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At least 757 records · Page 42Linked to original sources
PubMed1988

The chronic effects of desipramine and sertraline on platelet and synaptosomal 5HT uptake in olfactory bulbectomised rats.

1. Depressed patients show a characteristic decrease in the rate of uptake of serotonin into their platelets, which is normalised only by clinically effective antidepressant treatment. 2. We also find a decrease in platelet 5HT uptake rates in the olfactory bulbectomised (OB) rat model of depression, which return to normal following three weeks of treatment with desipramine or sertraline. 3. Synaptosomal 5HT uptake appears to consist of a low affinity, high capacity component and a high affinity, low capacity component, both of which are increased in the OB rat, compared to its sham operated control, and normalised by chronic antidepressant treatment. 4. The low affinity uptake of serotonin is not inhibited by in vitro incubation with sertraline, which suggests that the low affinity system may be associated with a non-specific uptake of 5HT into noradrenergic or dopaminergic nerve endings.

1-Naphthylamine↗
PubMed1990

A double-blind comparison of fluvoxamine, desipramine and placebo in outpatients with depression.

1. The efficacy of fluvoxamine is compared to that of desipramine in a multicenter double blind placebo controlled six-week flexible dose trial of 90 outpatients with major depressive disorder. 2. Although overall drug effects were relatively weak, there were trends suggesting separation of both active drugs from placebo at week six. Both drugs were well tolerated. 3. Studies of major depression ought to be designed to last 8-10 weeks in order to demonstrate placebo active drug differences and the stability of such a difference should it occur in the first six weeks.

Adult↗
PubMed1996

Changes in thyroid hormone levels associated with desipramine response in adolescent depression.

1. The authors recently reported that acutely ill depressed adolescents have elevated plasma T4 and fT4 compared to controls. Studies in adult depression suggest antidepressant response is associated with decreases in these elevated levels. The effect of antidepressant treatment on adolescent thyroid indices has not been examined. 2. Thyroid indices were examined in 12 adolescent patients (4 male, 8 female; age 14-19y) in the active treatment arm of a double-blind, placebo-controlled desipramine trial (200 mg/day for 6 weeks). Antidepressant responders had higher pre-treatment levels of T4 and larger decreases were observed responders vs. nonresponders. 3. These results replicate findings observed in adult depressed patients and suggest similar alterations in the hypothalamic-pituitary-thyroid (HPT) axis function in adolescent depression.

Adolescent↗
PubMed1982

Autoradiographic demonstration of binding sites for [3H]desipramine in rat brain.

Many of the characteristics of [3H]desipramine ([3H]DMI) binding sites, previously established with brain homogenates, were confirmed in slide-mounted sections of rat forebrain. A 1:1 ratio of specific to non-specific binding was established. The proportion of specifically bound [3H]DMI was reduced in brain sections from rats pretreated with 6-hydroxydopamine but not with 5,6-dihydroxytryptamine. High resolution localization of [3H]DMI binding sites was achieved by exposing the sections to tritium-sensitive film.

Animals↗
PubMed1989

Reversal of desipramine-induced suppression of paradoxical sleep by a long-acting somatostatin analogue (octreotide) in rats.

EEG sleep recordings were performed in rats under intraperitoneal injections of saline, desipramine (DMI, 4 mg/kg) an inhibitor of noradrenaline reuptake, and DMI plus the octapeptide somatostatin analogue (octreotide, 0.2 mg/kg). As already reported, DMI resulted in selective suppression of paradoxical sleep (PS) and increased slow wave sleep (SWS). The administration of the octapeptide somatostatin analogue totally reversed the DMI-induced suppression of PS, but had no effect on SWS. This finding confirms previous results demonstrating a role of somatostatin in the generation of PS. In addition, it suggests that the suppression of PS by DMI may be due to an inhibitory effect on somatostatin release, rather than to an alteration of brain noradrenaline.

Animals↗
PubMed1992

Semiquantitative analysis of immunoreactivities of tyrosine hydroxylase and aromatic L-amino acid decarboxylase in the locus coeruleus of desipramine-treated mice.

The influence of antidepressant drugs on catecholaminergic neuron groups of the mouse brain was studied immunohistochemically, using a microphotometric semiquantitative method. The immunoreactive level of tyrosine hydroxylase (TH) and aromatic L-amino acid decarboxylase (AADC) in the locus coeruleus (LC) was significantly decreased after 2 weeks of antidepressant administration. Our results suggest that long-term exposure to an antidepressant drug, desipramine, significantly affects intracellular catecholamine-synthesizing enzymes. These results may suggest some significant roles of the catecholaminergic neuronal groups to the action of the tricyclic antidepressant drugs.

