bioenergetics and dysfunction of neurotrophins are included in many neurodegenerative and psychiatric diseases. We investigated in vitro effects of Cleocin Reviews pharmacologically different antidepressants and mood stabilizers on mitochondrial enzymes to discover, which mitochondrial functions could be involved in pathophysiology of mood disorders.

tofranil dosage forms 2016-12-04

The purpose of the present study was to compare the extent of salivary flow and finger sweating after single acute oral doses of mianserin Flomax Generic Equivalent (30 mg), amitryptiline (75 mg), imipramine (75 mg) and maprotiline (75 mg) and placebo in healthy volunteers in a double-blind assay. Maprotiline and mianserin were less active in reducing salivary flow but were more active than amitryptiline and imipramine in reducing finger sweating. The lack of association between these methods for the measurement of the anticholinergic effect of antidepressant drugs is analyzed in terms of possible mechanisms for the control of palmar sweating.

tofranil 300 mg 2015-03-24

A growing body of data suggests that the glutamatergic system may be involved in the pathophysiology and treatment of severe mood disorders. Chronic treatment with the antimanic agents, lithium and valproate, resulted in reduced synaptic expression of the AMPA(-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) receptor subunit GluR1 in the hippocampus, while treatment with an antidepressant (imipramine) enhanced the synaptic expression of GluR1. The anticonvulsants, lamotrigine (6-(2,3-dichlorophenyl)-1,2,4-triazine-3,5-diamine) and riluzole (2-amino-6-trifluoromethoxybenzothiazole), have been demonstrated to have efficacy in the depressive phase of bipolar disorder. We therefore sought to determine the role of these anticonvulsants, compared to that of the predominantly antimanic anticonvulsant valproate, on AMPA receptor localization. We found that the agents with a predominantly antidepressant profile, namely lamotrigine and riluzole, significantly enhanced the surface expression of GluR1 and GluR2 in a time- and dose-dependent manner in cultured hippocampal neurons. By contrast, the predominantly antimanic agent, valproate, significantly reduced surface expression of GluR1 and Cytoxan Tablets GluR2. Concomitant with the GluR1 and GluR2 changes, the peak value of depolarized membrane potential evoked by AMPA was significantly higher in lamotrigine- and riluzole-treated neurons, supporting the surface receptor changes. Phosphorylation of GluR1 at the PKA (cAMP-dependent protein kinase) site (S845) was enhanced in both lamotrigine- and riluzole-treated hippocampal neurons, but reduced in valproate-treated neurons. In addition, lamotrigine and riluzole, as well as the traditional antidepressant imipramine, also increased GluR1 phosphorylation at GluR1 (S845) in the hippocampus after chronic in vivo treatment. Our findings suggest that regulation of GluR1/2 surface levels and function may be responsible for the different clinical profile of anticonvulsants (antimanic or antidepressant), and may suggest avenues for the development of novel therapeutics for these illnesses.

tofranil 25 mg 2015-03-01

Positive chronotropic and inotropic responses to etilefrine (alpha-[(ethylamino)methyl]-m-hydroxybenzyl alcohol), an orally active cardiovascular agent, were investigated in isolated dog right atrial and left ventricular preparations. Intravenous administration of etilefrine to a support dog increased heart rate and mean systemic blood pressure, and increased sinus rate and atrial contractile force in the isolated right atrium perfused with blood from the support dog. Etilefrine injected intra-arterially to isolated atria and ventricles induced dose-dependent positive chronotropic and inotropic effects. Etilefrine was about 100 times less potent than isoproterenol. The effects of etilefrine in isolated atria were significantly inhibited by treatment with atenolol, but were not significantly Nexium Medication inhibited by ICI 118,551. The effects of etilefrine were partially inhibited by imipramine. These results indicate that etilefrine is a highly selective beta-1 adrenoceptor agonist and suggest a moderate catecholamine-releasing activity by tyramine-like action in the blood-perfused dog heart.

tofranil overdose symptoms 2016-11-09

Atypical depression, one of the 4 historically important ways of subdividing depression, was first used by West and Dally to describe a patient subgroup that was nonresponsive to imipramine but responsive to iproniazid. The definition was later refined to include reverse vegetative and hysteroid dysphoria symptoms, presaging adoption of the current DSM definition in 1984. However, focusing on hysteroid dysphoria symptoms drew attention away from anxiety symptoms, some of which are more strongly linked to atypical depression. Studies that have attempted to validate atypical depression have reinforced reverse vegetative symptoms criteria and have shown that atypical depression is probably more common than melancholia. Studies suggest that atypical depression is not preferentially responsive to monoamine oxidase inhibitors, but rather less responsive to tricyclic antidepressants.

