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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:
Antidep, Antideprin, Depramine, Depranil, Deprinol, Depsonil, Ethipramine, Imavate, Imidol, Imipramin, Imipramina, Imipramini, Imipraminum, Imiprex, Impril, Janimine, Melipramin, Melipramine, Mepramin, Norfranil, Novopramine, Pinor, Primonil, Pryleugan, Talpramin, Tipramine, Tofranil mite, Tolerade, Venefon

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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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Cocaine abuse may lead to overdose (related to seizures and/or status epilepticus) and to diseases (schizophrenia, depression, and anxiety). This work was designed to study the influence of drugs used to treat psychopathologies associated with cocaine abuse on cocaine-induced seizures and mortality in mice. Fluoxetine (10, 20, 40 mg/kg), imipramine and buspirone (5, 10 mg/kg), pimozide (10, 20 mg/kg), lithium (56.3, 112.5 mg/kg), and naltrexone (25, 50 mg/kg) were administered intraperitoneally, 30 minutes prior to cocaine (90 mg/kg, ip). The animals were observed (30 minutes) to determine: latency to first seizure, number of seizures, and number of deaths after cocaine overdose. Fluoxetine, imipramine, buspirone, and pimozide had pro- or anticonvulsant effects depending on the dose. Smaller doses protected and higher doses increased cocaine-induced seizures and/or mortality. Naltrexone worsened and lithium protected against seizures. Thus, these results suggest that caution should be taken in the selection of pharmacotherapy and dosages for patients with cocaine addiction because of the possibility of potentiating cocaine toxicity.

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An antidepressant drug, imipramine, given chronically increased the social interaction between rats. A neuropeptide, vasopressin, demonstrated a similar, although weaker effect.

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The role of the serotonin receptor 4 (5-HT4R) pathway in cardiac excitation-contraction coupling (ECC) remains unclear. In the brain, induction of the calcium (Ca(2+))-binding protein p11 enhances 5-HT4R translocation and signaling and could therefore be considered as a modulator of the 5-HT4R pathway in the myocardium. p11 expression is increased by brain-derived neurotrophic factor (BDNF) or antidepressant drugs (imipramine). Thus, we investigated whether p11 regulates the 5-HT4R pathway in the heart in physiological conditions or under pharmacological induction and the effects on calcium handling.

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The catalytic activity of cytochrome P450 enzymes is known to be affected by presence of organic solvents in in vitro assays. However, these effects tend to be variable and depend on the substrate and CYP450 isoform in question. In the present study, we have investigated effect of ten water miscible organic solvents (methanol, ethanol, propanol, isopropanol, acetone, acetonitrile, dimethylsulphoxide, dimethylformamide, dioxane and PEG400) on water soluble substrates of CYP450, metoprolol and imipramine, at 0, 0.1, 0.25, 0.5, 0.75 and 1% v/v concentration in rat liver microsomes. Organic solvents studied had a concentration dependent inhibitory effect on the metoprolol and imipramine metabolism activity. Metoprolol metabolism was found to be more susceptible to the organic solvents, almost all the ten solvents had more or less inhibitory effect compared to imipramine metabolism. Except acetone, PEG400 and dimethylsulphoxide, all solvents had ~50% inhibition of total metoprolol metabolism activity, while in case of imipramine metabolism activity, only n-propanol, isopropanol and PEG400 had ~50% inhibition at 1% v/v. Interestingly, methanol, dimethylsulphoxide and acetonitrile had negligible effect on the imipramine metabolism (less than 10% inhibition at 1% v/v) while, total metoprolol metabolism activity was substantially inhibited by these solvents (MeOH 52%, DMSO 29% and ACN 47% at 1% v/v). In both cases, dioxane was found to be the most inhibitory solvent (~90% inhibition at 1% v/v).

