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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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The effect of bupropion, a new clinically active antidepressant drug, administered repeatedly to rats and mice, was compared with that of imipramine. The drugs were given orally twice a day for 14 days, bupropion in a dose of 20 mg/kg, imipramine--10 mg/kg. The action of bupropion was studied in the following tests: clonidine-induced aggression in mice, open field in rats, amphetamine-induced hypermotility in rats, clenbuterol-induced hyperthermia in rats kept at high ambient temperature. Moreover, the effect of bupropion on 3H-prazosin binding to membranes from the cerebral cortex was measured. On the basis of the results obtained it may be concluded that in some tests chronically administered bupropion acts like imipramine; as both drugs potentiate the amphetamine-enhanced locomotor activity, attenuate the hyperthermic response to clenbuterol and increase the number of 3H-prazosin binding sites in the cerebral cortex.

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It has been shown that non-aqueous capillary electrophoresis (NACE) can provide improved separations in comparison to those obtained using conventional CE under aqueous conditions (ACE). Previous work carried out in our laboratories involving initial investigations into the technique have been reported. Based on the findings of that work it was possible to separate a variety of basic pharmaceuticals from selected impurities and to obtain the successful separation of some hydrophobic sulphonic acids. The successful coupling of NACE to mass spectrometry (NACE-MS) has also been demonstrated.

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With the object of studying the kinetics of imipramine and desipramine five healthy volunteers received single intramuscular, oral and intravenous doses and multiple oral doses of imipramine hydrochloride on different occasions. Two of the volunteers also received single intramuscular and oral doses of desipramine hydrochloride. Great interindividual differences were noted in the plasma concentrations of imipramine and the formed desipramine after single doses of imipramine hydrochloride. In all subjects more desipramine was formed after oral than after parenteral adminstration of imipramine. The bioavailability of an orally administered dose of imipramine ranged between 29.5 and 54.7%. The concentration of imipramine was generally lower in the blood cells than in the plasma, unlike the concentration of desipramine which was considerably higher in the blood cells. The half-lives of imipramine ranged from 4.0-17.6 hrs (M = 7.6 +/- 2.5) after single oral doses and between 9.2 and 20.2 hrs (M = 14.0 +/- 1.9) after multiple oral doses. The half-lives of the formed desipramine ranged between 13.5 and 61.5 hrs (M = 29.9 +/- 8.7) after multiple oral doses of imipramine hydrochloride. The observed mean steady-state plasma concentration after multiple oral doses of imipramine hydrochloride, 50 mg t.i.d. varied from 21.4-69.0 mug/1 (M = 38.2 +/- 8.7) for imipramine and from 33.7-136.0 mug/1 (M 72.3 +/- 19.5) for desipramine. The great difference in the ability to form desipramine after oral and parenteral administration of imipramine hydrochloride may have therapeutic consequences as imipramine and desipramine have differing pharmacological properties.

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The authors examined dose-response relationships in 62 agoraphobic patients receiving either imipramine or placebo under double-blind conditions in conjunction with behavioral interventions. At the end of 12 weeks, patients treated with imipramine had improved significantly more than placebo patients. Results revealed that the beneficial therapeutic effect of imipramine was dose dependent and suggested that optimal response in agoraphobia may require doses of 150 mg/day or more. The results also indicated that side effects can significantly interfere with the buildup of optimal dose in agoraphobic patients treated with imipramine. The authors briefly discuss the implications of these findings for clinical practice and future research.

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The platelet is one of the most researched biological markers in psychiatry. Characteristics of MAO activity, 5-HT uptake, imipramine and alpha 2-adrenergic receptor binding, for example, are similar in platelet and CNS. Methodological factors are not negligible, and range from diagnostic specificity and drug effects to the normal physiological variability of age and hormone-related changes, circadian and seasonal rhythms. As yet, there are no clear state or trait platelet markers in affective disorders and schizophrenia that can be unequivocally used to detect vulnerability to the illness, predict therapeutic response, define clinical diagnostic entities or follow the course of the illness. However, platelet markers are increasingly being used in careful studies to monitor psychopharmacological effects (an in vivo assay of all active metabolites), different ligands can be specific markers for certain aspects of a psychiatric illness (e.g. alpha 2-adrenergic receptors and weight loss), and this homogeneous preparation of human cells is an increasingly important tool in studying mechanisms in pathophysiology. More longitudinal studies are required to establish functional relationships between platelet variables and psychopathology.

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Continuing our earlier study in a group of purine-2,6-dione derivatives of long chain arylpiperazines (LCAPs), a series of 8-unsubstituted 7-phenylpiperazin-4-yl-alkyl (4-14) and 7-tetrahydroisoquinolinyl-alkyl (15-17) analogues were synthesized and their serotonin 5-HT1A, 5-HT2A, 5-HT6, 5-HT7 and dopamine D2 receptor affinities were determined. The study allowed us to identify some potent 5-HT1A receptor ligands with additional moderate affinity for 5-HT2A, 5-HT7 and dopamine D2 receptors. Compounds 9, 12, 13 and 14, with the highest 5HT1A receptor affinity, were selected for further functional in vivo studies and behavioural evaluation of antidepressant- and antianxiety-like activity. Compounds 9, 12 and 13 showed features of agonists of pre- and/or post-synaptic 5-HT1A receptors, whereas 14 was classified as an antagonist of postsynaptic sites. Moreover, derivatives 9 and 14 acted as antagonists of 5-HT2A receptors. In behavioural studies, compounds 9 and 13 showed antidepressant-like activity in the mouse forced swim test, and their effects were similar or stronger than those of imipramine. Compounds 9, 12 and 14 displayed potential anxiolytic-like properties in the mouse four-plate test, similar or even greater than those of the reference anxiolytic drug, diazepam.