Animals↗
PubMed1996

Trypanocidal resistance in Trypanosoma evansi in vitro: effects of verapamil, cyproheptidine, desipramine and chlorpromazine alone and in combination with trypanocides.

A study was conducted in vitro to assess the ability of calcium antagonists to reverse trypanocidal resistance in Trypanosoma evansi. Susceptibility patterns of sensitive and resistant parasites were evaluated against calcium antagonists of several chemical classes (verapamil, cyproheptidine, desipramine and chlopromazine), alone and in combination with suramin, diminazene aceturate or melarsen oxide cyteamine. The putative resistance modulators were intrinsically antitrypanosomal, but were unable to reverse resistance to any of the trypanocides tested. It was thus concluded that resistance to these trypanocides in T. evansi may differ from drug resistance mechanisms occurring in cancer cells, malaria or in South American trypanosomosis, where calcium antagonists have successfully reversed resistance.

Animals↗
PubMed1989

The effects of desipramine (DMI) and electroconvulsive shock (ECS) on the function of the hypothalamo-pituitary-thyroid axis in the rat.

Monoaminergic systems influence the hypothalamo-pituitary-thyroid (HPT) axis. Since two different antidepressant treatments, desipramine (DMI) and electroconvulsive shock (ECS), are known to alter monoaminergic function in the rat central nervous system (CNS), the effects of DMI and ECS on the function of the HPT axis in the rat were examined. Animals were treated with either DMI (5 mg/kg) twice daily for 14 days (DMI x 14) or once only (DMI x 1) or ECS five times in 10 days (ECS x 5) or once only (ECS x 1). Three and 24 hours after the final treatment, blood samples were taken for measurement of plasma total thyroxine (TT4), total tri-iodothyronine (TT3), free thyroxine (FT4), free tri-iodothyronine (FT3) and thyroid stimulating hormone (TSH). Plasma TSH concentrations were decreased by the DMI x 14 and increased by the ECS x 5 regimen. Small decreases in thyroid hormones (T3 and T4) occurred after DMI x 14. No other consistent changes were observed in the animals treated with ECS. The effect of DMI or ECS treatment on the responsiveness of pituitary thyrotrophs was assessed in vitro. Isolated superfused pituitary glands from rats treated in vivo with either DMI x 14 or ECS x 5 were exposed to a pulse of thyrotropin releasing hormone (TRH; 1 ng/ml). No significant change in TSH secretion was observed in response to TRH in either case. Therefore, the changes observed in circulating plasma TSH levels are unlikely to have resulted from either direct or indirect effects on pituitary thyrotroph TRH receptor sensitivity.

Animals↗
PubMed1990

Influence of clenbuterol, a beta-adrenergic agonist, on desipramine induced growth hormone, prolactin and cortisol stimulation.

We report herein the effects of the beta-adrenergic agonist clenbuterol on desipramine (DMI)-induced growth hormone (GH), prolactin (PRL) and cortisol secretion in healthy male subjects. In the first study, nine subjects were treated with either clenbuterol (0.04 mg, p.o.) or placebo. In the second study, 12 subjects received either DMI (50 mg, i.v.) alone or in combination with clenbuterol (0.04 mg, p.o.) given 60 min prior to DMI administration. Clenbuterol alone had no influence on GH, PRL, or cortisol concentrations, compared to placebo. DMI alone caused GH stimulation (mean maximum = 15.7 +/- 3.4 ng/ml), which was significantly lower after combined administration of DMI and clenbuterol (mean maximum = 7.7 +/- 1.6 ng/ml) (p less than or equal to 0.01). DMI-induced PRL and cortisol stimulation was not influenced by clenbuterol pretreatment. These results indicate the inhibiting influence of noradrenergic beta-receptors on GH stimulation.

Adolescent↗
PubMed1993

Effects of chronic desipramine administration on the locus coeruleus neuronal activity in the learned helplessness paradigm.

One week after inescapable shock (IS) exposure, animals showed an increased number of escape failures in the shuttlebox and a decreased noradrenergic (NA) transmission. The latter was assessed by electric activity of locus coeruleus (LC) neurons. Seven daily injections of desipramine (DMI) were effective in reducing the number of escapes failures in the shuttlebox, but such treatment did not modify the decreased electric activity of LC NA neurons observed 7 days after IS. These results are discussed in terms of the action of DMI on NA terminals in reversing the behavioral deficit induced by IS.

Action Potentials↗
PubMed1995

Rapid microsample analysis of imipramine and desipramine by reversed-phase high-performance liquid chromatography with ultraviolet detection.

