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PubMed1983

Uptake of [3H]dopamine into dopaminergic and noradrenergic neurones of the isolated neurointermediate lobe of the rat hypophysis. Effects of desipramine and nomifensine.

The isolated neurointermediate lobe (NIL) of the rat hypophysis accumulates [3H]dopamine from the incubation medium. Column chromatographic analysis showed that 92% of the tissue radioactivity was contained in the catecholamine fraction. [3H]Dopamine represented 70% and [3H]noradrenaline 30% of the [3H]catecholamines. Desipramine (1 microM) prevented the formation of [3H]noradrenaline without affecting the storage of [3H]dopamine. Nomifensine (10 microM) blocked the storage of [3H]dopamine and [3H]noradrenaline. Thus, in the NIL, [3H]dopamine is taken up into dopaminergic and noradrenergic neurones. In the latter, [3H]dopamine is converted to [3H]noradrenaline, indicating a significant dopamine beta-hydroxylase activity in the NIL tissue. A selective labeling of the dopamine stores with [3H]dopamine can be achieved in the presence of desipramine.

Animals↗
PubMed1991

[3H]MK-801 binding to N-methyl-D-aspartate receptors solubilized from rat brain: effects of glycine site ligands, polyamines, ifenprodil, and desipramine.

The N-methyl-D-aspartate (NMDA) receptor is thought to contain several distinct binding sites that can regulate channel opening. In the present experiments, the effects of ligands for these sites have been examined on [3H]MK-801 binding to a soluble receptor preparation, which had been passed down a gel filtration column to reduce the levels of endogenous small-molecular-weight substances. Glycine site agonists, partial agonists, and antagonists gave effects similar to those observed in membranes [EC50 values (in microM): glycine, 0.31; D-serine, 0.20; D-cycloserine, 1.46; (+)-HA-966, 4.06; and 7-chlorokynurenic acid, 1.81]. Spermine and spermidine enhanced [3H]MK-801 binding to the soluble receptor preparation (EC50, 4.3 and 20.1 microM, respectively), whereas putrescine and cadaverine gave small degrees of inhibitions. When spermine and spermidine were tested under conditions where [3H]MK-801 binding approached equilibrium, their ability to enhance [3H]MK-801 binding was much reduced, a result suggesting that the polyamines increase the rate to equilibrium. Putrescine antagonised the effects of spermine. Ifenprodil reduced [3H]MK-801 binding under both equilibrium and nonequilibrium conditions, although the high-affinity component of inhibition described in membranes was not observed. Ifenprodil antagonised spermine effects in an apparently noncompetitive manner. Desipramine was able to give total inhibition of specific [3H]MK-801 binding under nonequilibrium conditions with an IC50 of 4 microM, and this value was unaltered when [3H]MK-801 binding was allowed to reach equilibrium. These results suggest that the sites mediating the effects of glycine and its analogues, polyamines and desipramine are integral components of the NMDA receptor protein.

Animals↗
PubMed1971

Effect of central catecholamine alterations on the hypothermic response to 6-hydroxydopamine in desipramine treated rats.

The hypothermia observed in rats kept in a cold environment after the intracisternal administration of 6-hydroxydopamine was enhanced by desipramine. Since pretreatment with 6-hydroxydopamine virtually eliminated the temperature fall in response to a subsequent dose of 6-hydroxydopamine, brain catecholamines were implicated in the response. Preferential reduction of brain noradrenaline antagonized the hypothermia after 6-hydroxydopamine in desipramine-treated rats to a greater extent than did the preferential reduction of dopamine. The results indicate the importance of noradrenergic fibres in this hypothermic response, but do not exclude an involvement of brain dopaminergic pathways.

Animals↗
PubMed1978

Comparison of the responses of single cortical neurones to tyramine and noradrenaline: effects of desipramine.

