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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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Pinealectomy and reserpine advanced the reorganization of the circadian rhythm of motor activity of rats following a ten-hour shift in the photoperiod. Bilateral electrolytic lesion of the hypothalamic suprachiasmatic nuclei and administration of the antidepressant drug, imipramine, on the contrary, delayed the rhythm change. The results suggest a possible antagonistic reciprocal relationship between the pineal gland and the main pacemaker, whose balance causes a gradual adaptation of animals to the changing environment. Fast reorganization of motor activity at pineal dysfunction or under the influence of depressogenic drugs could cause desynchronization and psychiatric disorders in a form of depression.

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The effects of imipramine (single dose of 100 mg orally) and lofepramine (single dose of 140 mg orally) in comparison to placebo on the EEG power spectra were examined in 24 non-selected healthy male volunteers. All subjects received the three drugs in a completely counterbalanced sequence. On the basis of their relative alpha-intensity the Ss were divided in two groups of 12 Ss each (high and low alpha-intensity). Two-way analyses of variance were computed for the absolute power in the alpha-, beta-, delta- and theta-frequency-bands. Imipramine increased the intensity of the delta-, theta- and beta-frequency-bands and decreased the power in the alpha-band. Lofepramine increased the intensity of the beta-band. The effects of imipramine and lofepramine are dependent on the relative power in the alpha-band of the Ss.

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The cardiovascular effects and toxicity of tricyclic antidepressants (TCAs) have been well documented in medical literature. The most common manifestation of such effects is slowing of intraventricular conduction, manifested by prolonged PR, QRS and QT intervals on the standard electrocardiogram (ECG) and postural hypotension. In contrast to TCAs, selective serotonin reuptake inhibitors (SSRIs), including fluoxetine and citalopram, are considered to cause less effect on cardiac impulse conduction. In addition, these compounds induced significantly less anticholinergic, antihistaminergic and cardiotoxic side-effects than TCAs. However, there is an increasing number of case reports on dysrhythmias, like atrial fibrillation or bradycardia and syncope associated with fluoxetine and another SSRI treatment and overdose. Although such reports have not been common, they do raise concerns. In cardiac tissues isolated from canine, rabbit, rat and guinea pig hearts we have found that fluoxetine and citalopram inhibited cardiac Na+ and Ca2+ channels. These direct cardiac electrophysiological effects were similar to those of observed for tricyclic antidepressants clomipramine and imipramine. The inhibition of cardiac Ca2+ and Na+ channels by fluoxetine may explain most cardiac side-effects observed occasionally with the drug and mild but significant bradycardia reported during chronic treatment. Our results suggest that fluoxetine and citalopram may have antiarrhythmic (class I + IV type), as well as proarrhythmic properties (due to impairment of atrioventricular or intraventricular conduction and shortening of repolarization). Taking all these into consideration, in depressed patients having also severe cardiac disorders, ECG control may be suggested during fluoxetine and probable another SSRI therapy. The primary goal of this review is to compare these direct cardiac effects of fluoxetine and citalopram to those of previously reported for TCAs. This paper also summarizes the recently observed effects of fluoxetine apparently not related to the blockage of 5-HT transporter based on literature.

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Paroxetine increases serotonergic neurotransmission by inhibiting presynaptic reuptake of serotonin (5-hydroxytryptamine; 5-HT) and thereby increasing the level of the neurotransmitter at the synaptic cleft. In vitro, it is a more potent inhibitor of serotonin uptake than the selective serotonin reuptake inhibitors (SSRIs) Citalopram, fluvoxamine and fluoxetine. Paroxetine was more potent than sertraline in one study that compared mean inhibition constants for serotonin uptake, but not in another study that compared the concentrations required to inhibit serotonin uptake by 50%. In contrast to the tricyclic antidepressants, paroxetine has little effect on the uptake of dopamine or noradrenaline (norepinephrine) in vitro. It has negligible affinity for αr(1-), αr(2-) and βr-adrenoceptors, dopamine D(1) and D(2) receptors, hi starnine H(1) receptors and serotonin 5-HT(1A), 5-HT(2A) and 5-HT(2C) receptors. However, paroxetine does have weak affinity for muscarinic cholinergic receptors. As shown in rats, paroxetine appears to indirectly activate somatodendritic 5-HT(1A) autoreceptors when initially administered, thereby inhibiting firing of 5-HT neurons and release of serotonin. This may explain why the onset of therapeutic effect of paroxetine is delayed. However, repeated administration of paroxetine causes adaptive changes in synaptic serotonergic receptors, including a decrease in the responsiveness of somatodendritic and terminal serotonin autoreceptors. Central βr-adrenoceptors are not down-regulated by administration of paroxetine to rats. Various studies in healthy volunteers without sleep disorders or volunteers reporting poor sleep have indicated that paroxetine disturbs normal sleep patterns by reducing rapid eye movement (REM) sleep time and lengthening REM latency. The effect of paroxetine on sleep in patients with panic disorder has not been determined, but in patients with depression the drug improves subjective quality of sleep. In electroencephalographic studies in healthy volunteers, administration of a single dose of paroxetine 30mg produced changes indicative of a sedative profile, whereas administration of 70mg produced changes indicative of activating properties. No significant impairment of psychomotor function was observed after administration of single or multiple doses of paroxetine 20 or 30mg to healthy volunteers or patients with depression. The sedation and impairment of psychomotor function caused by haloperidol, amobarbital, oxazepam or alcohol (ethanol) were not potentiated by the administration of paroxetine 30mg. In contrast to amitriptyline 150 mg/day or doxepin 150 mg/day, 2 to 6 weeks' treatment with paroxetine 20 or 30 mg/day did not produce clinically significant haemodynamic or electrophysiological effects on cardiac function in healthy volunteers or patients with depression. Fewer adverse cardiac effects were reported by paroxetine than nortriptyline recipients in a study in patients with depression and ischaemic heart disease. The anxiolytic activity of paroxetine has been demonstrated after 7 or 21 days' administration in several rodent models.