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Recent studies suggest that ketamine produces antidepressant actions via stimulation of mammalian target of rapamycin (mTOR), leading to increased levels of synaptic proteins in the prefrontal cortex. Thus, mTOR activation may be related to antidepressant action. However, the mTOR signalling underlying antidepressant drug action has not been well investigated. The aim of the present study was to determine whether alterations in mTOR signalling were observed following treatment with antidepressant drugs, using ketamine as a positive control. Using Western blotting, we measured changes in the mTOR-mediated proteins and synaptic proteins in rat hippocampal cultures. Dendritic outgrowth was determined by neurite assay. Our findings demonstrated that escitalopram, paroxetine and tranylcypromine significantly increased levels of phospho-mTOR and its down-stream regulators (phospho-4E-BP-1 and phospho-p70S6K); fluoxetine, sertraline and imipramine had no effect. All drugs tested increased up-stream regulators (phospho-Akt and phospho-ERK) levels. Increased phospho-mTOR induced by escitalopram, paroxetine or tranylcypromine was significantly blocked in the presence of specific PI3K, MEK or mTOR inhibitors, respectively. All drugs tested also increased hippocampal dendritic outgrowth and synaptic proteins levels. The mTOR inhibitor, rapamycin, significantly blocked these effects on escitalopram, paroxetine and tranylcypromine whereas fluoxetine, sertraline and imipramine effects were not affected. The effects of escitalopram, paroxetine and tranylcypromine paralleled those of ketamine. This study presents novel in vitro evidence indicating that some antidepressant drugs promote dendritic outgrowth and increase synaptic protein levels through mTOR signalling; however, other antidepressant drugs seem to act via a different pathway. mTOR signalling may be a promising target for the development of new antidepressant drugs.

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The effects of long-term amphetamine treatment were examined on self-stimulation responding from the substantia nigra. Rates of self-stimulation responding were substantially depressed among rats chronically treated with amphetamine and tested in the absence of the drug. When rats were subsequently retested after a two day hiatus in which they received imipramine or amitriptyline, the post-amphetamine depression of rates of self-stimulation responding was mitigated. The efficacy of imipramine and amitriptyline in reversing the post-amphetamine depression of self-stimulation responding was also evident during a continuation of the drug (imipramine or amitriptyline)/test sequence, for seven test sessions. The results of the present investigation were related to changes in dopamine and acetylcholine neurotransmission following long-term amphetamine treatement.

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40 patients with endogenic depression, who exhibited an inhibited-mel ancholic symptomatology received Dibenzepin (30 patients) and Imipramin (10 patients) as a mood-elucidating and activating anti-depressant. Exact determinations of blood pressure, pulse rate, the orthostatic-reaction, Schellong's test and the cold-pressure test were carried out on these patients. The results were tabulated. They show fundamentally that (1) the thymoleptic circulatory reaction as a sign of the influence of the vegetative functions makes possible in many cases a prognosis of the secondary effects of treatment and (2) a strong acceleration in the rate of pulse, and a rise in the systolic blood pressure at rest as well as the normalization of the orthostatic-test chiefly indicate an improvement or remission of depression.

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Although there are controversial issues (the "American view" and the "European view") regarding the construct and definition of agoraphobia (AG), this syndrome is well recognized and it is a burden in the lives of millions of people worldwide. To better clarify the role of drug therapy in AG, the authors summarized and discussed recent evidence on pharmacological treatments, based on clinical trials available from 2000, with the aim of highlighting pharmacotherapies that may improve this complex syndrome.

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In an attempt to clarify the possible role of a serotonergic and dopaminergic dysfunction in obsessive-compulsive disorder (OCD), we measured platelet 3H-imipramine (3H-IMI) binding, serotonin uptake, and platelet sulfotransferase activity in 17 drug-free OCD patients and an equal number of healthy controls. Serotonin uptake and 3H-IMI binding sites in platelets have been shown to constitute peripheral markers of those present in presynaptic serotonergic neurons. Sulfotransferase, an enzyme involved in the catabolism of phenolic compounds and of cathecholamines such as dopamine, has similar kinetic characteristics in brain and platelets. Our results showed a lower number of 3H-IMI binding sites and a higher level of sulfotransferase activity in OCD patients compared with those in controls. These preliminary results suggest involvement of both the serotonin and dopamine systems in OCD.

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Human hair contains methamphetamine, amitriptyline, imipramine, nicotine, and their metabolites in some amount, which can be detected by routine toxicological methods. Sometimes, the level of drugs reaches over 100 micrograms/g. Animal experiments indicate that these drugs are found solely in sections of hair grown after administration of the drugs. The negative stage after the administration of drugs means that the hair section containing drugs has not come out of the hair follicle. Toxicological examination of the hairs may give some clue helping to identify the chronology of the intoxication.

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Binedaline is a new antidepressant drug which is not a tricyclic compound. In animal investigations it showed a greater therapeutic index than imipramine and amitriptylene and a smaller ED50. It also showed less anticholinergic and antihistaminic activity. In this study the effects of 100 mg (females) and 150 mg (males) of binedaline was compared with 50 mg and 75 mg of amitriptylene and placebo in healthy volunteers. Binedaline was better tolerated than amitriptylene and produced less sedation and fewer instances of dry mouth. Binedaline was devoid of the marked postural hypotension produced by amitriptylene but caused the same degree of tachycardia as amitriptylene at rest, when subjects were tilted and when subjected to ergometry. It was concluded that binedaline causes less alpha-adrenergic blockade than amitriptylene but that the sympathomimetic effects were similar. At the doses employed no major changes in electrocardiogram or systolic time intervals occurred.

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Imipramine is a well-established tricyclic antidepressant which was first approved for the treatment of depression in the late fifties. Antidepressant effect of imipramine is attributed to inhibition of serotonin (5HT) and noradrenaline (NA) reuptake in brain. These monoamines have been implicated in a variety of neurological disorders including tremor. In the present investigation attempt was made to study the effect of imipramine on harmaline-induced tremor in rats. Male Sprague Dawley rats weighing 115+/-2.5 g were given harmaline (10 mg/kg, i.p.) alone or along with imipramine (30 min before harmaline) in doses of 60 and 90 mg/kg respectively. The latency of onset, intensity and duration of tremor and EMG were recorded. To substantiate the role of 5HT in aetiopathology of tremor the above experiment was repeated in the rats pretreated with P-chlorophenylalanine (PCPA), a potent 5HT depleter. The levels of 5HT and 5-hydroxyindole acetic acid (5HIAA) in the brain stem were measured using high performance liquid chromatography. Imipramine dose-dependently exacerbated the duration, intensity and amplitude of EMG following harmaline-induced tremor. Imipramine treatment further decreased harmaline-induced 5HT turnover in the brain stem. However, this was statistically insignificant. Depletion of 5HT produced a significant reduction in the intensity and duration of harmaline-induced tremor. In conclusion, this study suggests that imipramine exacerbates harmaline-induced tremor. Clinical use of imipramine for the treatment of depression in patients who also suffer from tremors may require a close monitoring.