tofranil buy canada 2017-05-29

High pressure stress was found to induce immunosuppression accompanied with the enhancement of motor activity in mice. Citrus fragrance restored stress-induced immunosuppression and induced calm behavior in mice. In the forced swimming test using rats, citrus fragrance reduced the total immobility time and potentiated the imipramine-induced reduction in total immobility time. The application of citrus fragrance to depressive patients made it possible to markedly reduce the doses of antidepressants needed for the treatment of patients.

tofranil drug study 2015-08-12

It has been reported that imipramine reduces the titre of rheumatoid factor in schizophrenic patients. Twenty out-patients suffering from classical rheumatoid arthritis and having rheumatoid factor titre equal to, or greater than 1:64, were treated in a double-blind trial with imipramine 75 mg or matching placebo. In this study the dose of imipramine used failed to affect the levels of rheumatoid factor.

tofranil 10 mg 2017-01-14

A daily dose of at least 3.0 mg clonazepam as augmentation of ongoing antidepressant treatment should be considered in prolonged depressive patients with suboptimal improvement.

tofranil 25mg tab 2015-02-09

The spontaneous activity of the norepinephrine-containing cells of the locus coeruleus was recorded in chloral hydrate-anesthetized rats. The effect of seven tricyclic antidepressants on the firing rate of single cells in the locus coeruleus was studied. All the drugs tested, except iprindole markedly decreased the rate of firing of the noradrenergic cells. Antidepressants having a secondary amine in the side chain, desipramine, nortriptyline and chlordesipramine, were more potent than their respective tertiary amine analogues, imipramine, amitriptyline and chlorimipramine. Alteration of the rate of drug metabolism by pretreatment with SKF-525A or phenobarbital did not change the doses of tertiary antidepressnats required to decrease norepinephrine cell firing. Depletion of the norepinephrine stores by pretreatment with alpha-methyl-p-tyrosine and reserpine markedly increased the dose of desipramine required to depress the norepinephrine cells. The results are in good agreement with previous studies showing that secondary amine antidepressants are more potent than their tertiary amine homologues in blocking the uptake of norepinephrine into brain and peripheral tissues. Despite their lower potency it is concluded that tertiary antidepressants act on noradrenergic neurons in their unchanged form and not via secondary amine metabolites formed during the recording experiments since alterations in liver metabolism did not influence the response. The findings are consistent with the suggestion made from studies on transmitter turnover that antidepressants by inhibiting reuptake of norepinephrine cause a stimulation of postsynaptic receptors which decreases the activity of the presynaptic neurons by a feed-back mechanism. This view is further supported by the finding of an inverse relation between the norepinephrine content of the brain and the dose of desipramine required to decrease the firing rate of the noradrenergic neurons.

tofranil tablet uses 2015-02-16

Duchenne muscular dystrophy, a genetic disease caused by the absence of functional dystrophin, remains without adequate treatment. Although great hopes are attached to gene and cell therapies, identification of active small molecules remains a valid option for new treatments. We have studied the effect of 20 approved pharmaceutical compounds on the muscles of dystrophin-deficient mdx5Cv mice. These compounds were selected as the result of a prior screen of 800 approved molecules on a dystrophin mutant of the invertebrate animal model Cænorhabditis elegans. Drugs were administered to the mice through maternal feeding since 2weeks of life and mixed in their food after the 3rd week of life. The effects of the drugs on mice were evaluated both at 6weeks and 16weeks. Each drug was tested at two concentrations. Prednisone was added to the molecule list as a positive control. To investigate treatment efficiency, more than 30 histological, biochemical and functional parameters were recorded. This extensive study reveals that tricyclics (Imipramine and Amitriptyline) are beneficial to the fast muscles of mdx mice. It also highlights a great variability of responses according to time, muscles and assays.

tofranil 5 mg 2017-12-17

We have measured the levels of kainate receptor mRNA in rat brains following the injection of antidepressant drugs over a time course up to 32 days. Over this period imipramine and fluvoxamine elicited a rise in kainate receptor mRNA levels to a maximum of three and two fold increase respectively, relative to untreated rat brain samples. Mianserin and amitriptyline did not induce significantly elevated kainate mRNA levels compared to untreated specimens, but were elevated compared to vehicle injected controls.

tofranil 35 mg 2015-05-21

Six subjects with DSM-III defined unipolar major depressive disorder had positron emission tomography scans using 18F-2-fluoro-2-deoxy-D-glucose (2FDG) before and after treatment with imipramine. Their 12 scans were compared to the scans of six controls matched for age. Significant reductions in metabolism for subjects in the depressed group were found on scans for both the anterior and right frontal regions. significant reductions in metabolism occurred more often in the right hemisphere than the left. No significant changes in metabolism could be attributed to imipramine. In addition, absolute metabolic rates were not related to the degree of depression pre- and post-treatment. The findings suggest that hypometabolism in the frontal cortex and right hemisphere may occur in major depressive disorders.