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A participation of neuronal and tissue uptake mechanism in responses to periarterial electrical sympathetic nerve stimulation (ES) and intra-arterial applications of norepinephrine (NE) was investigated in the isolated and perfused canine ophthalmic arteries (OA), using key pharmacological drugs such as imipramine, tyramine, cocaine, cortisol and diltiazem. Results were as follows: (1) NE, KCl and ES induced marked vasoconstrictions in a dose- and frequency-related manner, but tyramine induced only a slight constriction even at large doses; (2) cortisol, an uptake2 blocker, did not significantly modify KCl- and ES-induced vasoconstrictions, but significantly enhanced NE-induced responses; (3) small doses of imipramine, a neuronal uptake1 blocker, did not modify NE-induced vasoconstrictions, but large doses decreased them. On the other hand, the ES-induced response was slightly increased by a relative small dose of imipramine; (4) cocaine, another uptake1 blocker, slightly enhanced NE- and ES-induced responses; (5) ES-induced response was reduced by not only diltiazem, but also Ca2+-free solution with EGTA (1 mM l-1). The NE-induced response was not affected by diltiazem (Ohkubo and Chiba, 1987, Exp. Eye Res. 45, 263-70), and slightly but significantly depressed by Ca2+-free solution with EGTA. These results suggest that tissue and neuronal uptake mechanisms exist in responses to ES and NE1, the response to ES was markedly dependent on Ca2+ influx to the cell membrane2, and exogenous NE may induce Ca2+ movement mainly from the intracellular store site.

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Beyond the current hypothesis of depression, several new biological substrates have been proposed for this disorder. The present study investigated whether the anti-inflammatory drugs celecoxib and piroxicam have antidepressant activity in animal models of depression. After acute administration, we observed antidepressant-like effects of celecoxib (10 mg/kg) and piroxicam (10 mg/kg) in the modified forced swim test in rats. Piroxicam increased serotonin and norepinephrine levels in the hippocampus. Prolonged (21-day) treatment with celecoxib (10 mg/kg) and piroxicam (10 mg/kg) rescued sucrose preference in a chronic mild stress model of depression. Additionally, the chronic mild stress-induced reduction of hippocampal glutathione was prevented by treatment with celecoxib and piroxicam. Superoxide dismutase in the hippocampus was increased after chronic mild stress compared with the non-stressed saline group. The non-stressed celecoxib and piroxicam groups and stressed piroxicam group exhibited an increase in hippocampal superoxide dismutase activity compared with the stressed saline group. Lipid hydroperoxide was increased in the stressed group treated with vehicle and non-stressed group treated with imipramine but not in the stressed groups treated with celecoxib and piroxicam. These results suggest that the antidepressant-like effects of anti-inflammatory drugs might be attributable to enhanced antioxidant defenses and attenuated oxidative stress in the hippocampus.

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This paper describes a procedure for the synthesis and application of a citalopram-derived affinity resin in purifying the 5HT-reuptake system from human blood platelets. A two-step scheme has been developed for partial purification, based on wheat germ agglutinin-lectin (WGA) affinity and citalopram affinity chromatographies. Upon solubilization of the carrier with 1% digitonin, a 50-70-fold increase in specific [3H]imipramine binding activity with a 70% recovery could be accomplished through WGA-lectin chromatography. The WGA pool was then subjected to affinity chromatography on citalopram-agarose. At least 90% of the binding capacity adsorbed to the column. Specific elution using 10 microM citalopram resulted in a 22% recovery of binding activity. A 10,000-fold overall purification was obtained by using this two-step procedure. Analysis of the fractions on SDS-PAGE after 125I labeling revealed specific elution of 78- and 55-kDa proteins concomitant with the appearance of [3H]imipramine binding activity. The pharmacological profile of the partially purified reuptake system correlated well with that derived from the crude membrane-bound reuptake system, suggesting a copurification of the 5HT binding activity and [3H]imipramine binding activity.

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D-cycloserine (DCS), a partial N-methyl-D-aspartate (NMDA) agonist, facilitates the extinction of conditioned fear in animals and promotes the efficacy of exposure-based therapies in humans. The current study examined whether pre-exposure to the antidepressant imipramine affects the enhancement of extinction by DCS.

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The effects of tricyclic antidepressants drugs (TCA) amitriptyline, imipramine and nortriptyline, on purified Electrophorus electricus (L.) acetylcholinesterase (AChE; acetylcholine hydrolase, EC were studied using kinetic methods and specific fluorescent probe propidium. The antidepressants inhibited AChE activity by a non-competitive mechanism. Inhibition constants range from 200 to 400 microM. Dimethylated amitriptyline and imipramine were more potent inhibitors than the monomethylated nortriptyline. Fluorescence measurements using bis-quaternary ligand propidium were used to monitor ligand-binding properties of these cationic antidepressants to the AChE peripheral anionic site (PAS). This ligand exhibited an eight-fold fluorescence enhancement upon binding to the peripheral anionic site of AChE from E. electricus (L.) with K(D)=7 x 10(-7)M. It was observed that TCA drugs displaced propidium from the enzyme. On the basis of the displacement experiments antidepressant dissociation constants were determined. Similar values for the inhibition constants suggest that these drugs have similar affinity to the peripheral anionic site. The results also indicate that the catalytic active center of AChE does not participate in the interaction of enzyme with tricyclic antidepressants. These studies suggest that the binding site for tricyclic antidepressants is located at the peripheral anionic site of E. electricus (L.) acetylcholinesterase.

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To improve a gas chromatography/electron impact ionization mass spectrometry (GC/MS) method for determining the concentration of procaterol in human plasma.