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Baseline studies showed significantly larger and less concentrated nocturnal urine among enuretics compared with controls. We observed a marked antidiuretic effect of imipramine in 6 enuretics with severe nocturnal polyuria. The imipramine induced decrease in urine output was accompanied by reduced osmolal clearance. Approximately a third of the observed decrease in solute excretion was attributed to lower excretion of sodium and potassium. The remaining two-thirds were most likely caused by an increased tubular reabsorption of urea, which may be secondary to a sympathomimetic effect of imipramine tubules, possibly because of altered adrenal medullary function with an increase in proximal tubular sodium and water reabsorption. The resultant lower tubular flow rate facilitates tubular reabsorption of urea in the distal part of the nephron.

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A long-term follow-up assessment was conducted in 25 chronically depressed patients who had participated in a 6-week trial of imipramine to determine if imipramine responders would sustain a more favorable long-term outcome than nonresponders or noncompleters. Imipramine responders tended to remain on imipramine treatment throughout the follow-up interval and had a significantly better outcome. Eighty-nine percent of the imipramine responders met the criteria for recovery at follow-up compared with 31% in the comparison groups. Imipramine responders also fared significantly better at follow-up on measures of depression, global severity of illness, and social/vocational functioning. The results supported a more favorable long-term outcome in chronic depression patients who had responded to imipramine and suggest that maintenance therapy may be indicated and effective for this disorder.

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A method is described for the analysis of amitriptyline, doxepin, imipramine, nortriptyline, desmethyldoxepin, desipramine, and protriptyline in human plasma utlizing GLC-chemical-ionization mass spectrometry with selected ion monitoring. The assay is highly specific and is quantitative to at least 1 ng/ml with a standard error typically less than 5%. Representative concentrations of the parent compounds and their monodemethylated metabolites, as meeasured in plasma samples from patients under treatment with tertiary amine tricyclic antidepressants, are given.

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The effect of acute (single dose) and repeated (twice daily, for 21 days) administration of imipramine, amitriptyline, citalopram, mianserin and rolipram (the latter drug in a dose of 5 mg/kg po, all the other drugs in a dose of 10 mg/kg po) on drinking induced by isoprenaline (50 micrograms intracerebroventricularly (icv), 2 h after the single dose, 2 and 72 h after the last does of the antidepressants) was studied in rats. It was found that repeated, but not acute, treatment with imipramine, amitriptyline and rolipram significantly reduced the response to isoprenaline. The effect of amitriptyline and rolipram was observed 2 and 72 h after their last administration, while that of imipramine only 72 h after its last dose. Citalopram and mianserin were ineffective after both acute and repeated administration.

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This study tested the hypothesis that stimulants (indirect dopamine agonists) attenuate the discriminative stimulus of naltrexone in monkeys chronically treated with L-alpha-acetylmethadol (LAAM). Four rhesus monkeys (Macaca mulatta) received LAAM (1.0 mg/kg s.c.) twice daily and discriminated a withdrawal-precipitating dose of naltrexone (0.0178 mg/kg s.c.) from saline. Cocaine (0.1-1.78 mg/kg), amphetamine (0.32-1.78 mg/kg), haloperidol (0.01-0.1 mg/kg), sulpiride (1.0-10.0 mg/kg), propranolol (0.32-3.2 mg/kg), clonidine (0.001-0.1 mg/kg), desipramine (0.32-3.2 mg/kg), and imipramine (1.0-10.0 mg/kg) were given s.c. before cumulative doses of naltrexone. Cocaine and amphetamine antagonized the discriminative stimulus effects of naltrexone, each shifting the naltrexone dose-effect curve significantly (e.g., 100-fold) rightward or downward. In contrast, the dopamine antagonist haloperidol shifted the naltrexone dose-effect curve 5-fold leftward. Sulpiride, desipramine, clonidine, and propranolol had comparatively less effect on the naltrexone discriminative stimulus, whereas some doses of imipramine attenuated the naltrexone stimulus in a manner similar to that of cocaine and amphetamine. These results support the notion that multiple neurotransmitter systems are involved in the discriminative stimulus effects of opioid withdrawal. Furthermore, these data are consistent with reports that dopamine levels decrease during opioid withdrawal and provide evidence that enhancing dopamine or other monoamine levels may attenuate subjective effects of opioid withdrawal.

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Behavioral effects of psychollatine, a new glycoside indole monoterpene alkaloid isolated from Psychotria umbellata, was investigated in models of anxiety, depression, memory, tremor, and sedation related to 5-HT and/or GABA neurotransmission. The GABA antagonist picrotoxin and the 5-HT2 antagonist ritanserin were used to examine the role of GABA and 5-HT2 receptors in psychollatine-induced effects. In the light/dark and hole-board models of anxiety, diazepam (0.75 mg/kg) and psychollatine (7.5 and 15 mg/kg) showed anxiolytic-like effect at doses that do not increase sleeping time nor alter spontaneous locomotor activity. The anxiolytic effect of psychollatine was prevented by prior administration of ritanserin, but not of picrotoxin, indicating that 5-HT2 but not GABA receptors are implicated. In the forced swimming model of depression, psychollatine (3 and 7.5 mg/kg) effects were comparable to the antidepressants imipramine (15 mg/kg) and fluoxetine (20 mg/kg). Psychollatine suppressed oxotremorine-induced tremors in all doses. In the step-down learning paradigm, diazepam (0.85 mg/kg), MK-801 (0.15 mg/kg), and psychollatine 100 mg/kg impaired the acquisition of learning and memory consolidation, without interfering with retrieval. It is concluded that the effects of psychollatine at the central nervous system involve serotonergic 5HT2(A/C) receptors.