1 The technique of microelectrophoresis was used in order to compare the actions of tyramine and noradrenaline on single neurones in the cerebral cortex of the rat.2 Tyramine could both excite and depress cortical neurones. Each tyramine-sensitive cell was also sensitive to noradrenaline. There was a high correlation between the directions of responses to tyramine and noradrenaline, most cells excited by tyramine being excited by noradrenaline, and most cells depressed by tyramine being depressed by noradrenaline.3 In the case of both excitatory and depressant responses, tyramine appeared to be less potent than noradrenaline.4 Tyramine evoked ;slower' responses than noradrenaline, both the latencies to onset and the recovery times being longer for responses to tyramine than for responses to noradrenaline.5 When the rates of release of tyramine and noradrenaline from micropipettes were measured in vitro, no significant difference could be observed between the transport numbers of the two drugs. Thus the difference in potency between the two drugs, and the difference in the time courses of responses to the two drugs, are presumably of biological origin.6 Desipramine could discriminate between neuronal responses to tyramine and noradrenaline: responses to tyramine were antagonized, while responses to noradrenaline were either potentiated or unaffected. Responses to DL-homocysteic acid were not affected by desipramine.7 The results are consistent with the hypothesis that tyramine is an indirectly acting sympathomimetic amine in the brain, and desipramine acts by blocking the uptake of both tyramine and noradrenaline into presynaptic noradrenergic nerve terminals.

Animals↗
PubMed1983

Effects of cocaine and desipramine on the neurally evoked overflow of endogenous noradrenaline from the rat heart.

1 Stimulation of postganglionic cardiac sympathetic nerves produced a stimulation frequency-dependent overflow of endogenous noradrenaline from the otherwise isolated rat heart. 2 Such nerve stimulation also produced increases in heart rate. There was significant correlation between heart rate increases and corresponding noradrenaline concentrations in the coronary venous effluent. 3 Cocaine (3 X 10(-5)M) caused a significant reduction in both the noradrenaline overflow and the heart rate increase, produced by nerve stimulation for 1 min at 4 Hz. 4 Desipramine (10(-6)M) caused a significant increase in the noradrenaline overflow produced by stimulation for 1 min (4 Hz) with a mean increase of approximately 60%. There was no significant effect on the heart rate increase produced by such stimulation. 5 The opposite effects of cocaine (3 X 10(-5)M) and desipramine (10(-6)M) on noradrenaline overflow are attributed to differences in the local anaesthetic properties of these agents.

Animals↗
PubMed1982

Double-blind comparison of doxepin and desipramine in patients with primary affective disorder.

A double-blind comparison of doxepin versus desipramine was performed in carefully defined patients with research diagnosis of Primary Affective Disorder. While both drugs showed equal efficacy after 4 weeks, doxepin demonstrated a more rapid onset of action and surprisingly few side effects. Desipramine did not prove to be "activating" and did not worsen agitated depression. Although doxepin showed few autonomic side effects, it was nevertheless sedating, indicating that tricyclics with more anticholinergic effects are not necessarily more sedating drugs.

Adult↗
PubMed1982

A double-blind study of zimelidine, a serotonin uptake inhibitor, and desipramine, a noradrenaline uptake inhibitor, in endogenous depression. I. Clinical findings.

A comparative evaluation of zimelidine, a potent and selective serotonin (5-HT) uptake inhibitor, and desipramine, a potent noradrenaline (NA) uptake inhibitor, was carried out in a 4-week randomized, double-blind study in 65 hospitalized patients with endogenous depression. For evaluation of the clinical effect, Hamilton Rating Scale for depression (HRS) and a 14-item scale chosen from the Comprehensive Psychopathological Rating Scale (CPRS) were used. The concentration of drug in plasma was determined on the same days as the clinical ratings. There were no significant difference in the overall therapeutic effect between the two drugs. However, zimelidine had significantly better effect on anxiety. Although both agents were well tolerated, the zimelidine-treated patients reported significantly less severe anticholinergic side effects. Body weight did not change significantly in either treatment group. In the total material ther were no significant correlation between plasma concentrations of zimelidine, norzimelidine and desipramine and the amelioration score of either HRS and CPRS.