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For a rational treatment approach, further studies are needed, particularly in depression and conduct disorder; psychosocial-environment contributions and possible biological markers should be investigated in order to identify children who require psychopharmacological treatments and those who will respond to psychosocial interventions or the combination of both. Symptoms targeted to require pharmacotherapy and symptoms targeted to respond to psychosocial interventions have to be identified.

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Lennon and Carnegie have proposed that the clinical symptomatology of experimental allergic encephalitis (EAE), an acute autoimmune demyelinating disease, may be due, at least in part, to an immune response directed against CNS serotonin receptors. To test this hypothesis we treated strain 13 guinea pigs, which had been immunized with guinea pig basic protein (GPBP) in complete Freund's adjuvant (CFA), with drugs known to affect central nervous system (CNS) serotonin levels. These drugs included imipramine hydrochloride, tryptophan and carbidopa which increase CNS serotonin and reserpine which decreases it. Five experiments were conducted in which all immunized animals treated with saline only died, as expected, as did all animals treated with reserpine which died even more quickly. A significant proportion of animals treated with the other three drugs, alone or in combination, survived or lived longer than controls. We conclude that survival of animals with EAE is enhanced by treatment with these drugs. We suggest that further evaluation of a possible blockade in serotonin transmission in EAE and multiple sclerosis (MS) is warrented, since, if such a blockade were demonstrated, it is possible that these drugs may have potential for therapeutic efficacy in patients with MS.

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The effects of several neurotransmitters on prostaglandin (PG) D2-induced cataleptic behavior in rats were investigated by the high bar test. Intracerebroventricular administration of PG D2 elicited cataleptic behavior in a dose-dependent manner without producing a marked change in spontaneous motor activity. The incidences of cataleptic behavior were 20% and 100% at doses of 2 nmol and 50 nmol of PG D2, respectively. Intraperitoneal pretreatment with L-DOPA (100 mg/kg), apomorphine (1 mg/kg), amantadine (0.2 mg/kg), atropine (0.5 mg/kg) or p-chlorophenylalanine (300 mg/kg) significantly decreased the cataleptic behavior induced by 50 nmol of PG D2. Conversely, simultaneous treatment with 5-hydroxy-L-tryptophan (30 mg/kg), 5-methoxy-N,N-dimethyltryptamine (5 mg/kg), imipramine (20 mg/kg) or clomipramine (10 mg/kg) markedly increased the cataleptic behavior induced by 2 nmol of PG D2. Propranolol (10 mg/kg) and phenoxybenzamine (10 mg/kg) did not affect the induction of cataleptic behavior by either 2 nmol or 50 nmol of PG D2. These results suggest that PG D2 might be involved in inducing cataleptic behavior by modulating serotonergic, cholinergic and dopaminergic systems.

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New uses are still being discovered for a number of psychotropic agents that have been available for some time. Among the more important recent discoveries are the efficacy of the tricyclic antidepressants for panic disorder and agoraphobia with panic attacks; the use of the monoamine oxidase inhibitors for the above disorders and for atypical depression and hysteroid dysphoria; the use of propranolol for anxiety disorders and for uncontrollable violent outbursts; the antianxiety and antipanic effects of clonidine; and the usefulness of lithium in treating schizophrenia and schizoaffective disorder and for emotionally unstable character disorders. In addition to strengthening the therapeutic armamentarium, the author says, the discovery of new drug response patterns helps generate or strengthen hypotheses about the pathophysiology of various psychiatric disorders.

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We investigated the incidence of convulsions observed during treatment with antidepressants. Among the patients observed in this department, 582 cases received the antidepressants for more than 2 months were selected. 8 cases (1. 4%) of these patients showed convulsions. Detailed evaluation revealed a high incidence of convulsions occurred in patients who were administered more than two kinds of antidepressants. Among tetracyclic antidepressants, viz. maprotiline and clomipamine, and tricyclic antidepressants, viz. amitriptyline indicated a high incidence rate of convulsions. On the contrary, mianserin and imipramine tended to show a lower incidence. In 4 cases, acute toxic symptoms were seen before the convulsion, and the serum concentration of antidepressants in these patients was high. If toxic symptoms and elevated level of serum concentration are useful indicator for prediction of convulsion by treatment with antidepressants, these might be a noteworthy clinical findings. At present, if doctors are required to administer more than moderate amounts of more than two antidepressants, careful administration is desirable. With the accumulation of such cases, it is necessary to obtain further evaluation of the relationship between toxic symptoms and serum concentration of antidepressants.

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The binding characteristics of [3H]-imipramine in slide mounted tissue sections of rat forebrain have been studied to ascertain the optimal binding conditions for labeling the sites prior to autoradiographic localization. The conditions for the experiments and the kinetics of the imipramine binding correspond reasonably well with those used in membrane preparations to initially define the imipramine binding site. Subsequent labeling of sections, using these parameters, allowed the autoradiographic localization of high concentrations of imipramine binding sites in such areas as the cerebral cortex, striatum, and several limbic and visual system structures. In addition, there was a marked overlap between regions demonstrating imipramine binding and areas known to be innervated by serotonergic neurons. This study outlines the potential sites of action of imipramine in the brain and defines areas for future investigations which attempt to localize brain regions involved in the etiology of depression and areas involved in the side effects of antidepressant drug therapy.