A rapid and highly sensitive HPLC assay method was developed to measure small amounts of imipramine and its major metabolite, desipramine. The assay involved simple extraction procedures using clomipramine as the internal standard. The mobile phase consisted of acetonitrile (60%) and 0.01 M triethylamine in distilled water (40%) with the pH adjusted to 3.0. Separations were achieved on a C18 column and the effluent measured for UV absorption at 260 nm. The chromatographic separation was excellent, with no interference from endogenous serum constituents. This assay was suitable for measuring drug concentrations in the range of 10-1000 ng/ml using a 0.1-ml serum sample. The method was applied to a drug disposition study in transgenic mice with increased plasma alpha 1-acid glycoprotein.

Animals↗
PubMedDate not supplied

Effects of fluoxetine and desipramine on palatability-induced ethanol consumption in the alcohol-nonpreferring (NP) line of rats.

Three groups of NP rats (n = 5/group) received food, water and one of 3 Polycose solutions ad lib. One group received a solution containing 3% (w/v) Polycose, 0.125% (w/v) saccharin, 0.5% (w/v) NaCl (3% POL solution) to which ethanol was gradually added over three weeks until the concentration of 10% (v/v) ethanol (E) was reached (3% POL + E group). Alcohol ingestion by the 3% POL + E group reached an average of 9 g of ethanol/kg b. wt./day; the rats attained average blood alcohol concentrations of 61 +/- 8 mg%. One control group (3% POL) was given the same solution as above but without ethanol. The second control group (17% POL) had access to a 17.6% Polycose solution supplemented with 0.125% saccharin and 0.5% NaCl and was isocaloric to the 3% POL + E solution. Although the three groups differed significantly in the amounts of food and Polycose solutions consumed, their total caloric intakes were equivalent. The IP administration of the serotonin (5-HT) uptake inhibitor fluoxetine (5 and 10 mg/kg) significantly reduced drinking of the group receiving the 3% POL + E solution by 23% and 67%, respectively, but did not alter intakes of the Polycose solutions by the 3% or 17% POL control groups. The IP administration of the norepinephrine (NE) uptake inhibitor desipramine (5 and 10 mg/kg) significantly reduced intake of the Polycose solution by the 17% POL group by 52 and 83%, respectively, but only the 10 mg/kg dose attenuated drinking of the solutions by the 3% POL and 3% POL + E groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Drinking↗
PubMed1993

Effects of desipramine and alprazolam in the forced swim test in rats after long-lasting termination of chronic exposure to picrotoxin and pentylenetetrazol.

Rats were treated for 5 weeks with three subconvulsant doses of picrotoxin (PTX) and pentylenetetrazol (PTZ) per week to induce a persistent reduction of the GABAA receptor function which results in chemical kindling. Fifteen days after termination of this treatment schedule, the effect of desipramine (DMI) and alprazolam (ALP) on immobility time in the forced swim test (FST) was evaluated. Chronic PTX and PTZ did not alter the immobility time. Acute PTX and PTZ reduced the immobility of rats chronically treated with vehicle but not of those exposed chronically to PTX and PTZ. Chronic PTX did not influence the anti-immobility effect of DMI, but blocked that of ALP. Chronic PTZ markedly potentiated the anti-immobility effect of DMI but blocked that of ALP. Concomitant administration of chlordiazepoxide prevented the effects of chronic PTX and PTZ. These findings suggest that a long-lasting reduction in GABAA receptor function, unlike acute reduction, does not play an important role in the mobility of rats in the FST and in the anti-immobility effect of DMI while it blocks that of ALP.

Alprazolam↗
PubMedDate not supplied

Influence of desipramine on the contractile responses to noradrenaline, clonidine and to electrical field stimulation in the rat isolated seminal vesicle.

The effect of desipramine (DMI) on the contractile responses to noradrenaline (NA), clonidine and to electrical field stimulation (FS), was studied in the rat isolated seminal vesicle. The aim was to analyse the mechanism of action of DMI in this preparation and compare the results obtained with those already published for other similar preparations, e.g. the guinea-pig seminal vesicle. The results showed that DMI, which on its own had little effect on contractility of rat seminal vesicle, significantly (P less than 0.001) enhanced the Na-induced contractions (by 30-50%), whereas it markedly reduced (by 40%) the contractions produced by clonidine. DMI also enhanced the FS-induced contractions (by about 50%) in the same preparation. The enhancement of the NA-induced responses by DMI can be explained in terms of inhibition of the NA uptake by the preparation, whereas the reduction in clonidine response may be due to blockade of adrenoceptors in the rat seminal vesicle. Other possibilities and mechanisms are also discussed in this and other types of smooth muscle preparations.

Animals↗
PubMed1995

Simultaneous quantification of fluoxetine, norfluoxetine, and desipramine using gas chromatography with nitrogen-phosphorus detection.