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The findings from this study suggest antidepressant-like effect of C. thonningii involving interaction with serotonergic (5-HT2), dopaminergic (D2), noradrenergic (α1 and α2), and muscarinic cholinergic systems; and anxiolytic effect through an interaction with GABAA benzodiazepine receptor.

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The effects of viloxazine and zimelidine on reverse monoamine neurotransmitter uptake by crude synaptosomal fraction of the rat brain were studied and compared to those of imipramine, amphetamine and cocaine. Imipramine noncompetitively inhibited the uptake of all the monoamines under study, with a greater specificity as regards serotonin. Viloxazine and zimelidine strongly inhibited the transport of noradrenaline, dopamine and serotonine, the transport of the latter being inhibited to a greater degree. Kinetic analysis showed the active centers of noradrenaline and dopamine carriers to be very much alike, those of catecholamine and serotonin carriers to be less alike. The data obtained made it possible to describe (at least partly) the structure of the active centers of monoamine carriers and to specify the action modes of antidepressants and psychostimulants.

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Depressed patients with HIV illness respond to imipramine at the same rate as medically healthy depressed patients. Severity of immunosuppression is not associated with imipramine treatment outcome. There is no evidence that imipramine has negative effects on enumerative measures of immune status.

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Therapeutic drug monitoring (TDM) of tricyclic antidepressants (TCAs) is considered useful in patients with major depressive disorder, since these drugs display large individual differences in clearance, and the therapeutic windows of these drugs are relatively small. We developed an assay for determination of amitriptyline (ATP), nortriptyline (NTP), imipramine (IMP), desipramine (DSP) clomipramine (CMP) and desmethyl-clomipramine (DCMP) in dried blood spots (DBS). A fast and robust LC-MS/MS method was developed and analytically validated for simultaneous determination of ATP, NTP, IMP, DSP, CMP, and DCMP in DBS. Six mm circles were punched out from DBS collected on Whatman DMPK-C paper and mixed with acetonitrile: methanol 1:3 containing the internal standard. The extract was analyzed by LC-MS/MS. Total LC-MS/MS runtime was 4.8 min. The assay was linear in the range 20-500 µg/L for all compounds. Overall-assay accuracy and precision were<20% for the lower limit of quantification (LLOQ), except for CMP (CV=22.3%), and <15% at other concentrations. The initial LLOQ was 20 µg/L however for CMP and DMCP it was increased to 40 µg/L. The blood volume per spot did not influence the results, but a low hematocrit (≤ 30%) was associated with a >15% negative bias for all compounds. Punching at the perimeter of the blood spot instead of the center was associated with a positive bias. A good correlation was found between patients plasma and DBS samples of ATP, NTP and DMCP, but not for CMP. In addition, proportional differences were found. This LC-MS/MS method was analytically validated for determination of TCAs in DBS. Future validation will focus on the clinical application of the method.

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Our findings suggest that the effects of fluoxetine, mianserin, buspirone, imipramine, meclobemide and DOI on exploration, spontaneous motor activity and isolation-induced aggression in mice are different, which may involve different pharmacological mechanisms underlying their anti-aggression in isolation mice. 5-HT1A and 5-HT2A/2C receptors may mediate isolation-induced aggressive behavior in mice. The involvement of 5-HT receptor subtypes needs further clarification.

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A murine graft versus host (GVH) model was developed as a tool for drug discovery. A pharmacological survey revealed that as a class the anti-rheumatics (e.g., auranofin, azathioprine, and methotrexate) were the most potent inhibitors of GVH induced splenomegaly. The immunosuppressants, cyclophosphamide and cyclosporine A, and the glucocorticoids (e.g., dexamethasone, hydrocortisone, and corticosterone) were all able to suppress the GVH response. Anti-inflammatory agents (e.g., indomethacin and piroxicam), and a series of central nervous system affecting drugs, including serotonin agonists (e.g., trifluromethylphenylpiperazine (tfMPP), 1-(3-chlorophenyl)piperazine (mCPP), and quipazine), and tricyclic antidepressants (e.g., amitriptyline, desipramine, imipramine, and nortriptyline) typically were ineffective at doses up to 10 mg/kg. However, at high dose levels (30 mg/kg) piroxicam enhanced while amitriptyline and cyproheptadine (a mixed serotonin and histamine antagonist) suppressed GVH induced splenomegaly. These data provide a pharmacological profile for a series of immunomodulator, anti-inflammatory, and central nervous system active compounds in a classic immunologic model.

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Antidepressant neuroleptics, perazine (PZ), levomepromazine (LMZ) and flupenthixol (FPX) given to rats jointly with imipramine (IMI) for 2 weeks affected the plasma concentration of IMI only slightly but markedly elevated the concentration of its metabolite, desipramine (DMI). In the brain PZ significantly elevated both IMI and DMI concentrations while LMZ and FPX showed a tendency to increase the concentration of IMI and decrease the concentration of DMI. All three neuroleptics markedly decreased the DMI/IMI ratio in the brain and (except FPX) increased it in the plasma. Given alone for two weeks PZ, LMZ, FPX did not affect the levels of cytochromes P-450 and b-5 in liver microsomes. Chronic treatment with IMI significantly elevated the concentration of cytochrome P-450 in the liver and had a tendency to increase the concentration of cytochrome b-5. FPX, but not PZ or LMZ abolished this effect. Neuroleptics coadministered with IMI to rats did not affect the activity of the enzymes responsible for the IMI biotransformation as compared with IMI-treated animals. The neuroleptics added to the incubation mixture in vitro inhibited IMI hydroxylation noncompetitively. The demethylation was inhibited competitively by LMZ but noncompetitively by PZ and FPX. The inhibitory effect of neuroleptics on the hydroxylation was much more marked than that on the demethylation. FPX was the weakest inhibitor of IMI metabolism among the neuroleptics studied.