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

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Ethanolic- and isopropanolic-aqueous extracts of Cimicifuga racemosa are used for the treatment of climacteric complaints. As hot flushes and psychic complaints seem to be special targets for Cimicifuga extracts in clinical studies, these parameters were studied in experimental animals. Hot flush equivalents were measured in castrated rats as a quick increase in peripheral temperature with the aid of a transmitter implanted subcutaneously on the ventral side. The hot flush equivalents proved to respond to estrogen and the antidopaminergic drug veralipride but they were also reduced very effectively by Cimicifuga extract BNO 1055 (which is contained in Klimadynon/Menofem). In addition, an ethanolic-aqueous extract of C. racemosa was studied in the tail suspension test (TST), a behavioural test indicative for antidepressant activity. A significant decrease of the period of immobility was observed after treatment with 30 mg/kg body weight (bw) imipramine or with 50 or 100 mg/kg bw Cimicifuga extract. These findings in pharmacological tests-a reduction of the frequency of hot flush equivalents and hints on antidepressant activity of Cimicifuga extracts-are in good agreement with the therapeutical responses in climacteric women.

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Tests conducted on isolated and denervated preparations of the rat seminal duct brought evidence that tricyclic antidepressants (melipromine, noverile and azaphen) when employed in low concentrations (1-10(-9) g/ml) produced an adrenosensitizing effect. Denervation with the subsequent block by desoxycorticosterone (1-10(-5) g/ml) of exteraneuronal amine uptake did not alter the position, shape and inclination of the "concentration-effect" noradrenaline curves received in the presence of noverile and cocaine. It is believed that there exists a predominance of the postsynaptic mechanism of the aminosensitizing action of tricyclic antidepressants on the smooth muscle organ.

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The diffusional transport of a series of small drug molecules (<400 Da) in agarose gel with and without kappa-carrageenan (a negatively charged polysaccharide) is studied. The drug molecules have amphiphile character, the hydrophilic part being a tertiary amine which is the same in all six drugs. The difference in structure resides in the hydrophobic part which give these molecules different properties such as a difference in CMC-values (critical micelle concentration). The transport studies show that the apparent diffusion coefficients (Dapp) of all the drugs in 1% (w/w) agarose gel are almost identical and with a value similar to that in water. These results were anticipated because of the small size of the drugs, the low concentration of agarose, and the lack of interaction between the diffusant and the polymer. In agarose gels also containing 0.02% (w/w) kappa-carrageenan, however, the Dapp-values are significantly decreased for all drugs, except for lidocaine. This lowering of the Dapp is ascribed to the interaction between the drug molecules and kappa-carrageenan. The Dapp-values of the drugs in the gel system containing kappa-carrageenan correlate well with the adsorption isotherms of the same drugs in the drug/kappa-carrageenan/water system obtained previously [1] and the Dapp-values follow the order: chlorpromazine

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A number of epidemiological studies have established a link between insulin resistance and the prevalence of depression. The occurrence of depression was found to precede the onset of diabetes and was hypothesized to be associated with inherited inter-related insufficiency of the peripheral and central insulin receptors. Recently, dicholine succinate, a sensitizer of the neuronal insulin receptor, was shown to stimulate insulin-dependent H2O2 production of the mitochondrial respiratory chain leading to an enhancement of insulin receptor autophosphorylation in neurons. As such, this mechanism can be a novel target for the elevation of insulin signaling.

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Liquid-liquid chromatography based on the ion-pair partition technique gives separation systems of high efficiency when silica micro-particles are used as the support for the stationary phase. With 10-mum particles, plate heights of the order of 40-70 mum have been achieved with a linear velocity of 0.25 cm/sec. The retention in ion-pair partition systems is determined by the nature and concentration of the counter ion, and the properties of the mobile phase also have a major influence. It is often possible to predict the selectivity, and this can be controlled by varying the composition of the mobile phase. This paper describes the application of ion-pair partition chromatography to the bioanalysis of drugs, drug metabolites and biogenic substances. Typical counter ions in the stationary phase were methanesulphonate and perchlorate for ammonium compounds and tetrabutylammonium for the separation of organic anions. Determinations by liquid chromatography were demonstrated for quinidine and dihydroquinidine, metanephrine and normetanephrine and for imipramine and its demethyl metabolite in plasma. A quaternary ammonium compound, QX-572, was determined in urine and chromatograms are shown for the isolation of indoleacetic and hydroxyindoleacetic acid in urine. The methods have been used in routine analysis. Ultraviolet detection has permitted the determination of highly absorbing compounds down to the 10-ng level in plasma and urine.

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Our findings suggest that Aβ metabolism may be affected in depression; these findings also possibly answer the question of why even early-onset depression is a risk factor for developing Alzheimer's disease.

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The present study investigated the potential of therapeutic drug monitoring data to document pharmacokinetic drug interactions with psychotropic medication, both in terms of methodology and applicability. It focused on 105 patients exposed to one of five agents known for their capacity to induce (phenytoine, phenobarbital, and carbamazepine) or to inhibit (thioridazine and levomepromazine) the metabolism of psychotropic drugs. These patients were matched by gender, age, and monitored psychotropic medication to 105 patients randomly selected from a pool of subjects nonexposed to target comedication. Such a paired approach was shown to be effective in reducing variability for a majority of substances. Power analysis suggested that eight to 10 pairs of exposed and nonexposed patients would effectively allow the detection of twofold effects of interacting substances. In keeping with the literature, analysis of the ratios of dose-normalized exposed to nonexposed concentrations indicated that phenothiazine comedication led to significantly higher concentrations of desmethylated metabolites but not parent compounds, when clomipramine, imipramine, or amitriptyline were administered. A similar, as yet undocumented interaction was observed for the tetracyclic antidepressant mianserine. In contrast, the present study revealed that maprotiline concentrations were increased, but its metabolite was largely unaffected by phenothiazine comedication. Increased concentrations were also observed for moclobemide, but not citalopram or its metabolite. In addition to its long recognized capacity to decrease haloperidol concentrations, carbamazepine was shown to induce the metabolism of clopenthixol and possibly flupenthixol. The consistency of such a picture substantiates the need to consider therapeutic drug monitoring databases as cost-effective and reliable tools for postmarketing surveillance.