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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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There is increasing evidence suggesting that depression is associated with a certain degree of cognitive dysfunction. However, there is still debate on whether this dysfunction is only substantially associated with the most severe forms of depression, on whether or not it decreases in parallel with clinical response, and on the role played in these changes by psychotropic medications. In order to clarify these questions, we analyzed the performance in several cognitive tasks that involved attention and working memory of 40 untreated subjects with a diagnosis of dysthymia or major depressive disorder without melancholia. The protocol used included three audioverbal tasks: vocal reaction time (VRT), inverse spelling (IS) and text repetition (TR). The protocol was also administered to 20 healthy volunteers that were used as a comparison group. The same battery of assessments was administered 2 months later to all 60 subjects. At the time of the second assessment, patients (but not healthy volunteers) were on antidepressant medication, in accordance with common clinical practice. The authors found a longer VRT in patients versus healthy volunteers at baseline. VRT did not decrease in patients that responded to treatment. However, there was an improvement in VRT in patients that took sertraline (n=16) compared to subjects taking imipramine (n=11). This fact was not attributable to differences in antidepressant response. Performance in the two other tasks was globally worse in the patient group than in the comparison group, and there was also an absence of improvement in the scores of patients who responded to treatment. However, when the sample was stratified by illness duration, individuals with less than 10 years from the first episode of depression showed a decrease in IS errors compared to the healthy volunteers. It is concluded that patients with nonmelancholic depression suffer from cognitive dysfunction, that this dysfunction persists after clinical improvement and that at least attention is influenced by the type of medication taken. Time from onset of the disorder also seems to influence changes in cognitive performance.

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Uptake of serotonin and [3H]imipramine binding were studied in parallel in the platelets of control, depressed and schizophrenic patients. In the depressed patient group, uptake of serotonin was consistently reduced while [3H]imipramine binding was only decreased in a number of these patients. In the schizophrenic group, uptake of serotonin was reduced to 62% of control with no changes in [3H]imipramine binding being observed. These data demonstrate a clear dissociation between uptake of serotonin and [3H]imipramine binding sites in human platelets. The possible functional role of these [3H]imipramine binding sites remains to be determined.

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A tricyclic antidepressant, C-labeled imipramine was synthesized by N-methylation of desipramine with 11CH3I to assist in the imaging of the human imipramine receptor by positron emission tomography. The radiochemical yield after purification of 11C-imipramine by high performance liquid chromatography was 28-63% at a specific activity of 26-53 Ci/mmol. The time required for synthesis, including purification was 30 min from the end of 11CH3I trapping. The organ distribution of 11C-imipramine was investigated in mice at various times after i.v. injection. The main accumulation of radioactivity was in the kidney, followed by the lung and the heart. In the brain, the radioactivity levels in the hypothalamus and striatum were the highest and remained constant, differentiating them from other portions of the brain. Furthermore, the result of a binding assay with 3H-labeled imipramine suggested that the regional distribution of 11C-imipramine in the same mouse brain correlated to that of the high affinity imipramine binding site.

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The biochemical mechanism of action produced by a new antidepressant pyrazidol (1,10-trimethylene-8-methyl-1, 2, 3, 4-tetrahydropyrazino[1,2-a] indole hydrochloride) includes the inhibitory influence on the neuronal uptake of norepinephrine and a reversible comparatively short-lived inhibitory effect on the MAO activity.

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Dopamine (DA) receptor sensitivity to apomorphine (APO) was assessed in the rat nigrostriatal system following chronic antidepressant treatment. Imipramine (IMI), iprindole (IPR) or vehicle was administered to rats for 10 days (10 mg/kg i.p., b.i.d.). Two and a half days after the last injection 3,4-dihydroxyphenylacetic acid (DOPAC) levels were measured in rat striata following injection of APO (50 or 100 micrograms/kg s.c.) or vehicle. In contrast with rats receiving chronic vehicle injections, rats chronically treated with IMI or IPR failed to exhibit a significant APO-induced fall in striatal DOPAC levels. Antidepressant-treated animals, however, exhibited significantly lower basal DOPAC levels than vehicle-treated rats. In an effort to localize the diminished APO response, DA autoreceptor sensitivity to APO was assessed in drug- and vehicle-treated animals. Employing gamma-butyrolactone (GBL) and a dihydroxyphenylalanine (DOPA) decarboxylase inhibitor to elevate striatal DOPA, the APO-induced reversal of DOPA elevation was used as an index of DA autoreceptor sensitivity. This GBL-stimulated in vivo tyrosine hydroxylation was similarly reversed by APO (125, 250 or 500 micrograms/kg i.p.) in IMI-, IPR- and vehicle-treated animals. In view of these findings, we propose that the blunted biochemical response to APO observed in animals pretreated with antidepressants does not originate as a result of alterations in the sensitivity of DA autoreceptors located on the striatal presynaptic nerve terminal.