Adult↗
PubMed1983

Effects of amitriptyline, desipramine and zimeldine, alone and in combination with ethanol, on information processing and memory in healthy volunteers.

Interactions of three antidepressants--amitriptyline, desipramine and zimeldine--with a single 0.8 g/kg body weight dose of alcohol were studied in healthy male volunteers. The dependent variables were performance measurements in the Continuous Performance Task and a cognitive memory task. Alcohol and desipramine showed different and specific deleterious effects on cognitive and memory functions, whereas amitriptyline produced a more generalized impairment. Zimeldine slightly improved performance in the Continuous Performance Task and antagonized effects of alcohol in both tasks.

Adult↗
PubMed1988

Comparison of desipramine, amitriptyline, zimeldine and alaproclate in six animal models used to investigate antidepressant drugs.

In the present paper the acute actions primarily of the tricyclic antidepressants amitriptyline and desipramine, the atypical antidepressant zimeldine and the potential antidepressant alaproclate were evaluated in six models used for studying antidepressant agents. These included the forced swim test, a modified learned helplessness procedure, the clonidine hypothermia test, the social dominance test (using the interaction with clonidine), a differential-reinforcement-of-low-rates (DRL-72s) schedule and conditioned avoidance response. The results showed desipramine to be effective in all the tests employed. Zimeldine was effective in the learned helplessness, DRL-72s and domination tests, but also caused notable deficits in two-way active avoidance response. Alaproclate was effective in all the tests except the domination paradigm. Amitriptyline was effective in all tests employed. The results are discussed in relation to the possible mechanism of action of these compounds in the test models employed.

Alanine↗
PubMed1990

Desipramine and nortriptyline antagonize apomorphine and reserpine hypothermia by a different mechanism.

The reversal of hypothermia, induced by reserpine or by a high (16 mg) dose of apomorphine, in male Swiss mice, does not seem to utilize a common mechanism. Desipramine (20 mg kg-1 i.p., 60 min) or nortriptyline (8 mg kg-1 i.p., 60 min) increased temperature in both reserpine (2.5 mg kg-1 s.c., 18-19 h) and apomorphine (16 mg kg-1 s.c., 30 min) treated mice. In apomorphine-treated animals the effect of both drugs was reversed by the mixed dopaminergic D1- D2-antagonist haloperidol (1 mg kg-1 i.p., 90 min), the D1-receptor blocking drug SCH 23390 (0.05 mg kg-1 s.c., 30 min), the alpha 1-adrenoceptor blocking drugs prazosin (3 mg kg-1 s.c., 90 min) and phenoxybenzamine (20 mg kg-1 i.p., 65 min), the beta-adrenoceptor blocking drug (+/-)-propranolol (10 mg kg-1 i.p., 120 min), and the opioid antagonist naloxone (2 mg kg-1 i.p., 15 min). In contrast the selective D2-antagonist (+/-)-sulpiride (100 mg kg-1 i.p., 90 min), and the alpha 2-antagonist yohimbine (2 mg kg-1 i.p., 75 min), failed to effect the reversal of apomorphine hypothermia brought about by desipramine or nortriptyline. Their temperature effects in reserpinized mice were not modified by any of the antagonists tested.

Animals↗
PubMed1981

Increased intracranial self-stimulation in rats after long-term administration of desipramine.

The effects of long- and short-term administration of the tricyclic antidepressant desipramine on intracranial self-stimulation in rats were studied with electrodes in the A10 region of the dopamine-containing cell bodies of the ventromedial tegmentum. Long-term desipramine administration resulted in a significant shift to the left in the ascending portion of the rate--current intensity function, indicating that the activity of the mesolimbic dopamine system was enhanced. These findings point to a possible dopaminergic mechanism of action of antidepressants and support speculations concerning the role of dopamine-containing neurons in the pathophysiology of depression.