tofranil drug classification

To investigate the role of erythropoietin (EPO) in the central nervous systems, we assayed EPO concentrations in the cerebrospinal fluid (CSF) of patients with depression or old cerebrovascular injuries and controls. Concentrations of EPO in the CSF were significantly higher in 13 patients with depression (3.21+/-0.46 mU/mL) than in 10 patients with old cerebrovascular diseases (1.80+/-0.32 mU/mL, P < 0.01), and in 10 healthy controls (0.98+/-0.26 mU/mL, P < 0.01). Serum EPO concentrations did not differ among these three groups. In the patients with depression, 5 months of treatment with imipramine and/or nortriptyline significantly reduced EPO concentrations in the CSF (1.56+/-0.34 mU/ mL, P < 0.01). Results suggest that the brain of patients with depression may be in an hypoxic state, and that the increased EPO in the CSF may act to limit hypoxia-induced damage to neurons in these patients.

tofranil 25mg medication

The isolated field-stimulated vas deferens of the rat (0.1 Hz, 3 ms, 30-40 V) was used to study the relationship between the in vivo inhibition of neuronal uptake of noradrenaline (NA) by cyclic antidepressant drugs and the subsequent activation/desensitization of presynaptic alpha 2-adrenoceptors. Receptor activation was indirectly measured by quantifying the ability of each drug to inhibit basal twitch responses after their acute administration. Receptor desensitization was also indirectly measured by quantifying the ability of the drugs to reduce the inhibitory effects of selective alpha 2-adrenoceptor agonists on the electrically-induced twitch responses after their long-term administration. The acute in vivo administration of desipramine and other antidepressants (0.5-10 mg kg-1; i.p.; 2 h) resulted in dose-dependent inhibitions of the basal twitch responses which were rapidly reversed to control values by idazoxan (10-5 M). In vitro, desipramine and other antidepressants also inhibited in a concentration-dependent manner (10(-9)-10(-5) M) the twitch responses. In rats pretreated 12 h earlier with reserpine (1 mg kg-1; i.p.) or oxypertine (4 mg kg-1; i.p.), desipramine (10 mg kg-1; 2 h) did not induce inhibition of the basal twitch responses or it induced a smaller effect, respectively. For the various antidepressants the degree of inhibition of the basal twitch responses (desipramine greater than protriptyline greater than nortriptyline greater than maprotiline = imipramine greater than amitriptyline greater than viloxazine greater than iprindole much greater than zimelidine) was highly correlated (r = 0.914) with the potency for blockade of [3H]-NA uptake into rat brain synaptosomes. Clonidine and xylazine inhibited in a concentration-dependent manner (10(-9)-10(-6) M) the twitch responses. The long-term (7-14 days) administration of antidepressants or cocaine (10 mg kg-1, i.p.) resulted in significant decreases in sensitivity to clonidine or xylazine. Short-term (3 days) treatment with desipramine did not reduce the sensitivity to clonidine. The results indicate that the acute in vivo inhibition of NA neuronal uptake by antidepressants leads to the activation (through endogenous NA) of presynaptic inhibitory alpha 2-adrenoceptors which results in inhibition of the twitch responses. In contrast, prolonged in vivo inhibition of NA reuptake is followed by a slow desensitization process of the same receptors which results in a reduction of sensitivity to clonidine.

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tofranil street drug 2017-11-26

1. Nomifensine is a new substance which showed, in tests for antidepressant activity, a pronounced effect which is quantitatively better than that of the reference substances. 2. With regard to thymoleptic effects in animal studies the effect of nomifensine is similar to that of tricyclic antidepressants, but nomifensine has no pronounced anticholinergic activity. 3. buy tofranil online Nomifensine influences the cardiovascular system very slightly. 4. The mechanism of action of nomifensine differs from that of tricyclic antidepressants and must be clearly differentiated from phenylalkyl amines with sympathomimetric activity. 5. Nomifensine is a compound with a special, new profile of action, and thus cannot be calssified in known categories.

tofranil drug 2016-02-16

Serotonergic implication in panic disorder has been demonstrated by the efficacy of serotonin reuptake blockers in treatment. Fluoxetine, a potent 5-HT reuptake blocker, has been suggested to have anti-panic efficacy. This open study examines 30 patients (eight males and 22 females) with an average age of 36.9 years, ranging from 18 to 62, who were treated for eight weeks with fluoxetine (mean dose 20 mg per day). All patients fulfilled DSM-III-R criteria of panic disorder with agoraphobia as determined in a SCID interview schedule. Out of 28 patients who started medication buy tofranil online , 64% of the patients completed the clinical trial and 36% of the patients dropped out of treatment because of increased anxiety or a lack of efficacy. Thirty-two percent of the patients had zero panic attacks by week 3. By the end of eight weeks of treatment, 48% of the patients had zero panic attacks. There was a significant reduction in anxiety and phobic avoidance and panic attacks. Tritiated platelet imipramine and paroxetine bindings revealed significantly lower maximal binding for patients with panic disorder in comparison with controls. Paroxetine Bmax showed a trend to increase in the direction of control values by the end of the trial.

recommended tofranil dosage 2017-12-27

After chronic treatment with imipramine (20 mg/kg, i.p., twice daily for 14 days) the pressor dose-response curves to phenylephrine, methoxamine and cirazoline (alpha 1-adrenoceptor agonists) significantly shifted to the left with decreased PD50 values in pithed rats; however, the dose-response curve to Sgd 101/75, a selective alpha 1-adrenoceptor agonist was not affected. On the other hand buy tofranil online , the alpha 2-adrenoceptor agonists such as B-HT 920, xylazine and clonidine produced a rightward shift for both the pressor (increased PD50) and cardioinhibition (increased ID50) dose-response curves in these rats. These results required treatment with imipramine over 2 weeks. Chronic treatment with imipramine has reduced the antagonism by prazosin of the pressor effect of phenylephrine when compared with the dose-ratios between the 2 groups. On the contrary, the antagonism by piperoxan of the cardioinhibitory effect of B-HT 920 was rather enhanced by the treatment, but that of the pressor effect of B-HT 920 was little changed. In cerebrocortical membrane fractions obtained from rats pretreated with imipramine, Ki of phenylephrine to displace [3H]prazosin was decreased, whereas that of clonidine and yohimbine to displace [3H]yohimbine was increased. In conclusion, it is demonstrated that after chronic imipramine treatment the peripheral alpha 2-adrenoceptors (both presynaptic and postsynaptic sites) as well as central alpha 2-adrenoceptors respond with a decreased sensitivity to the alpha 2-adrenoceptor agonists, and moreover, this treatment produces an increased sensitivity of the central and peripheral alpha 1-adrenoceptors to the alpha 1-adrenoceptor full agonists.