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Electrogenic H(+)-ATPase was found in neurosecretory granules from bovine posterior pituitary. This enzyme was sensitive to bafilomycin, a specific inhibitor of vacuolar H(+)-ATPase, and was inactivated completely by cold treatment in the presence of MgATP and NaNO3. Immunoblot analysis showed the presence of immunologically identical polypeptides (72, 57, and 34 kDa) in the ATPases of the neurosecretory granules and chromaffin granules. The granules showed MgATP-dependent activity for 5-hydroxytryptamine (serotonin) uptake. This uptake was temperature-dependent and showed saturation kinetics (apparent Km for 5-hydroxytryptamine, 2 microM) and counter-flow. Reserpine and tetrabenazine at 1 microM inhibited the uptake, whereas imipramine at 2 microM had no effect. Dopamine, epinephrine and norepinephrine were also inhibitory. The uptake was abolished by various treatments that dissipated the electrochemical H+ gradient or inhibited the H(+)-ATPase. These results indicate that a vacuolar type H(+)-ATPase in the neurosecretory granules forms an electrochemical H+ gradient that drives 5-hydroxytryptamine uptake by a specific transport system. A similar granular fraction from the anterior pituitary had no ATP-dependent activity for 5-hydroxytryptamine uptake.

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To describe a middle-aged patient with Charles Bonnet syndrome (CBS) suffering from concurrent major depression.

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To explore the hypothesis that depressed patients with low pretreatment levels of urinary 3-methoxy-4-hydroxyphenylglycol (MHPG) respond more favorably to antidepressant drugs which act on noradrenergic neuronal systems than do patients with high MHPG levels, the authors administered 150--200 mg/day of imipramine or maprotiline to 13 depressed patients. All of the 5 patients with low pretreatment MHPG levels responded to treatment compared with 1 of the 14 patients with high MHPG levels; 4 patients dropped out of the study.

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The purpose of this study was to investigate the effects of two lipidosis-inducing drugs (the anorectic drug chlorphentermine and the tricyclic antidepressant-imipramine) upon the estrous cycle of rats and upon the morphology of the vaginal and uterine epithelia. After two weeks of continuous administration of high daily drug doses, the estrous cycle became stagnant. Ultrastructurally, the vaginal and uterine epithelia contained storage lysosomes which were filled with undigested polar lipids appearing as multilamellated material. The uterine luminal epithelium was most severely affected. The estrous cycle was abolished also by treatment with the anorexigenic drug phentermine, although this compound does not cause lipidosis. Therefore, the cessation of the estrous cycle cannot be attributed to the lipidosis as induced by chlorphentermine and imipramine; probably it is a consequence of the main actions of these psychotropic drugs. The biological basis for the exceedingly severe lipidosis in the uterine luminal epithelium is suggested to be the heavy load of polar lipids physiologically delivered to the lysosomal apparatus as long as the cycle-dependent apoptotic and autophagic processes were going on during the early period of drug treatment.

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Young male Sprague-Dawley rats were allocated to two placebo (restraint and sham transcranial magnetic stimulation), one active control (imipramine), and four transcranial magnetic stimulation groups at 1, 5, 15 and 25 Hz and 1000 stimuli each. The Porsolt Swim Test was performed on day 1 (experiment 1). In an extension (experiment 2), the treatments were repeated on days 2 through 5, and the Swim Test repeated on days 3, 5, and 7.

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tofranil overdose 2017-12-21

Patients with moderately severe depressive illness were matched for age, sex, severity of symptoms and number of previous episodes of affective illness. Eleven pairs of patients were randomly assigned to four weeks' treatment with either viloxazine (100 mg three times a day) or imipramine (50 mg three times a day). Both treatments were associated with significant reductions in Antabuse Half Dose the scores on depression rating scales. With a sequential testing plan based on repeated significance tests and formed into a skewed restricted plan, no difference in the two treatments was shown. Significantly fewer side effects were reported by patients receiving viloxazine.