Animals↗
PubMed1973

Interaction between clonidine and desipramine in man.

Interaction between the tricyclic antidepressant desipramine and the antihypertensive agent clonidine has been investigated in five hypertensive patients in a double-blind placebo controlled study. Introduction of the tricyclic antidepressant led to loss of blood pressure control in four of the patients. The average blood pressure rise in the desipramine period compared with the placebo period was 22/15 mm Hg in the lying position and 12/11 mm Hg standing. Thus addition of a tricyclic antidepressant may lead to loss of blood pressure control in a hypertensive patient treated with clonidine.

Adult↗
PubMed1998

Thyroid accumulation and adverse effects of imipramine and desipramine in rats after long-term administration.

The respective adverse effects of imipramine and desipramine on serum thyroid hormone levels and their accumulation in thyroid were investigated in male Wistar rats. Two groups of 30 rats were gavaged for 4 weeks with 30 mg/kg/day imipramine hydrochloride (IMI) or desipramine hydrochloride (DESI), while the control group (12 rats) received the arabic gum vehicle only. In the IMI-treated group, the serum thyroxine (T4) level significantly decreased (by 13%) and IMI and its metabolite DESI were accumulated in the thyroid, as pointed out by mean thyroid-to-serum concentration ratios close to 12 and 8, respectively. In the DESI-treated group, the mean thyroid-to-serum concentration ratio of the drug was close to 14, and significant decreases in both serum T4 (-20%) and triiodothyronine serum levels (-14%) were found. The accumulation of antidepressant drugs in the thyroid was more pronounced and the thyroid serum levels were even lower after DESI administration than after IMI administration. These results are in favour of an antithyroid action of IMI and DESI due to the formation of a complex in the thyroid between molecular iodine and the drugs or metabolites.

Animals↗
PubMed1981

Concentrations of desipramine in elderly women.

Seven elderly depressed women were given desipramine, and plasma concentrations of the drug were measured from blood samples drawn after a single dose and during long-term use. The concentrations were no different from those found in younger patients. Aging does not seem to alter the plasma concentration of desipramine, and the authors conclude that the increased incidence and severity of the drug's side effects are probably not due to high drug concentrations.

Aged↗
PubMed1984

A case of severe acute desipramine overdose.

The authors describe a patient who ingested a toxic quantity of desipramine. His initial desipramine plasma concentration of 1627 ng/ml was associated with generalized seizures, bradycardia, and a respiratory arrest.

Acute Disease↗
PubMed1989

A controlled trial of desipramine in 18 men with posttraumatic stress disorder.

Eighteen male U.S. veterans meeting DSM-III criteria for posttraumatic stress disorder (PTSD) completed a 4-week double-blind, crossover study comparing administration of 200 mg/day of desipramine with placebo. Response was measured by using the Beck Depression Inventory, the Hamilton Rating Scale for Depression, the Hamilton Rating Scale for Anxiety, and the Impact of Event Scale. Overall, the only apparent response to desipramine was in some symptoms of depression; there were no changes in anxiety and other PTSD symptoms.

Adult↗
PubMed1990

Value of the DST for predicting response of patients with major depression to hospitalization and desipramine.

The authors examined the value of the dexamethasone suppression test (DST) for predicting response of patients with unipolar, nonpsychotic major depression to 1 week of hospitalization without antidepressant drugs and to a 4-week trial of desipramine at a fixed plasma level. The rates of response to hospitalization without drug treatment (defined as a score of 12 or less on the Hamilton Rating Scale for Depression) were not significantly different for the patients with a positive DST and those with a negative DST. This finding differs from those of prior studies of the DST and response to placebo. The responses of the DST-positive and DST-negative patients to desipramine also did not differ, a finding that replicates those in some prior reports.

Adult↗