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Human SK-N-SH neuroblastoma cells accumulate and store the adrenal imaging agent metaiodobenzylguanidine (MIBG) with minor involvement of specialized cytoplasmic storage granules (Smets LA et al., Active uptake and extravesicular storage of meta-iodo-benzylguanidine in human neuroblastoma SK-N-SH cells. Cancer Res 49: 2941-2944, 1989). In the present study the mechanism of extravesicular MIBG retention was investigated and compared with granular storage of MIBG and norepinephrine (NE) in PC-12 pheochromocytoma cells. SK-N-SH cells concentrated both MIBG and NE by neuron-specific Uptake-1 but long-term retention was only observed with MIBG. Retention of accumulated NE was, however, promoted by inhibition of intracellular catecholamine degradation with pyrogallol. Drug release by controlled cell permeabilization and by KCl-induced exocytosis indicated that MIBG was mainly stored as freely diffusible, cytoplasmic molecules. SK-N-SH cells were depleted from stored MIBG by the Uptake-1 inhibitor imipramine but poorly so by the granule-depleting drug reserpine. Conversely, PC-12 cells were depleted by reserpine but insensitive to imipramine. The data suggest that extravesicular retention of MIBG in SK-N-SH cells is not based on intracellular sequestration but is solely due to efficient re-uptake of accumulated drug after leaking from the cells. The accumulation of MIBG in SK-N-SH cells, reflecting "pure" Uptake-1, appears to be a powerful system for exploring various cellular and molecular aspects of catecholamine uptake.

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In this study, a platinum wire coated with poly(3,4-ethylenedioxythiophen) was used as an electro-assisted solid-phase microextraction fiber for the quantification of tricyclic antidepressant drugs in biological samples by coupling to GC employing a flame ionization detector. In this study, an electric field increased the extraction rate and recovery. The fiber used as a solid phase was synthesized by the electropolymerization of 3,4-ethylenedioxythiophen monomers onto a platinum wire. The ability of this fiber to extract imipramine, desipramine, and clomipramine by using the electro-assisted solid-phase microextraction technique was evaluated. The effect of various parameters that influence the extraction efficiency, which include solution temperature, extraction time, stirring rate, ionic strength, time and temperature of desorption, and thickness of the fiber, was optimized. Under optimized conditions, the linear ranges and regression coefficients of calibration curves were in the range of 0.5-250 and 0.990-0.998 ng/mL, respectively. Detection limits were in the range of 0.15-0.45 ng/mL. Finally, this method was applied to the determination of drugs in urine and wastewater samples and recoveries were 4.8-108.9%.

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Antidepressants (AD) need to be chronically administered (weeks to months) to provide beneficial effects. Evidence suggests that combined administration of inhibitors of monoamine reuptake and phosphodiesterase type 4 allows a highly effective therapeutic action. Also, this coadministration more rapidly boosts the cyclic adenosine monophosphate (cAMP) pathway, which is normally activated during chronic treatment of single compounds. Little is known, however, about how this augmentation therapy affects the core mechanism of glutamatergic plasticity. We therefore investigated how in vivo combinational subchronic rolipram and imipramine (scRI) treatment affects depressive behavior, cAMP-dependent transcription, and glutamatergic transmission in the hippocampus, a region critically implicated in depression.

tofranil medicine

3-Cyano-imipramine (cianopramine) is a potent and selective inhibitor of serotonin uptake into synaptosomes. In a double-blind trial, 60 patients with various types of depression fulfilling the DSM-III criteria of depressive episodes were treated with either cianopramine (n = 20, mean daily dose 3.3 +/- 0.6 mg) amitriptyline (n = 20, mean daily dose 86.4 +/- 21 mg) or placebo (n = 20) orally. According to the ratings of the Hamilton Scale of Depression and clinical global evaluations, both active drugs showed statistical superiority over placebo (P less than 0.02). The frequencies of anticholinergic side effects in the cianopramine group were comparable to those of the placebo group and were less than in the amitriptyline group. The findings suggest that cianopramine is a promising new antidepressant.

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Ziprasidone is a novel antipsychotic agent with a unique combination of pharmacological activities at human receptors. Ziprasidone has high affinity for human 5-HT receptors and for human dopamine D(2) receptors. Ziprasidone is a 5-HT(1A) receptor agonist and an antagonist at 5-HT(2A), 5-HT(2C) and 5-HT(1B/1D) receptors. Additionally, ziprasidone inhibits neuronal uptake of 5-HT and norepinephrine comparable to the antidepressant imipramine. This unique pharmacological profile of ziprasidone may be related to its clinical effectiveness as a treatment for the positive, negative and affective symptoms of schizophrenia with a low propensity for extrapyramidal side effects, cognitive deficits and weight gain.

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tofranil street drug 2015-01-03

There is a need for safe effective alternatives to benzodiazepines in the treatment of panic disorder. Buspirone, a new nonbenzodiazepine anxiolytic, is compared to imipramine and placebo in the treatment of panic disorder in an 8 week double-blind controlled study of 52 randomly assigned patients. Weekly assessments were made using the Hamilton Anxiety Scale, the Sheehan Clinician Rated Anxiety Scale, the Sheehan Patient Rated Anxiety Scale, the Phobia Scale, the Disability Scale, the Hamilton Depression Scale, the Montgomery Asberg Depression Scale, the Investigator Rated Global Improvement Scale and the Patient Rated Global Improvement Scale. Preliminary results of repeated measures Anovas are reported. Imipramine was superior to placebo on many of the outcome measures. Imipramine was superior to buspirone on the Patient Rated Global Improvement Scale and buy tofranil on the Investigator Rated Global Improvement Scale, but not on other measures. Although buspirone appeared to be more effective than placebo, differences were not statistically significant. Some buspirone patients did very well compared to others, suggesting a possible bimodal distribution of response. Patients on buspirone had fewer and less disruptive side effects than those on imipramine.