The combination of fluoxetine (FLU) and desipramine (DMI) has been reported to be useful for the treatment of depression, and these drugs are also known to undergo a metabolic drug-drug interaction because of their effects on cytochrome P-450 2D6. A procedure that separates these two drugs and norfluoxetine (NFLU), the N-demethylated metabolite of FLU, and that allows simultaneous quantification of their levels would be of value and has been developed in our laboratories. The procedure involves an initial extraction into ethyl acetate after basification of the homogenate. The organic phase is retained and taken to dryness; the residue is reconstituted in water and acetylated with acetic anhydride under slightly basic conditions. Ethyl acetate is then used to extract the acetylated compounds from the aqueous medium. The organic layer is taken to dryness and the residue reconstituted in toluene. An aliquot of the solution in toluene is injected directly into a gas chromatograph equipped with a nitrogen-phosphorus detector, a fused silica capillary column, and an integrator/printer. Maprotiline is added to the initial homogenate and carried through the procedure as the internal standard. The assay is rapid and sensitive and has been applied successfully to liver and brain tissue taken from rats treated with FLU, DMI, or the combination.

Animals↗
PubMed2005

Tyrosine administration does not affect desipramine-induced dopamine levels as measured in vivo in prefrontal cortex.

Using in vivo microdialysis, we examined whether tyrosine administration would potentiate the desipramine (DMI)-induced elevation of medial prefrontal cortex (MPFC) dopamine (DA) levels. DMI (10 or 20 mg/kg IP) increased MPFC DA levels but not DOPA accumulation. Tyrosine (12.5-100 mug/ml) administered by reverse microdialysis did not affect DMI-induced MPFC DA levels. The data support our hypothesis that DA synthesis must be significantly increased in order for administered tyrosine to increase extracellular DA levels.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2005

Ejaculation induces long-lasting behavioural changes in male rats in the forced swimming test: evidence for an increased sensitivity to the antidepressant desipramine.

Copulation to exhaustion induces a sexual inhibitory state featured by a decreased motivation. Since diminished motivation is a key symptom of depression, we analysed if sexually exhausted animals showed increased levels of depressive-like behaviour in the forced swimming test (FST). Besides, sexual activity has been reported to have reinforcing properties. Thus, we analysed whether different levels of sexual activity modified the development of the behavioural despair in the FST. Finally, the effect of a sub-threshold dose of desipramine (DMI, 2.5mg/kg) was evaluated in animals with different sexual conditions. Male adult rats were divided into: (a) naive rats and (b) animals executing one intromission (1-INTR) or (c) one ejaculation (1-EJ) and (d) sexually satiated rats, classified as sexually responsive (R) and non-responsive (NR). No differences were found in immobility behaviour between sexually exhausted and naive rats. In the pre-test sessions of the FST males attaining ejaculation (1-EJ, R and NR) had lower levels of immobility or showed a tendency towards such a diminution, while animals with sexual activity not involving ejaculation did not. Data suggest a "protective" effect of ejaculation against the development of depressive-like behaviour. Finally, the sub-effective dose of DMI produced an antidepressant-like action in all animals that ejaculated. In conclusion, sexual experience involving ejaculation modifies the behavioural expression of rats in the FST and their sensitivity to antidepressant drugs like DMI. Both responses reflect brain plastic changes induced by ejaculation.

Analysis of Variance↗
PubMed2005

Quantitative in vitro phosphor imaging using [3H] and [18F] radioligands: the effects of chronic desipramine treatment on serotonin 5-HT2 receptors.

Traditionally, autoradiography of neuroreceptors is performed in vitro using tritiated ligands and low sensitivity X-ray film, requiring long exposure times. In vivo imaging of neuroreceptors using positron emission tomography (PET) suffers poor spatial resolution, but in vitro PET autoradiography is difficult with film due to the short half-life of the isotopes. Storage phosphor screens provide an extremely sensitive alternative to film. To demonstrate and validate quantitative in vitro phosphor imaging with PET and tritiated ligands, we treated rats chronically with the antidepressant desipramine, which results in decreased binding to serotonin 5-HT(2) receptors. Serotonin 5-HT(2) binding decreased significantly in all cortical regions examined as measured by both [(3)H]ketanserin and [(18)F]setoperone. The data from the two radioligands were not significantly different, and the distribution of the receptors was in agreement with previous reports. We also present data on the reusability of tritium-sensitive phosphor screens, and show that the use of simple corrections allows receptor binding data with PET ligands to be compared across different days. The results indicate that phosphor imaging is a valid, fast, and quantifiable technique for measuring neuroreceptor regulation, and that it provides an excellent tool to corroborate in vivo PET data in vitro at higher resolution.

Animals↗