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PubMed1987

TRH test, DST, and response to desipramine in primary degenerative dementia.

The relationship of primary degenerative dementia (PDD) to major depressive disorder (MDD) is important clinically and theoretically. Neuroendocrine challenge strategies in PDD have focused primarily on the hypothalamic-pituitary-adrenal axis, have had varied results, and have not been coupled with assessment of response to antidepressant therapy. We studied the Thyrotropin-Releasing Hormone (TRH) test, the Dexamethasone Suppression Test (DST), and response to desipramine in 12 patients with PDD and 10 patients with MDD. The PDD patients had a high percentage of abnormal TRH tests and DSTs. This was not associated with improvement on desipramine.

Aged↗

PubMed1988

Effect of desipramine treatment on 3H-imipramine binding in the blood platelets of depressed patients.

Platelet imipramine binding (IB) was studied in depressed patients before and after treatment with desipramine for 17-28 days. Administration of desipramine was associated with a significant increase in Bmax. There was a trend for an increase in Kd, but it did not reach statistical significance. The net result of the changes in Bmax and Kd was an increase in IB. There were significant correlations between the change in depression ratings and pretreatment Kd, as well as the change in Kd during treatment. These results suggest that decreased IB is not a trait-dependent marker, but a state-dependent marker for depression.

Adult↗

PubMed1991

Fluvoxamine versus desipramine: comparative polysomnographic effects.

Electroencephalogram sleep measures over a 4-week period were obtained on 35 inpatients with major depression (unipolar) who received either fluvoxamine or desipramine in a randomized double-blind trial. Fluvoxamine showed immediate rapid eye movement (REM) sleep suppression and an alerting effect on sleep continuity measures. In contrast, desipramine administration was associated with REM suppression and sleep continuity improvement. The "alerting" quality of fluvoxamine, similar to other serotonergic antidepressants, appears to be unrelated to a lack of clinical efficacy, but may be related to persistent REM sleep suppression. However, it is premature to comment on the serotonin specificity for REM sleep.

Adult↗

PubMed1982

Effects of REM sleep deprivation and desipramine on beta-adrenergic binding sites in rat brain.

Rats were subjected to REM sleep deprivation by the flower pot method for 7 days. Another group of rats received either desipramine (10 mg/kg, i.p.), a tricyclic antidepressant, or saline (i.p.) once daily for 7 days. beta-Adrenergic receptor sensitivity in rat brain cortices was assessed by determining the maximum number of [3H]dihydroalprenolol binding sites by Scatchard analysis. Administration of desipramine caused a 26% reduction in beta-adrenergic receptor density (P less than 0.01) while REM sleep deprivation reduced beta-adrenergic receptor density by 13%, which was not statistically significant.

Animals↗

PubMed1983

The antidepressant agents desipramine, fluoxetine, fluvoxamine and norzimelidine inhibit uptake of [3H]noradrenaline and [3H]5-hydroxytryptamine in slices of human and rat cortical brain tissue.

The stability of uptake of [3H]noradrenaline and [3H]5-hydroxytryptamine in rat neocortical brain slices, prepared up to 4-5 h after decapitation, was established. Subsequently, monoamine uptake inhibition by 4 antidepressant agents: desipramine, fluoxetine, fluvoxamine and norzimelidine was compared in human post-mortem neocortical brain slices vs rat neocortical brain slices. In both species, desipramine exhibited considerable selectivity for noradrenaline uptake, while fluoxetine, fluvoxamine and norzimelidine showed varying degrees of selectivity for 5-hydroxytryptamine uptake. These results support the use of rat brain as a model for the study of neurochemical correlates of depression and antidepressant drug action.

Absorption↗

PubMed1987

Release of norepinephrine from rat hypothalamic slices: effects of desipramine and tyrosine.