tofranil maximum dosage 2015-07-22

Seasonal rhythmicity in the occurrence of acute depressive episodes and the therapeutic efficacy of light exposure suggest the possible involvement of the pineal gland or other biological oscillators in the pathophysiology of depressive illness. We have performed studies to clarify whether different light/dark (LD) cycle schedules may induce changes in the biochemical targets of antidepressants in the rat CNS. In particular, we have investigated the effect of short- (LD 8:16) or long-day (LD 14:10) photoperiods on different biochemical parameters of serotonergic neurons. A significant increase in the density of [3H]imipramine ([3H]IMI) binding and in the Vmax of 5-[3H]hydroxytryptamine (5-[3H]HT) uptake was found in the hypothalamus of LD 8:16-with respect to LD 14:10-exposed rats, whereas no difference was found in the kinetic properties of postsynaptic 5-HT receptors and in 5-HT metabolism in the hypothalami and cerebral cortices of rats exposed to the two different photoperiods. A seasonal rhythm of [3H]IMI binding sites and 5-HT uptake seems to exist only in certain brain areas, such as the hypothalamus, because no differences were found in the cerebral cortex of LD 14:10- and LD 8:16-accustomed rats. [3H]IMI binding and 5-HT uptake were significantly increased in the hypothalamus of rats accustomed to a light/dark-inverted cycle (DL 10:14) and killed 6 h after the stopping of lighting in comparison to rats exposed to normal LD 14:10 cycles and killed 6 h after the beginning of lighting. Therefore, a buy tofranil circadian modification of the serotonergic presynaptic sites seems to be present and related to light/dark exposure. Because the existence of endogenous compounds able to modulate [3H]IMI binding and 5-HT uptake, other than 5-HT, has been postulated in the mammalian brain, the involvement of these substances in the periodic changes observed could be suggested.

tofranil overdose 2017-01-13

Psychoactive drugs should be prescribed cautiously in patients with known narrow angles and should be buy tofranil monitored by an ophthalmologist.

tofranil 300 mg 2015-08-23

In the placebo group, 80% (12/15) of the patients relapsed compared with 18% (2/11) in the imipramine group. The Cox regression analysis showed a significant reduction in the risk of relapse of 85.6% with imipramine compared to placebo (p=.007; 95% confidence interval [CI]=24.6% to 97.2%) adjusted for the covariables. There was an 18% increase in the relapse buy tofranil rate (p=.032; 95% CI=2% to 36%) per unit increase in HAM-D score before the start of the trial; psychotic features had no significant effect (p=.794).

tofranil pm generic 2015-06-04

The effect of neuroleptics (chlorpromazine, trifluoperazine, haloperidol), antidepressants (amitryptyline, imipramine), tranquilizers (diazepam, chlordiazepoxide, benactyzine) and stimulant d-amphetamine on the domination and subordination relations formed as a result of competitive behaviour in a pair of rats was studied. The drugs in question proved to violate the set relations of domination and subordination weakening the attacking ability of dominating rats and strengthening buy tofranil the defensability of the subordinate ones. With increase of antidepressants dosage received by a subordinate rat its competing ability becomes enhanced too; this may cause a change in domination.

tofranil diet pill 2017-07-05

1 The minimal dose which significantly potentiates the hyperthermia induced by thyrotrophin releasing hormone (TRH, 40 mg/kg i.p.) in mice has been established for tricyclic and other antidepressants (imipramine, amitriptyline, clomipramine, nortriptyline, maprotiline, nomifensine, viloxazine) including a specific inhibitor of noradrenaline (NA) uptake (nisoxetine). 2 The minimal effective dose in this test has been compared with the minimal dose of the same compounds antagonizing reserpine-induced hypothermia. The ratio of the two doses for each substance indicates buy tofranil that potentiation of TRH-induced hyperthermia is, in general, the more sensitive test. 3 A correlation seems to exist between the alpha-adrenergic effect of antidepressants and the potentiation of TRH- induced hyperthermia. Those antidepressants which do not act on alpha-adrenergic systems (butriptyline, amineptine, trazodone, danitracen, fluoxetine) are inactive in this test. 4 This property may be used to select antidepressants that activate alpha-adrenoceptor systems.

tofranil generic 2016-08-12

Eighty patients with panic disorder with agoraphobia were randomly assigned, for an 8-week, double-blind dose-ranging trial, to placebo or to a weight-adjusted dose of imipramine: (low) 0.5 mg/kg per day, (medium) 1.5 mg/kg per day, or (high) 3.0 mg/kg per day. Plasma levels of imipramine and N-methylimipramine, patients' and clinicians buy tofranil ' ratings of panic and phobic symptoms, and response to treatment according to operationalized criteria were ascertained after 4 and 8 weeks.

tofranil tablets 2015-06-25

Cerebrospinal fluid (CSF) concentrations of beta-endorphin-like immunoreactivity (END-IR) were determined in 11 female and 6 male patients fulfilling the diagnostic criteria of panic disorder (PD) and in matched controls. Eleven of the PD patients had been taking moderate doses of benzodiazepines (BZD) irregularly without satisfactory effect against the panic attacks while six were totally drug-free. No medication was allowed for at least 24 hours before the lumbar puncture. In six patients a second lumbar buy tofranil puncture was performed after 2 to 3 months of treatment with imipramine or clomipramine. In PD patients, CSF levels of END-IR were significantly higher than in controls. Patients that had been taking BZD had somewhat higher concentrations of END-IR than those taking no medication; however, totally drug-free patients also displayed END-IR levels that were significantly higher than in controls. Although they effected a dramatic reduction of the panic attacks, antidepressants did not influence CSF END-IR concentrations.

