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PubMed1988

Urinary MHPG, platelet 3H-imipramine binding and symptomatology in depression: an exploratory study of clinical heterogeneity.

Urinary MHPG concentrations and platelet 3H-imipramine binding (Bmax, Kd) were measured in 20 psychiatric inpatients with diagnoses of major depressive disorder. Clinical assessments were performed using the Present State Examination (PSE) interview, and several dimensions of symptomatology were constructed on the basis of the PSE items. There was a significant positive relationship between Bmax and items reflecting both psychomotor retardation and anxiety. Urinary MHPG bore a comparatively complex nonlinear relationship to Bmax and to the psychomotor retardation symptom dimension. Urinary MHPG also showed an inverse, curvilinear correlation with certain neurotic symptoms. The implications of these findings are briefly discussed in the light of the "dysregulation" hypothesis of affective disorder.

Adult↗

PubMed1988

Seasonal variation of imipramine binding in the blood platelets of normal controls and depressed patients.

Imipramine binding (IB) was studied in the blood platelets from normal controls and depressed patients over a 4-year period (1981-1984) to determine if seasonal variation was present in Bmax or KD. Bimonthly variation in the Bmax of IB was found in normal controls studied longitudinally. No such variation was found when individual values from normal controls were examined on a monthly or seasonal basis. Bmax in depressed patients showed a significant seasonal, but not monthly, variation. KD of IB varied in normal controls using monthly or seasonal data, but not in the probably more reliable bimonthly data. These results suggest that IB studies comparing groups of subjects should match groups for season of the year or, for greater accuracy, month of the year.

Adult↗

PubMed1989

Seasonal rhythm of platelet 3H-imipramine binding in normal controls.

The densities of platelet 3H-imipramine sites were determined by repetitive measures of 11 normal controls over the course of 1 year. A significant seasonal variation was found, with a circannual peak on February 17 and a nadir on August 18. The estimated amplitude of this rhythm was +/- 599.54 fmol/mg, which fluctuated about a yearly mean of 2647.5 fmol/mg. The present results underscore the importance of including seasonally matched controls in the evaluation of potential patient differences in platelet binding.

Adult↗

PubMed1990

A test of the tridimensional personality theory: association with diagnosis and platelet imipramine binding in obsessive-compulsive disorder.

We administered the Tridimensional Personality Questionnaire (TPQ) to a sample of 25 individuals with obsessive-compulsive disorder (OCD) and 35 normal controls. As predicted, OCD cases scored much higher on the harm avoidance dimension than normal controls. Findings for the novelty seeking and reward dependence dimensions were less dramatic, although compatible with the underlying theory. Despite a theoretical link between the harm avoidance dimension and serotonin-mediated neuropathways, we failed to find an association between this dimension and platelet imipramine binding in either OCD cases or controls.

Arousal↗

PubMed1991

Decreased seasonal mesor of platelet 3H-imipramine binding in depression.

Seasonal cycles of platelet 3H-imipramine binding were compared in 49 endogenous unipolar depressed patients and 20 normal volunteers. A significant sinusoidal component was detected in the Bmax of binding in both patients and controls with similar amplitudes and seasonal peaks. However, the yearly average (mesor) of the patient group was significantly lower (20.0%) than that of the normal controls. The results support earlier claims of a diminished platelet binding in endogenous depression and indicate that this decrease was still evident in the presence of a 48.2% (controls) to 65.8% (patients) seasonal variation. Control Bmax values were normally distributed about a best-fit mean (cosinor fit). In contrast, patient values appeared to be bimodally distributed with one mode that was similar to controls and one mode that was substantially lower. In general, psychiatric symptoms failed to distinguish between patients with high and low platelet binding and no correlation was found between Bmax and severity of illness (HAM-D).

Adolescent↗

PubMed1980

Central noradrenergic adaptation to long-term treatment with imipramine in rhesus monkeys.

Rhesus monkeys were treated with the antidepressant drug imipramine; cerebrospinal fluid norepinephrine and dopamine-beta-hydroxylase were measured to assess central noradrenergic activity. Large changes occurred after short-term, but not long-term, treatment. Biochemical stabilization occurs at the time when therapeutic effects are seen in patients.

Acclimatization↗

PubMed1982

Attenuation by chronic imipramine treatment of [3H]clonidine binding to cortical membranes and of clonidine-induced hypothermia: the influence of central chemosympathectomy.