tofranil overdose death 2015-09-20

The effect of acute and chronic treatment with three antidepressant drugs on the cortical L-type calcium channel (measured as [3H]nitrendipine binding sites) and on the responsiveness to pain (assessed in the hot-plate test) was tested on the Wistar rat. Acute administration of antidepressants did not affect the characteristics of calcium channels and did not significantly prolong the hot-plate latency. However, a combination of antidepressants with nifedipine brought about analgesia. Chronic administration of imipramine did not significantly affect the characteristics of calcium channels buy tofranil online but produced a moderate analgesic effect. In contrast, chronic administration of citalopram and chlorprothixene increased the density of [3H]nitrendipine binding sites and induced hyperalgesia, which was nullified by acute administration of nifedipine. The results confirm that calcium channels may be involved in analgesia and hyperalgesia and indicate that chronic treatment with some antidepressant may induce an increase in the density of cortical calcium channels.

tofranil brand name 2016-05-12

Sphingolipid turnover has been shown to be activated at old age and in response to various stress stimuli including oxidative stress. Reduction of vitamin E content in the liver under the pro-oxidant action is associated with enhanced sphingolipid turnover and ceramide accumulation in hepatocytes. In the present paper, the correction of sphingolipid metabolism in the liver cells of old rats and in the palmitate-treated young hepatocytes using α-tocopherol has been investigated. 3- and 24-month-old rats, [(14) C]palmitic acid, [methyl-(14) C-choline]sphingomyelin (SM), and [(14) C]serine were used. α-Tocopherol administration to old rats or addition to the culture medium of old liver slices or hepatocytes prevented age-dependent increase of ceramide synthesis and lipid accumulation, and increased SM content in liver tissue and cells. α-Tocopherol treatment of old cells decreased the neutral and acid sphingomyelinase (SMase) activities in hepatocytes and serine palmitoyl transferase activity in the liver cell microsomes. Effect of α- or γ-tocopherol, but not of δ-tocopherol, on the newly synthesized ceramide content in old cells was correlated with the action of inhibitor of serine palmitoyl transferase (SPT) activity (myriocin) and SMase inhibitors (glutathione, imipramine). Addition of α-tocopherol as well as myriocin to the culture medium of young hepatocytes, treated by palmitate, abolished ceramide accumulation and synthesis. The data obtained demonstrate that α-tocopherol normalized elevated ceramide content buy tofranil online in the old liver cells via inhibition of acid and neutral SMase activities and lipid synthesis de novo. α-Tocopherol, reducing ceramide synthesis, prevented palmitate-induced aging-like ceramide accumulation in young liver cells.

tofranil low dose 2016-09-06

Pain induction and assessment are very important for the sensitivity of the pain models. Generally, experimental pain models need to be designed with careful consideration of the pharmacological mechanisms and pharmacokinetics of analgesics. The drawback with the different study designs is also discussed. This knowledge can aid the decisions that need buy tofranil online to be taken when designing experimental pain studies for compounds entering Phase I and II trials.

tofranil y alcohol 2017-03-09

A MEDLINE search was conducted, limiting searching to double-blind, randomized, controlled trials (1978 to present) of antiepileptic drugs (carbamazepine, gabapentin, pregabalin, topiramate, and lamotrigine) used in buy tofranil online the treatment of chronic neuropathic pain.

tofranil online 2015-01-08

The GPR39-Zn(2+)-sensing receptor seems to be involved in buy tofranil online the pathophysiology of depression. GPR39 knockout animals show depressive- and anxiety-like behavior. Chronic treatment with selective antidepressants (ADs) up-regulates GPR39.

tofranil 25 mg 2015-04-02

Psychoendocrinology studies of depressed patients focus on the disregulation of the hypothalamic-pituitary-adrenal (HPA) axis. Abnormalities in the HPA axis have been noted in depressed patients. Numerous data have demonstrated the existence of reciprocal interactions between the central serotonin (5-HT) system and HPA axis. These interactions are of particular relevance when considering pathological conditions, such as depression, in which modifications of both the 5-HT system and HPA axis have been evidenced. In our laboratory, we examined the effects of adrenocorticotropic hormone (ACTH) on the immobilization of rats in the forced swim test and on the wet-dog shakes induced by the DOI, 5-HT2 receptor agonist with the administration of imipramine and lithium. The reduction of immobility, induced by the buy tofranil online chronic administration of imipramine for 15 days, was blocked by treatment with ACTH for 14 days. And, chronic ACTH treatment for 14 days increased the wet-dog shake response. This effect of ACTH was not inhibited by a 14-day administration of imipramine. Accordingly, the chronic treatment of rats with ACTH may prove to be an effective model for antidepressant-treatment-resistant depression. We believe that behavioral pharmacological and molecular biological research into the interaction between the 5-HT and HPA axis will elucidate the pathogenesis of depression or antidepressant-treatment-resistant depression and the mechanism of antidepressants action.