We studied the release of endogenous norepinephrine (NE) from rat hypothalamic slices. The slices were superfused with Krebs-bicarbonate buffer and field-stimulated with 960 or 1800 pulses applied 40 min apart. The spontaneous and stimulation-evoked overflow of NE into the medium were both enhanced by addition of a NE reuptake inhibitor, desipramine (10 microM). Repeated stimulations in the presence of desipramine decreased the evoked release of NE during the second and third stimulation periods (S2 and S3). The attenuation of NE release during S2 was not reversed by the addition of tyrosine (50 microM) to the medium.

Animals↗

PubMed1980

Effects of desipramine and yohimbine on alpha 2- and beta-adrenoreceptor sensitivity.

The effects of yohimbine on desipramine-induced adrenoreceptor alterations were examined in murine limbic forebrain areas. Treatment with both drugs in combination resulted in a significant decrease in [3H]dihydroalprenolol binding, which was not manifest after treatment with either drug alone. Moreover, co-administration of yohimbine was found to accelerate the time course and increase the magnitude of desipramine-induced increases in [3H]clonidine binding. The possible physiologic significance of these findings is discussed along with their pharmacologic implications.

Animals↗

PubMed1985

Involvement of amygdaloid catecholaminergic mechanism in suppressive effects of desipramine and imipramine on duration of immobility in rats forced to swim.

The suppressive effect of systemic injection of desipramine and imipramine on the duration of immobility in rats forced to swim was inhibited by 6-hydroxydopamine given into the medial amygdaloid nucleus as a pretreatment. Pretreatment with 5,7-dihydroxytryptamine given into the medial amygdaloid nucleus had no effect on the immobility-reducing effect of tricyclic antidepressants. The concentrations of catecholamines and serotonin in 6-hydroxydopamine- and 5,7-dihydroxytryptamine-pretreated rats, respectively, were significantly lower than those in the saline-injected rats. These results suggest that the suppressive effect of systemic injection of desipramine and imipramine on the duration of the immobility of rats forced to swim was mediated by the catecholaminergic but not the serotonergic mechanisms in the medial amygdaloid nucleus.

5,7-Dihydroxytryptamine↗

PubMed1990

Picrotoxin changes the effects of imipramine and desipramine in rats in the forced swimming test.

The aim was to find whether the chloride channel blocker, picrotoxin, at subconvulsant doses could affect the activity of imipramine or desipramine in the 'forced swimming' test with rats. It was found that picrotoxin enhanced the anti-immobility effects of imipramine and desipramine whereas open field activity remained unaffected or was even decreased by the same treatments. The results seem consistent with recent reports showing direct interactions between several antidepressant drugs and the GABAA receptor/benzodiazepine receptor/chloride ionophore complex (GABAA/benzodiazepine/Cl complex). The results also conform with the hypothesis that a reduction in the functionality of this complex could be related to the clinical effects of antidepressant drugs.

Animals↗

PubMed1991

Desipramine and the phencyclidine derivative BTCP differently inhibit [3H]TCP binding to high- and low-affinity sites.

The effects of N-[1-(2-benzo(b)thiophenyl)cyclohexyl]piperidine (BTCP) and desipramine on [3H]N-[1-(2-thienyl)cyclohexyl]piperidine ([3H]TCP) binding were investigated in vivo and in vitro. In the cerebrum, both drugs were competitive inhibitors of high-affinity [3H]TCP binding. Conversely, in the cerebellum, they were non-competitive inhibitors of low-affinity [3H]TCP binding. These results imply that the different [3H]TCP binding sites have distinct pharmacological properties, and show that, although chemically related to TCP, BTCP has an effect similar to that of desipramine.

Animals↗

PubMed1993

Inhibition of neuronal nicotinic acetylcholine receptors by imipramine and desipramine.

The actions of two structurally related tricyclic antidepressants on neuronal nicotinic acetylcholine receptors were investigated in human neuroblastoma (SY-SY5Y) cells, using whole-cell patch-clamp recordings. Both desipramine and imipramine reversibly inhibited inward currents evoked by application of the nicotinic receptor agonist dimethylphenylpiperazinium iodide (30-300 microM) with IC50 values of 0.17 microM and 1.0 microM respectively (holding potential -70 mV). The degree of current inhibition caused by either tricyclic compound was unaffected by agonist concentration (30-300 microM). The effects of desipramine were voltage-independent over the range -40 mV to -100 mV, and inhibition caused by imipramine only increased very slightly with membrane hyperpolarization over the same range. These results indicate that tricyclic antidepressants can inhibit neuronal nicotinic acetylcholine receptors by mechanisms which are distinct from their actions at non-neuronal nicotinic acetylcholine receptors.