Central chemosympathectomy with intraventricular injection of 250 microgram of 6-hydroxydopamine, resulting in depression of cerebral noradrenaline level by 75% led to an increase in specific binding of [3H]clonidine to cerebral cortical membranes, but did not affect the hypothermic response to clonidine. Chronic imipramine treatment depressed [3H]clonidine binding and attenuated clonidine-induced hypothermia similarly in non-chemosympathectomized and chemosympathectomized rats.

Animals↗

PubMed1983

Intrahypothalamic 5,7-dihydroxytryptamine facilitates feminine sexual behavior and decreases [3H]imipramine binding and 5-HT uptake.

5,7-Dihydroxytryptamine (5,7-DHT) injected into the hypothalamus facilitated feminine sexual behavior in ovariectomized, estrogen-treated female rats beginning 9 days post-lesion. 5,7-DHT treatment was associated with decreased [3H]5-HT but not [3H]NE uptake in the whole hypothalamus and with decreased [3H]-imipramine binding in some hypothalamic nuclei. These data provide the first demonstration using chemical lesions that 5-HT neurons may exert tonic inhibition on hormone-mediated feminine sexual behavior.

5,7-Dihydroxytryptamine↗

PubMed1981

Simultaneous liquid chromatographic analysis of amitriptyline, nortriptyline, imipramine, desipramine, doxepin, and nordoxepin.

A simultaneous method for the therapeutic monitoring of amitriptyline, doxepin, imipramine, and their active demethylated metabolites nortriptyline, nordoxepin, and desipramine, respectively, in plasma or serum by reversed-phase liquid chromatography (RPLC) is presented. The drugs and the internal standard (loxapine) are first extracted from 2 ml of serum into butylchloride at pH 14, and then back extracted into 200 microliter of 0.025 mol/l hydrochloric acid. An aliquot of the aqueous acid phase is injected into the chromatograph and eluted with acetonitrile-phosphate buffer (21: 79, by vol.) containing 0.6 nl of n-nonylamine per liter of phosphate buffer. The drugs are eluted in a total chromatographic time of approximately 13 min at ambient temperature and detected at 200 nm. A sensitivity of 5 microgram/l of serum for each drug is obtained. Recoveries for these drugs ranged from 77% to 103%; and the coefficient of variation (day-to-day) ranged from 4.2 to 7.8. Of 35 basic or neutral drugs tested for possible interference, only propoxyphene interferes with the analysis of nortriptyline.

Amitriptyline↗

PubMedDate not supplied

Comparison of 6- with 9-week trials of adjunctive imipramine in postpsychotic depression.

Outcome at 6 weeks versus outcome at 9 weeks was compared in 23 patients with syndromally defined episodes of postpsychotic depression who underwent a trial of adjunctive imipramine added to their continuing treatment with fluphenazine decanoate and benztropine. The global outcome after 9 weeks was found to be superior. The implications of this finding for the treatment of secondary depressions in patients with schizophrenia and schizoaffective disorder is discussed.

Adult↗

PubMed1978

"Behavioural despair" in rats and mice: strain differences and the effects of imipramine.

Rats and mice when forced to swim in a restricted space will rapidly cease attempts to escape and become immobile. Previous experiments have shown that immobility was selectively reduced by antidepressant agents. The present experiments show that important differences exist between strains in both the amount of immobility observed and the effects of imipramine. Strain differences should therefore be taken into account in attempts to replicate results from one laboratory to another.

Animals↗

PubMed1979

Antagonism by d,1-propranolol of imipramine effects in mice.

Three agents with known or suspected antidepressant activity, imipramine, salbutamol and dexamphetamine, were active in animal tests predictive of an antidepressant effect in man: antagonism of the hypothermia induced by reserpine, by oxotremorine or by a high dose of apomorphine, and the potentiation of the yohimbine-induced toxicity. These effects were antagonized by d,1-propranolol, suggesting that the stimulation of beta-adrenergic receptors could be a common mechanism underlying their effects. These results agree with the noradrenergic hypothesis of the pathophysiology of affective disorders.

Albuterol↗

PubMed1979

Forced swimming in rats: hypothermia, immobility and the effects of imipramine.

Rats when forced to swim in a restricted space not only became immobile but showed marked hypothermia. The hypothermia was greater than that observed after reserpine or Ro 4-1284 and was not antagonized by imipramine at doses which significantly reduced immobility. Hypothermia induced by forced swimming can therefore be dissociated from the immobility occurring in these conditions and also from drug-induced hypothermia.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗

PubMed1980

Rapid-eye-movement sleep deprivation decreases the density of 3H-dihydroalprenolol and 3H-imipramine binding sites in the rat cerebral cortex.