tofranil overdose 2017-12-13

Generalized anxiety disorder (GAD) is characterized by chronically persistent worry and therefore requires effective long-term treatment. This article reviews the benefits and risks associated with various pharmacologic and psychological therapies to assess their ability to achieve the elimination of GAD symptomatology and restoration of normal function. Psychotherapeutic approaches such as applied relaxation, cognitive therapy, and cognitive-behavioral therapy have all been shown to be effective when used as monotherapies and may be beneficial when used adjunctively. Current effective pharmacotherapies for patients with GAD include anxiolytic benzodiazepines, buspirone, and antidepressants including venlafaxine and paroxetine. Benzodiazepines have long been used to treat anxiety and are particularly appropriate in short-term treatment situations; however, buy tofranil online their adverse side-effect profile and their inability to treat depression commonly comorbid with GAD renders them less than ideal in many situations. Buspirone has demonstrated anxiolytic benefits but, like benzodiazepines, shows negligible antidepressant action. Antidepressants like paroxetine and venlafaxine are not only effective antidepressants but also effective anxiolytics, thus implying their special ability to treat GAD and concurrent depression, even over the long-term.

tofranil cost 2017-08-21

It has been suggested that maintenance treatment of patients who have remitted panic disorder with agoraphobia beyond the six months of acute phase imipramine treatment may decrease the risk of relapse. This study further explores the relationship between relapse and duration of imipramine treatment in this population.Fifty-one patients, all in remission at the end of six months acute phase open trial with imipramine 2.25 mg/kg/day and randomized to double-blind maintenance or placebo substitution, discontinued imipramine treatment eventually and were followed over a 12-month risk period: 27 during first year placebo substitution, 7 after 12 months of imipramine maintenance in placebo substitution, and 17 after variable durations of imipramine maintenance in open discontinuation. There were no behaviorally oriented interventions or instructions at any time during the acute and maintenance phases of treatment or during imipramine discontinuation. Duration of imipramine treatment, the method of discontinuation (open versus placebo substitution), or any of the 9 variables from the demographic, clinical, and open treatment domains that were entered in a Cox proportional hazard model did not predict relapse. The rate of relapse after only 6 months of treatment (10 out of 27, 37%) was identical to the rate of relapse after 12 to 30 months of treatment (9 out of 24, 37.5%). The results suggest a lack of specific protective effects beyond prophylaxis and underscore the difficulty in predicting relapse in fully remitted panic disorder with agoraphobia patients. Early detection of relapse in patients who discontinue treatment may be buy tofranil online a viable alternative to prediction.

tofranil generic 2016-04-28

Repeated buy tofranil online injections or oral administration of antidepressants: imipramine, amitriptyline and desmethylimipramine (10 mg/kg twice daily for 21 days) did not alter significantly [3H]flunitrazepam binding to frozen-thawed preincubated membranes from the brains of mice or rats.

tofranil and alcohol 2015-10-26

A review is presented of the diagnosis and drug treatment of the more common psychiatric and developmental disorders in the pediatric population. Where applicable, DSM III (Diagnostic and Statistical Manual of Psychiatric Disorders, III) criteria are utilized to describe the behavioral syndromes. The indications for usage and appropriate dosages of antipsychotics, antidepressants, anxiolytics, stimulants, and lithium are described. Those disorders discussed are attention deficit disorder Urispas Tab , conduct disorders, anxiety disorders, sleep disorders, schizophrenia, autism, Tourette's syndrome, mental retardation, depressive illness, manic depressive illness, eating disorders, and enuresis.

tofranil buy canada 2017-05-18

There is a shortage of compounds that are directed towards new targets apart from those targeted by the FDA approved drugs used against Mycobacterium tuberculosis. Topoisomerase I (Mttopo I) is an essential mycobacterial enzyme and a promising target in this regard. However, it suffers from a shortage of known inhibitors. We have previously used computational approaches such as homology modeling and docking to propose 38 FDA approved drugs for testing and identified several active molecules. To follow on from this, we now describe the in vitro testing of a library of 639 compounds. These data were used to create machine learning models for Mttopo I which were further validated. The combined Mttopo I Bayesian model had a 5 fold cross validation receiver operator characteristic of 0.74 and sensitivity, specificity and concordance values above 0.76 and was used to select commercially available compounds for testing in vitro. The Generic Levitra Reviews recently described crystal structure of Mttopo I was also compared with the previously described homology model and then used to dock the Mttopo I actives norclomipramine and imipramine. In summary, we describe our efforts to identify small molecule inhibitors of Mttopo I using a combination of machine learning modeling and docking studies in conjunction with screening of the selected molecules for enzyme inhibition. We demonstrate the experimental inhibition of Mttopo I by small molecule inhibitors and show that the enzyme can be readily targeted for lead molecule development.

tofranil brand 2015-08-16

[3H]Imipramine binding was studied in the prefrontal cortex and putamen of post-mortem brains from control and Parkinsonian subjects. Saturation and inhibition curves showed both high affinity [3H]imipramine binding related to the serotonin uptake mechanism and low affinity binding which was sodium-independent and unrelated to serotonergic uptake. After subcellular fractionation, high affinity [3H]imipramine binding sites were enriched in synaptosomal fractions. In Parkinson's disease, where brain serotonin concentrations are decreased, there was a significant reduction in the density of the high affinity binding in the prefrontal cortex and putamen while the characteristics of the low affinity binding sites remained unchanged. After subcellular fractionation of the putamen of Parkinsonian patients, the decrease in [3H]imipramine binding was found predominantly in the synaptosomal fractions. These results are consistent with a relation between the high affinity [3H] Lamictal Generic Cost imipramine binding sites and the neuronal serotonin uptake mechanism. Estimation of [3H]imipramine binding could be used as a specific marker for the study of serotonergic innervation in human post-mortem material. The reduction in the density of tricyclic antidepressant binding sites found in cortical and subcortical areas of Parkinsonian brains may be somehow implicated in the depression often seen in patients.