Desipramine↗

PubMed1995

Effects of desipramine and alprazolam on forced swimming behaviour of adult rats exposed to prenatal diazepam.

Pregnant rats were treated with a single daily s.c. injection of diazepam (2 mg/kg) over gestation days 14-20. This treatment led to a reduction in GABA receptor complex function since adult male offspring showed a strong decrease in electrographic hippocampal responses to alprazolam and a strongly increased response to picrotoxin after intra-locus coeruleus injection of the two compounds. No difference in immobility time in the forced swimming test and in spontaneous motor activity was observed between prenatally vehicle- and diazepam-exposed offspring. Conversely, prenatal exposure to diazepam potentiated the anti-immobility effect of subchronic desipramine (10 mg/kg i.p.) and made active a dose of desipramine (5 mg/kg i.p.) that was ineffective in prenatally vehicle-exposed rats. This effect was observed only in pretested rats. Prenatal exposure to diazepam blocked the anti-immobility effect of subchronic alprazolam (15 mg/kg i.p.) in both non-pretested and pretested rats. Spontaneous motor activity was strongly reduced in all groups. These findings suggest that a persistent reduction in GABA receptor complex function, induced by prenatal exposure to diazepam, does not alter the mobility of adult progeny in the forced swimming test, but it may have consequences when drugs acting on the GABA receptor complex are used.

Alprazolam↗

PubMed1993

Immunoassay reagents for psychoactive drugs. II. The method for the development of antibodies specific to imipramine and desipramine.

Imipramine and desipramine were structurally modified by the attachment of spacer arms to the aromatic ring which were subsequently attached to bovine serum albumin. This approach utilized novel spacer arms and conjugation methods. This method yielded antisera with excellent selectivity and good titers. Rabbits were used to raise the antisera and the antibodies produced were characterized with respect to their cross-reactivity with imipramine, desipramine and hydroxy metabolites as well as selected structurally related compounds.

Animals↗

PubMed1985

Long-term desipramine treatment attenuates clonidine-induced suppression of ventral tegmental self-stimulation.

Long-term administration of the tricyclic antidepressant desipramine did not change the rate of self-stimulation responding in the A10 (ventral tegmental) area but significantly attenuated the suppressive effect of the selective alpha 2-adrenergic agonist clonidine on this behavior. These findings demonstrate an involvement of noradrenergic mechanisms in the regulation of ventral tegmental self-stimulation and further suggest that adaptive changes in inhibitory presynaptic noradrenergic receptors may be involved in desipramine's antidepressant effects.

Animals↗

PubMed1990

Effect of desipramine on dopamine receptor binding in vivo.

Effect of desipramine (given i.p. 30 min prior to the tracer injection) on the in vivo binding of 3H-SCH23390 and 3H-N-methylspiperone (3H-NMSP) in mouse striatum was studied. The ratio of radioactivity in the striatum to that in the cerebellum at 15 min after i.v. injection of 3H-SCH23390 or 45 min after injection of 3H-NMSP were used as indices of dopamine D1 or D2 receptor binding in vivo, respectively. In vivo binding of D1 and D2 receptors was decreased in a dose-dependent manner by acute treatment with desipramine (DMI). A saturation experiment suggested that the DMI-induced reduction in the binding was mainly due to the decrease in the affinity of both receptors. No direct interactions between the dopamine receptors and DMI were observed in vitro by the addition of 1 mM of DMI into striatal homogenate. Other antidepressants such as imipramine, clomipramine, maprotiline and mianserin also decreased the binding of dopamine D1 and D2 receptors. The results indicated an important role of dopamine receptors in the pharmacological effect of antidepressants.