The high affinity binding sites for 3H-imipramine (3H-IMI) and 3H-dihydroalprenolol (3H-DHA) in the rat cerebral cortex were studied after 2,4 48 and 72 h of rapid-eye-movement (REM) sleep deprivation. Both the Kd and Bmax values for 3H-IMI and 3H-DHA binding remained unaffected after 24 or 48 h of REM sleep deprivation. After 72 or REM sleep deprivation there was a significant reduction in the Bmax for 3H-IMI and 3H-DHA binding with a concomitant increase in the apparent affinities. The reduction in high affinity 3H-IMI and 3H-dihydroalprenolol binding sites observed 72 h after REM sleep deprivation could be related to the antidepressant effects of REM sleep deprivation in man.

Alprenolol↗

PubMed1983

Effects of combined administration of imipramine and chlorpromazine on beta- and alpha 2-adrenergic receptors in rat cerebral cortex.

Administration of the combination of antidepressant and neuroleptic drugs has been reported to have a synergistic effect in the treatment of delusional depression. The effects of chronic coadministration of imipramine (IMIP) and chlorpromazine (CPZ) on beta-adrenergic and alpha 2-adrenergic binding sites in rat cerebral cortex were studied. The combination caused the same reduction in the number of beta-adrenergic receptors as IMIP alone. No changes in alpha 2-adrenergic receptors were observed with IMIP and/or CPZ.

Animals↗

PubMed1985

Antidepressive drugs can change the affinity of [3H]imipramine and [3H]paroxetine binding to platelet and neuronal membranes.

Serotonin transport in synapses and platelets is inhibited by tricyclic antidepressants as well as by more selective transport inhibitors. This inhibition is hypothesized to be of importance for the psychotropic effect, although it is known that some new antidepressants do not possess this transport inhibitory action. We now report that antidepressive drugs can influence the serotonin transport complex in platelets and brain in other ways: [3H]imipramine and [3H]paroxetine, which bind with high affinity to the serotonin transport complex, can be dissociated from the complex with velocity constants strongly influenced by the different antidepressants. This effect is not correlated to the inhibitory action of the drugs on serotonin transport. Furthermore the effect is seen in the micromolar range in contrast to the high affinity binding process which takes place in the pico- and nanomolar range. The effects of antidepressants on the dissociation rates of bound ligand make it possible to differentiate between serotonin reuptake inhibitors which appear identical in other assays. Antidepressive drugs can thus be divided into groups which differ from the usual classifications.

Animals↗

PubMed1985

Effect of imipramine on calcium and potassium currents in isolated bovine ventricular myocytes.

Isolated bovine ventricular myocytes were investigated with a two-microelectrode voltage clamp technique. The clamp currents were analyzed in terms of ICa and IK. Possible effects on INa were avoided by superfusing the cells with a Na-free medium. Imipramine (IMI) was applied at a concentration of 3.6 microM. Within the initial 3 min (early phase), IMI reduced peak ICa by 38 +/- 9% but IMI did not change the time constants of inactivation, the voltage dependence of peak ICa or its reversal potential. Therefore, we conclude that IMI reduced calcium conductance. After 10 min of exposure (late phase), IMI can also reduce the reversal potential of ICa. The inward rectifying potassium current (IK1) was transiently enhanced by 15 +/- 8% but later (8-10 min) reduced by 19 +/- 4%. Washout of IMI completely reversed all the effects within 10 min. Reduction of ICa diminished the rate of rise and the overshoot of the slow action potential and can explain the shortening of the AP seen in both Na-free and Na-containing media. Possible clinical implications are discussed.

Action Potentials↗

PubMed1986

Effect of chronic imipramine or baclofen on GABA-B binding and cyclic AMP production in cerebral cortex.

Long-term (14 days) treatment of mice with the antidepressant drug imipramine increased the number of GABA-B receptors in the cerebral cortex and also led to an increase in the potentiation of norepinephrine-induced cAMP accumulation by baclofen (a GABA-B agonist) in cortical slices. Chronic baclofen treatment decreased both of these measures. These results suggest that previous evidence of increased GABA-B binding by antidepressants is coupled to a functional increase in adenylate cyclase activity, but that the mechanism responsible for this effect is not due simply to direct GABA-B receptor stimulation.

Animals↗