tofranil drug category 2016-01-20

The paper describes the effect of amantadine (AMA) supplementation on imipramine (IMI) therapy in patients (with treatment-resistant unipolar depression) who fulfilled DSM IV criteria for major depression. Twelve patients were enrolled to the study on the basis of history of their illness and therapy. Following 2 weeks of washout period, the patients were treated with IMI twice daily (100-150 mg/day) for 6 weeks, and then AMA was introduced (twice daily, 100-150 mg/day) and administered jointly with IMI for further 6 weeks. Thereafter, AMA was withdrawn, and the patients were treated with IMI alone for 2 weeks. Hamilton Depression Rating Scale (HDRS) and Beck Depression Inventory (BDI) were used to assess efficacy of antidepressant therapy. IMI changed neither HDRS nor BDI score after 3 or 6 weeks of treatment when compared with washout (before treatment). AMA supplementation significantly reduced both HDRS and BDI scores after 3- or 6-week supplementation. AMA augmentation of IMI treatment was Prevacid Dose Infants beneficial and lasted even after AMA withdrawal. Moreover, pharmacokinetic data indicate that AMA did not influence significantly the plasma concentration of the IMI and its metabolite, desipramine, in the patients during joint treatment with AMA and IMI, what suggests the lack of pharmacokinetic interaction. These results suggest that joint therapy with IMI and AMA may be successful in the treatment-resistant unipolar depression.

tofranil medicine 2016-06-12

To assess the influence of drug concentration and incubation time on the plasma lipoprotein distribution of CSA, 3H-CSA (50 to 1000 ng/ml) was incubated in human plasma for 5 to 120 minutes at 37 degrees C. To determine if LTP I facilitated TG transfer activity regulates the plasma lipoprotein distribution of CSA, 3H-Triolein (TG)- or 3H-CSA-enriched high-density lipoproteins (HDL) or low-density lipoproteins (LDL) were incubated in T150 buffer (50 mM Tris-HCl, 150 mM NaCl, 0.02% Sodium Azide, 0.01% Disodium EDTA), pH 7.4 Flagyl Missed Dose which contained a 3H-Triolein (TG) or 3H-CSA-free lipoprotein counterpart +/- exogenous LTP I (1.0 microg protein/ml) or in delipidated human plasma which contained 1.0 microg protein/ml of endogenous LTP I for 90 minutes at 37 degrees C. These experiments were repeated in the presence of a monoclonal antibody TPI (15 microg protein/ml) directed against LTP I.

tofranil drug interactions 2016-06-20

The role of endogenous enkephalins in behavioural control in mice was investigated by i.v. injection of RB 101 (N-[(R,S)-2-benzyl-3[(S)(2-amino-4- methylthio)butyl dithio]-1-oxopropyl]-L-phenylalanine benzyl ester). RB 101 is a recently reported systemically active mixed inhibitor prodrug of the two enzymes which metabolize the enkephalins neutral endopeptidase 24.11 and aminopeptidase N. RB 101 (2.5-10 mg/kg) induced a dose-dependent long-lasting hyperlocomotion and attenuated the conditioned suppression of motility in mice placed in an environment where they had received footshocks 24 h before. In addition, RB 101 decreased the duration of immobility in the forced swim test. All these actions of RB 101 were antagonized by the selective delta antagonist, naltrindole, supporting the preferential involvement of delta opioid receptors in these enkephalin-controlled behavioural responses. The effects induced by RB 101 were also suppressed by prior administration of the selective dopamine D1 antagonist, SCH 23390, but not by the D2 antagonist, sulpiride. Attenuation of the conditioned suppression of motility was associated with increased striatal dihydroxyphenylacetic acid (DOPAC)/dopamine (DA) and homovanillic acid (HVA)/DA ratios, both effects being antagonized by naltrindole. This latter compound is also efficient to inhibit the effect of imipramine in the Amoxil Drug Label mouse forced swim test. Taken together, these results support the occurrence of tonic and phasic controls of mood-related behaviour by endogenous enkephalins through delta and D1 receptor stimulation and suggest a possible future use of these mixed inhibitors as new antidepressants.

tofranil 50 mg 2015-07-13

The high affinity binding of [3H]paroxetine was measured in rat cerebral cortex following chronic treatment (21 days) with imipramine (5 mg/kg), trimipramine (5 mg/kg) and fluoxetine (2 mg/kg), in adult (3-4 months) or neonatal (7 days of age) rats. Tissue concentrations of serotonin and of its metabolite 5-hydroxyindole-3-acetic acid were also determined by high-performance liquid chromatography in cingulate cerebral cortex, rostral neostriatum, hippocampus and midbrain raphe nucleus region. No differences were found in any of the parameters Luvox Reviews Australia of [3H]paroxetine binding after antidepressant administration, in either adult or neonatal animals. In addition, endogenous serotonin and 5-hydroxyindole-3-acetic acid levels were not different from control values in any of the regions examined. The present study shows that the serotonin uptake recognition site is resilient to changes after chronic treatment with therapeutic doses of antidepressants, and emphasizes the potential usefulness of uptake site ligands as markers to quantify innervation densities within the brain.

tofranil reviews anxiety 2015-02-02

Major depression disorder is a significant health problem with 10-20% of all adults suffering from this disease. The underlying causes of depression are still unclear and 15% of depressed patients are resistant to all known therapies. Monoamine therapies have so far been the most successful approach for treating depression. Triple monoamine reuptake inhibitors have recently been implicated in generation of potent antidepressant activity while possibly exhibiting a Avapro Dosing Information low side-effect profile in addition to treating anhedonia. The additional, previously under-appreciated involvement of dopaminergic systems in depression prompted our efforts to develop novel asymmetric trisubstituted and disubstituted pyran derivatives as triple reuptake inhibitors. One of the lead compounds, D-142, exhibited uptake inhibition (K(i)) values of 29.3 nM, 14.7 nM and 59.3 ± 13.7 nM for norepinephrine, serotonin and dopamine transporters, respectively. Its affinity for serotonin transporter was comparable to fluoxetine, a well known SSRI. In the rat forced swimming test, compound D-142 exhibited potent antidepressant activity in the dose range tested (2.5, 5 and 10mg/kg) and was far more efficacious than the reference compound imipramine. In the mouse tail suspension test, compound D-142 reduced immobility in a dose (2.5, 5 and 10mg/kg) dependent manner, indicating a potent antidepressant effect. In locomotor activity tests, compound D-142 did not exhibit any stimulation in the same dose ranges. In the extended CNS receptors screening assay this molecule exhibited little or no non-specific interaction in the CNS, indicating high specificity for monoamine transporters. These results advance D-142 as a potential potent antidepressant.