tofranil syrup 2017-06-05

The unusual co-occurrence of IBS with bipolar disorder provides direct evidence to indicate that depression does not necessarily lead to an increase in the reported severity of IBS, at least in the context of bipolar disorder, and may under certain circumstances buy tofranil actually be associated with a reduction in the severity of IBS symptoms. Factors that might moderate the relationship between depression and symptom severity are discussed.

tofranil medication 2016-08-24

Results show that modafinil induced an antidepressant property in TST and this effect apparently was mediated through interaction buy tofranil with the dopaminergic (D2 receptors) system.

tofranil drug interactions 2017-07-11

The present results indicate that water deprivation is not a necessary condition to engender drinking conflict buy tofranil behavior or to obtain pharmacological effects similar to those obtained with other classical conflict procedures.

tofranil drug study 2017-10-15

Responses to imipramine in its earliest controlled trials were much larger than buy tofranil in recent antidepressant trials. Drug-placebo differences declined significantly between 1959 and 1965, with rising placebo-associated responses. Frequent failure to find superior drug-over-placebo outcomes may reflect patient characteristics and limited statistical power. Antidepressant-trial methods have become much more standardized, samples larger and more complex, and effect-sizes much smaller since the 1960s.

tofranil user reviews 2016-05-27

The current study was aimed at comparing the behavioral and biochemical (5-hydroxytryptamine and 5-hydroxyindoleacetic acid levels) effects of monoamine reuptake inhibitors (fluoxetine, venlafaxine and imipramine) in sub-chronically forced swim stressed rats. At the given doses of 10, 20 and 30 mg/kg, among aforesaid antidepressants, the imipramine treatment alone caused significant decline in the immobility time of rats (IC(50) 20 mg/kg). In the hippocampus of rats, the imipramine treatment caused significant elevation of 5-hydroxytryptamine (5-HT) whereas, the fluoxetine and venlafaxine elicited significant increase in 5-hydroxyindoleacetic acid (5-HIAA) levels. Likewise, in the plasma of rats, the imipramine treatment significantly increased the 5-HIAA levels whereas, the fluoxetine and venlafaxine treatment significantly elevate the 5-HT levels. It can therefore be inferred that the imipramine did not act like other buy tofranil monoamine reuptake inhibitors in biochemical study, which could possibly underlie its ability to be detected in forced swim test (behavioral study). Moreover, the re-uptake inhibition of 5-HT is not accountable for the antidepressant action exhibited in forced swim test.

tofranil tablet uses 2017-03-26

Pooled data were analysed from seven short-term (4 - 8 weeks) and one long-term (up to 1 year) trials comparing reboxetine with placebo, imipramine, desipramine or fluoxetine. The tolerability of reboxetine Indocin 25mg Suspension was evaluated in 2613 patients with major depression or dysthymia. Data from 1959 patients with major depressive disorder were included to assess drug efficacy. Efficacy was principally assessed using the Hamilton Depression Rating Scale (HAM-D).

tofranil generic name 2017-06-09

The induction of lipid peroxidation in hepatic microsomes of rodents Prevacid Tablets treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is well documented. The potential mechanisms involved in TCDD-induced microsomal lipid peroxidation were investigated, using selected inhibitors and free radical scavengers in vitro. Rats were treated with 40 micrograms TCDD/kg orally as a single dose. Inhibitors of phospholipase A2, including a variety of phenothiazines, dibucaine, imipramine, and verapamil, inhibited in vitro microsomal lipid peroxidation in response to TCDD administration. In addition, the lipoxygenase inhibitor quercetin, and the hydrogen peroxide scavenger aminopyrine inhibited lipid peroxidation with microsomes from TCDD-treated rats. The singlet oxygen scavenger beta-carotene, the cytochrome P-450 substrate benzphetamine, and the cyclooxygenase inhibitor indomethacin produced moderate enhancement of hepatic microsomal lipid peroxidation. The results suggest that activation of phospholipase A2 may play a critical role in the metabolic events associated with hepatotoxicity and ultimate cell death produced by TCDD. The results also support the involvement of hydrogen peroxide in TCDD-induced microsomal lipid peroxidation.

tofranil 25mg medication 2017-01-16

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, and recent Cytoxan Medication Assistance 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 tablet 2017-07-31

The effect of acute administrations of three doses of imipramine (1, 5 and 10 mg/kg s.c.), a widely used tricyclic antidepressant, on extracellular levels of serotonin (5-HT) has been studied by intracerebral microdialysis in raphe nuclei and prefrontal cortex of conscious rats. Imipramine 1 mg/kg s.c. did not change extracellular 5-HT in either raphe nuclei and prefrontal cortex. However, with the dose of 5 mg/kg s.c. imipramine induced in raphe nuclei, a brief increase of extracellular 5-HT followed by a lowering (55-65% basal release) of the neurotransmitter. The same dose of imipramine decreased (60-70% of basal value) extracellular 5-HT in prefrontal cortex. Imipramine 10 mg/kg s.c. significantly increased 5-HT levels in both raphe nuclei (190 +/- 20% above basal value) and prefrontal cortex (280 +/- 15% above basal value). Pretreatment with (-)pindolol (5 mg/kg s.c.), a non-selective 5-HT1A subtype receptor antagonist, 30 min before imipramine 5 mg/kg, modified the effect of the antidepressant: an increase, instead Feldene Medicine of a decrease, on prefrontal cortex dialysate 5-HT was observed. (-)Pindolol (10 mg/kg s.c.) increased extracellular 5-HT in both raphe nuclei (155 +/- 20% above basal value) and prefrontal cortex (160 +/- 8% above basal value). These data show that acute administration of imipramine modifies extracellular 5-HT at the level of the raphe nuclei and prefrontal cortex. 5-HT1A autoreceptors in the raphe nuclei, which this study suggests to be tonically active, may be stimulated after systemic administration of high doses of imipramine.