Animals↗

PubMed1987

Differential effects of chronic administration of desipramine on the cyclic AMP response in cortical slices and membranes in the rat.

Chronic administration of desipramine resulted in a significant decrease in the degree of stimulation of production of cyclic AMP by noradrenaline, isoproterenol and forskolin in slices of the cerebral cortex of the rat. In preparations of membranes from similarly treated animals, GppNHp- and forskolin-stimulated adenylate cyclase activity was increased, while isoproterenol-, manganese- and sodium fluoride-stimulated activity was unchanged. It is concluded that chronic administration of desipramine exerts effects on the adenylate cyclase system additional to its action on beta-adrenergic receptors, possibly by modifying the catalytic or guanyl nucleotide binding units of the enzyme.

Adenylyl Cyclases↗

PubMed1993

Reduction of NMDA-induced behaviour after acute and chronic administration of desipramine in mice.

The mechanisms of the antinociceptive effect of desipramine (DMI) are only partly known. It is generally accepted that excitatory amino acids act as neurotransmitters in primary nociceptive fibres and recent in vitro studies have shown an interaction between tricyclic antidepressants and the N-methyl-D-aspartic acid (NMDA) receptor complex. In this study, the modulatory effect of DMI on the biting and scratching behaviour induced by intrathecal (i.th.) administration of NMDA (0.25 nmol) was investigated. Desipramine was administered acutely, either intrathecally (0.7-35 micrograms) or intraperitoneally (i.p., 10 mg/kg), or chronically in the drinking water (0.15 g/l) for 3 weeks. The NMDA-induced behaviour was significantly reduced both after acute and chronic administration of DMI. Several studies have shown a functional upregulation of the 5-HT1A receptor after chronic treatment with DMI. The activation of this receptor using the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT), leads to a reduction in NMDA-induced behaviour. Using the 5-HT1A antagonist NAN-190 (10 micrograms, i.th.), the effect of chronic administration of DMI on the NMDA-induced behaviour was reversed. However, NAN-190 also increased NMDA-induced behaviour in the control group, suggesting that a tonic inhibition of this behaviour, mediated by the 5-HT1A receptor, may exist. These findings indicate that DMI may reduce glutaminergic transmission at the spinal NMDA receptor. As this receptor is central in spinal nociceptive transmission, this could be one mechanism for the antinociceptive effect of DMI.

Animals↗

PubMed1988

Effects of Ro 15-4513, fluoxetine and desipramine on the intake of ethanol, water and food by the alcohol-preferring (P) and -nonpreferring (NP) lines of rats.

The effects of the IP administration of RO 15-4513 (1, 2 and 4 mg/kg), fluoxetine (5 and 10 mg/kg) and desipramine (5 and 10 mg/kg) on the intake of 10% ethanol, H2O and food were determined in the selectively bred alcohol-preferring (P) and -nonpreferring (NP) lines of rats with daily access to fluids being limited to single 2-hour sessions. The imidazobenzodiazepine Ro 15-4513 (a partial inverse benzodiazepine agonist) significantly reduced the intake of 10% ethanol by the P rats to 50-60% of control levels in the first 30 minutes without altering food or H2O intake. The attenuating actions of 2 mg/kg Ro 15-4513 on ethanol intake could be completely blocked by the central benzodiazepine receptor antagonist Ro 15-1788 (10 mg/kg). Ro 15-1788, by itself, produced no effects on alcohol and H2O consumption. The 5 mg/kg dose of fluoxetine significantly reduced 10% ethanol intake by the P rats to 20% of control values without altering either H2O or food consumption. The 10 mg/kg dose of fluoxetine further reduced ethanol intake by the P rats, but this dose also reduced daily food intake to approximately 70% of normal. Desipramine at both doses significantly (p less than 0.05) reduced both ethanol and food uptake by the P rats and had a tendency to reduce H2O consumption as well. In general, the three drugs had effects in the NP rats similar to those observed for the P group, although the effects on 10% ethanol intake were difficult to compare because of the low, variable intake of alcohol by the NP group.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Drinking↗