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Current evidences support inflammation, oxidative and nitrogen stress, as well as brain-derived neurotrophic factor (BDNF) signaling mechanisms as important in depression pathophysiology. Tetracycline antibiotics have anti-inflammatory and antioxidant properties. Preliminary evidence indicates that minocycline has antidepressant properties. Doxycycline (DOXY) has favorable pharmacokinetic and safety profiles when compared to other tetracycline congeners. The antidepressant activity of DOXY has not been adequately investigated. This study evaluated the effects of DOXY (25 and 50 mg/kg, i.p.) on LPS-induced (0.5 mg/kg, i.p.) depressive-like Flomax Open Capsule behavior. Doxycycline was administered 30 min before LPS (pre-LPS) or 1.5 and 23.5 h following LPS (post-LPS) administration in mice. LPS-treated animals presented an increase in immobility time in the forced swimming test (FST) when compared to controls 24 h after endotoxin administration. Similarly to imipramine (IMI-10 mg/kg, i.p.), DOXY at both doses prevented and reversed LPS-induced alterations in the FST. IL-1β content was increased 24 h after LPS administration in striatum, hippocampus and prefrontal cortex. IMI and DOXY prevented and reversed LPS-induced increase in IL-1β. IMI and DOXY also prevented and reversed LPS-induced alterations in nitrite content and oxidative stress parameters (lipid peroxidation and reduced glutathione levels). Both DOXY and IMI prevented LPS-induced decrease in hippocampal BDNF levels. Taken together, our results demonstrate that DOXY is comparable to IMI in effectively ameliorate LPS-induced depressive-like behavior, providing a rationale for testing DOXY's antidepressant efficacy in humans.

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Arousal disorders, which belong to parasomnias in ICSD, have some disfunction in the process from sleep to awakenings. And the undesirable behaviors, Menosan Medicine such as wandering and screaming, are observed in the middle of awakening. Arousal disorders contain 1) confusional arousal, 2) sleepwalking, and 3) sleep terrors. Their common characteristics are the following items. 1) these symptoms frequently can be observable in infants, 2) these symptoms appear after awakenings especially from slow wave sleep, 3) the organic change has not been proven, 4) patients lose memory about the episode in the next morning, 5) natural improvement of symptoms can be expected after puberty. Confusional arousal is considered as a partial episode of sleepwalking and sleep terrors.

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The patient Detrol La Reviews was treated with imipramine.

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In confirmation of previous studies, the tricyclic agent imipramine (10.0 mg/kg) and the "atypical" agent mianserin (40.0 mg/kg) significantly increased efficiency. In analogy, the selective NE reuptake inhibitors (NARIs) desipramine (20.0 mg/kg), nortriptyline (2.5 mg/kg) and reboxetine (0.63 mg/kg) all displayed marked enhancements in efficiency. In contrast, the selective 5-HT reuptake inhibitors (SSRIs) citalopram (10.0 mg/kg), fluvoxamine (10.0 mg/kg) and paroxetine (10.0 mg/kg) all significantly decreased efficiency. The mixed 5-HT/NE reuptake inhibitors (SNRIs) venlafaxine (2.5 mg/kg, 10.0 mg/kg) and S33005 (0.16-10.0 mg/kg), likewise, did not increase efficiency. Further, the DA reuptake inhibitors (DARIs) bupropion (0.16-10.0 mg/kg) and GBR12935 (0.63-10.0 mg/kg) had no effect on DRL 72-s performance. All drug classes exerted a similar, mild inhibitory influence on food intake and locomotor behaviour. Imipramine, mianserin and NARIs markedly increased extracellular levels of Diovan Similar Drugs NE, and SSRIs elevated levels of 5-HT, while SSRIs augmented levels of both.

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At the highest dose tested, all ADs, with the exception of the MAO inhibitors, significantly reduced RWA. Both tricyclics inhibited RWA only at doses that similarly affected LOC. In contrast, Singulair 30 Mg all SSRI and reboxetine inhibited RWA at doses that left LOC unaffected.

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A significantly lower number of Bmax wasfound in patients with PMS as compared Duphaston 10mg Tablets to controls, but no correlation between platelet [3H]-imipramine binding and Beck Depression Inventory scores was found.