tofranil cost 2016-12-29

The aim of the investigation was to find out the role of noradrenergic (NE) terminals of the medial preoptic area (mPOA), in the regulation of sleep-wakefulness. Studies were conducted on free-moving adult male rats with chronically implanted cannulae in the mPOA. Sleep-wakefulness was assessed on the basis of EEG, EMG, and EOG recordings along with behavioral observations. Lesioning of catecholamine terminals (with 6-hydroxydopamine) in the mPOA produced an increase in quiet wakefulness. Prevention of NE fiber destruction, by pretreating the rats with imipramine, prevented this effect. This demonstrated that the increased quiet wakefulness produced by 6-OHDA was the result of NE fiber destruction. Changes in sleep-wakefulness were also assessed after microinjection of NE into the mPOA, in Azulfidine Y Alcohol normal and ventral noradrenergic bundle (VNA)-lesioned rats. NE administration induced sleep in VNA-lesioned rats, and arousal in normal rats. The findings suggest that the NE terminals in the mPOA, projecting via VNA, play a role in the induction of sleep.

tofranil mg 2016-04-20

A statistically significant 28% increase in the mean (+/- SD Protonix 20 Mg ) number of serotonin2 receptors (127.8 +/- 13.4 vs 99.6 +/- 11.1 fmol/mg of protein) and a 73% increase in beta-adrenergic receptor binding (14.5 +/- 1.5 vs 8.4 +/- 1.5 fmol/mg) was found in the frontal cortices of violent suicide victims compared with matched controls. No significant differences were found in the number of serotonin1 binding sites (109.5 +/- 13.4 vs 99.9 +/- 8.8 fmol/mg). We have previously reported a reduced density of presynaptic tritiated imipramine binding sites on serotonergic nerve terminals in the frontal cortices of suicide victims. These data support the hypothesis that suicide completed by violent methods is associated with reduced presynaptic serotonergic activity that has generated compensatory upregulation of the postsynaptic serotonin2 receptor sites. The increase observed in beta-adrenergic binding suggests that there may also be a concomitant reduction in presynaptic noradrenergic activity associated with suicide. If antidepressant pharmacotherapies specifically downregulate cortical beta-adrenergic and/or serotonin2 receptors in depressed subjects, as has been demonstrated in animal studies, and since these effects would be in the opposite direction of the receptor changes found in suicide victims, they may account for the therapeutic action of antidepressants on suicidal behavior and depressive disorders.

tofranil 25mg tab 2015-03-11

We examined the effects of chronic activity wheel running and antidepressant treatment on brain-derived neurotrophic factor (BDNF) messenger RNA (mRNA) in multiple brain regions-hippocampal formation (HF), ventral tegmental area/substantia nigra (VTA/SN), nucleus accumbens (NAc), and piriform cortex (PFx)-after bilateral olfactory bulbectomy (OBX). Male, Long-Evans rats (n=72) underwent either sham or OBX surgery and were randomly divided into eight experimental groups in a 2 (sham vs. OBX) x 2 (sedentary vs. activity wheel)x2 (saline vs. imipramine) factorial design. Animals were killed after 21 days of treatment. Drug x exercise interaction effects were observed for HF (P=0.006-0.023) and VTA/SN (P=0.021); exercise increased BDNF mRNA in the saline treated animals but not in the imipramine treated animals. OBX did not affect BDNF mRNA in the HF or VTA/SN (P>0.05). BDNF mRNA levels in the PFx were not altered by exercise, drug, or OBX (P>0.05). These results suggest that the effect of exercise on BDNF mRNA extends beyond the HF to the mesolimbic ventral tegmental area and that the potentiation of BDNF Zofran 8mg Cost mRNA by exercise and antidepressant pharmacotherapy, reported by other investigators, is time limited.

tofranil with alcohol 2016-05-13

The psychotropic activity of a series of new aminouracil derivatives was studied on the widely applied models of pharmacological screening in rats. The Aciphex Tabs most expressed antidepressant effect at the stage of primary pharmacological screening was been revealed for compound PIR-03-52 in a dose of 10 mg/kg. A profound study of the antidepressant activity on models of pathological states, PIR-03-52 exhibited a pronounced antidepressant effect that was comparable with that of a reference drug (imipramine). The given effect is related to the positive influence of PIR-03-52 on the serotoninergic and dopaminergic systems.

tofranil y alcohol 2015-11-01

Previous work indicates that one consequence of the accumulation of several xenobiotics in the lung is compromised pulmonary disposition of 5-hydroxytryptamine (5-HT). In the present studies, we examined whether pulmonary accumulation of chlorpromazine (CPZ), propranolol (P), imipramine (IMP), and clomipramine (Cl-IMP) affected 5-HT disposition in rabbit lungs. Pulmonary extraction and metabolism of [14C]-5-HT during single pulmonary passage were examined using the reference indicator radioisotope dilution technique in male New Zealand albino rabbits. After control experiment, animals received CPZ or P (2.5, 5, or 10 mg/kg), IMP or Cl-IMP (0.25, 0.5 or 1.0 mg/kg) via the jugular vein. Pulmonary clearance was 83% of administered 5-HT. A significant proportion (28%) of total radioactivity in the bloodstream after single passage was recovered as 5-HIAA in control experiments. These values were reduced significantly to 70 and 20%, respectively upon prior administration of IMP (0.25 mg/kg). Cl-IMP Vantin Generic was more effective in reducing these values further. CPZ and P were marginally effective at the highest dose. While prior administration of IMP and Cl-IMP resulted in pulmonary accumulation of both drugs, the latter accumulated to a significantly greater extent. These results suggest that Cl-IMP has higher affinity to the rabbit lung than IMP and may inhibit pulmonary uptake of 5-HT by competition for uptake and binding sites more than IMP.