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Drugs with affinity for phospholipids, such as chlorpromazine, verapamil, tetracaine and imipramine, were found to inhibit accurate transcription from adenovirus 2 major late promoter in a nuclear extract of Ehrlich ascites tumor cells. The transcription activity of the Antabuse Medicine nuclear extract inhibited by chlorpromazine was restored by addition of acidic phospholipids. The nuclear extract was also shown to lose transcription activity when treated with phospholipase A2. Chlorpromazine was found to inhibit transcription at the step of initiation, not elongation. Moreover, it did not affect the activity of purified RNA polymerase II, suggesting the interaction of phospholipids with transcription factors in the nuclear extract. Some transcription factors in the nuclear extract were found to have affinity for cardiolipin, and were precipitated with excess cardiolipin. The transcription factors precipitated with cardiolipin could be solubilized with guanidine hydrochloride, and restored the transcription activity of the cardiolipin-treated nuclear extract.

tofranil and alcohol 2016-08-15

The authors report three cases of panic disorder with agoraphobia Combivir Tablets Price in children, with characteristic panic attacks, separation anxiety, and fear and avoidance of crowds and public places. The panic and agoraphobic symptoms responded to medications effective with agoraphobic adults, i.e., imipramine and alprazolam.

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In the first experiment the never-medicated depressed patients exhibited fewer platelet [3H]imipramine binding Paxil 30mg Generic sites than did the comparison subjects. In the second experiment the drug-free depressed patients had fewer platelet binding sites for both [3H]imipramine and [3H]paroxetine than did the comparison subjects.

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Since there exist conflicting results with regard to the possible effect of aging on platelet [3H]-imipramine binding, taken as a peripheral marker of the serotonin (5-HT) transporter, we reinvestigated this matter by comparing the binding of the more selective ligand [3H]-paroxetine in 20 aged and 23 young subjects. The results showed that neither the maximum binding capacity nor the dissociation constant (Kd) were significantly different in the two groups. When the subjects were compared according to sex, the young females revealed a statistically significant lower Kd than the males, while the contrary was true for the aged females. The Kd was significantly and negatively correlated to age in males. In addition, a significant age x gender interaction was also observed. Therefore, the sex of a subject would seem to provoke significant age-related changes in the Kd of [3H]-paroxetine binding to platelet membranes. This might indicate modifications in the 5-HT transporter that could form the basis of a sex-related difference in vulnerability to disorders, such as depression, where a dysfunction at this level is hypothesized.

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Alprazolam is a triazolobenzodiazepine which is related to diazepam and other 1,4-benzodiazepines, and has a similar pharmacological profile. Relative to the newer benzodiazepines, alprazolam has an intermediate half-life of 10 to 12 hours in healthy young subjects. In placebo-controlled and double-blind comparative trials in patients with anxiety, alprazolam was of comparable efficacy to diazepam and generally caused a lower incidence of drowsiness. Alprazolam has antidepressant activity and has been shown to be similar in efficacy to imipramine in the treatment of unipolar depression. Thus, alprazolam may be particularly useful in patients with mixed anxiety/depression. However, its general acceptance as an antidepressant awaits further studies.

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The phosphorylation of substrate proteins by protein kinases plays a key role in signal transduction and function of neurons. Protein kinases have been associated with several physiological and pathological states including depression. The aim of the present study was to investigate the effect of imipramine and electroconvulsive treatment (ECS), both clinically effective treatments of depression, on the activity of calcium/calmodulin dependent protein kinase II (CaM-KII) in the hippocampus. Our results indicate that repeated (but not acute) imipramine and ECS administration significantly decreased CaM-KII activity by 65 and 70%, respectively, in the soluble fractions from hippocampus. This decreased enzyme activity was accompanied by a proportional decrease (60-70%) of the amount of a-CaM-KII in the same fraction. A single and repeated administration of imipramine produced a significant increase in the activity of CaM-KII (50 and 337%, respectively) in the particulate fraction from hippocampus. Similarly, a single and repeated ECS produced an increase in the enzyme activity by 22 and 240%, respectively. The amount of a-CaM-KII in the particulate fraction was not significantly affected by repeated antidepressant administration. It is postulated that changes in CaM-KII activity following chronic antidepressant treatment might represent and important step in expression of its antidepressive action.

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Little is known about the effects of non-MAOI antidepressants on cognitive functions, despite their wide application to ambulant patients. Evidence from studies involving healthy volunteers suggests that differences exist between drugs, with imipramine, amitriptyline and mianserin being associated with the most marked detrimental effects. However, these findings have generally not been supported by the few studies using clinical populations, for which improvements in cognitive functions are often recorded following treatment. The reasons for this discrepancy are discussed, and the need for further research suggested.