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PubMed1982

Effects of chronic treatment with imipramine on the behavioural and electroencephalographic modifications induced by clonidine in the rat.

The influence of repeated administration of imipramine on the EEG and behavioural effects of clonidine has been studied in the rat bearing chronic electrodes. Clonidine induced behavioural depression and EEG synchronization in control rats. Mydriasis, hyperirritability, stereotyped behaviour and EEG desynchronization were elicited by clonidine on the first and second days after discontinuation of the treatment with imipramine (15 mg/kg, i.p., daily for 21 days). On the 9th. day the animals responded to clonidine with sedation and EEG synchronization. These results support the hypothesis that chronic treatment with tricyclic antidepressant drugs changes the sensitivity of central noradrenergic neurones.

Animals↗
PubMed1983

Effects of chronic treatment with imipramine, trazodone and electroshock on the behavioural and electroencephalographic modifications induced by clonidine in the rat.

The influence of some typical and atypical antidepressant drugs on the EEG and behavioural effects of clonidine has been studied. The results indicate that chronic administration of imipramine or of electroshock led to the abolition of the behavioural depression and of the EEG synchronisation induced by clonidine. Chronic administration of trazodone was without effect. These results support the hypothesis that chronic treatment with imipramine and electroshock elicits a down-regulation of noradrenergic presynaptic receptors. These structures seem to be largely unaffected by trazodone, which could have a favourable effect on depression through its influence on beta-adrenergic receptors and on the 5-HT system.

Animals↗
PubMed1984

Binding and function of serotonin 2 receptors following chronic administration of imipramine.

Experiments were undertaken to determine whether alterations in the binding of 5-HT2 receptors in the cerebral cortex of rat brain, induced by antidepressant drugs, are related to behavioral changes observed in response to the administration of a precursor of serotonin. Chronic (5 days), but not acute, administration of an imipramine-yohimbine combination resulted in a significant decrease in the binding of 5-HT2 receptors in the frontal cortex and wet-dog shakes induced by 5-hydroxytryptophan (5-HTP). The decrease in the binding to 5-HT2 receptors was due entirely to a change in the concentration of binding sites with no modification in receptor affinity. The behavioral alteration resulted from a decrease in the maximal response to 5-HTP. Further experiments revealed that chronic (5 days) administration of imipramine alone altered the behavioral response to 5-HTP without changing the binding of 5-HT2 receptor binding and that changes in 5-HT2 binding in the cortex were not always accompanied by an alteration in the response to 5-HTP. These results suggest a lack of correlation between the drug-induced change in 5-HT2 binding in frontal cortex and the function of serotonin 2 receptors.

5-Hydroxytryptophan↗
PubMed1977

Bladder muscle contractility. Comparative effects and mechanisms of action of atropine, propantheline, flavoxate, and imipramine.

The anticholinergic and antispasmodic activity of atropine, propantheline, imipramine, and flavoxate were judged by each drug's ability to inhibit bethanechol chloride and barium chloride-induced canine detrusor contractions. In this in vitro model, atropine and propantheline are pure anticholinergic agents. Imipramine significantly decreases both bethanechol and barium-induced contractions, while flavoxate only minimally inhibits the response to either stimulant.

Animals↗
PubMed1981

Treatment of imipramine overdose in children.

Enuresis is a common problem often treated effectively with imipramine hydrochloride. The usefulness of this therapy carries with it, however, the risk of accidental overdose by younger siblings of these enuretic patients. Traditional support measures are effective in the treatment of the mild to moderate overdose, while separate symptomatic treatment of seizures and cardiac arrhythmias is possible as outlined herein. Physostigmine offers a single alternate treatment which is effective in the full panorama of life-threatening manifestations of an imipramine overdose.

Adult↗
PubMed1976

Repeated acquisition of behavioral chains: effects of methylphenidate and imipramine.

A method involving repeated acquistion of behavioral chain was used to assess the effects of methylphenidate and imipramine in individual animals. Pigeons obtained food for completing a 4-response chain, which was changed from session to session. Learning was defined by the decrease in errors across trials within a session; overall accuracy was measured by total errors per session. For comparison, the drug tests were also conducted under a performance condition, in which the 4-response chain was the same from session to session. In general, both drugs increased total errors per session as a function of dose under both the learning and performance conditions. The error-increasing effect was greater with imipramine than with methylphenidate and was detected at lower doses under the learning condition than under the performance condition. Under the learning condition, the higher doses of both drugs decreased the rate of within-session error reduction. Although neither drug enhanced accuracy at any of the doses tested, the lower doses of methylphenidate slightly decreased total trial time under both the learning and performance conditions.

Animals↗
PubMed1976

Effects of imipramine, chlorimipramine, and fluoxetine on cataplexy in dogs.

Four narcoleptic dogs with cataplexy were given trials with the serotonin uptake blockers imipramine and chlorimipramine (known to be effective in treating cataplexy in humans). An even more selective serotonin uptake blocker, fluoxetine, was also tested. Injections of placebo, test compound, and placebo were given respectively on 3 successive days. Anticataplectic effects were measured approximately 30 min, 3 hr, and 6 hr postinjection by recording elapsed time and number of cataplectic episodes during the dogs' attempts to eat ten pieces of a desired food presented in a standard fashion. Imipramine (1 mg/kg) and fluoxetine (1.5 and 3.0 mg/kg)significantly improved performance, while chlorimipramine (0.5-5 mg/kg) had no clear effect. Data were not totally consistent with the notion that serotonin uptake blockers improve cataplexy in dogs, since chlorimipramine was not effective in these animals.

Animals↗
PubMed1980

A comparison of the effects of d-amphetamine, cocaine, imipramine and pentobarbital on local and overall rates of responding maintained under a four-component multiple fixed-interval schedule.

Key pecking of pigeons was maintained under a four-component multiple fixed-interval schedule with values of 1-min, 3-min, 5-min and 10-min. Each schedule value was correlated with a different key color, each of which controlled distinctively different performances. This schedule generated a range of response rates both within and across the different interval components that permitted a direct comparison of drug effects on local and overall rates of responding. d-Amphetamine, cocaine, imipramine and pentobarbital all increased low local response rates at doses that did not affect or decreased higher rates within each fixed interval. Similar effects were obtained when different overall rates of responding were analyzed except that imipramine and pentobarbital also increased the highest overall rates occurring under the 1-min schedule.

Animals↗
PubMed1987

The effect of chronic imipramine and electroconvulsive shock treatment on [3H]DADLE binding to cortical membranes of rats pretreated with chronic reserpine or 6-hydroxydopamine.

Repetitive electroconvulsive shock treatment (for 8 days) or chronic administration of imipramine (10 mg/kg/day IP for 14 or 21 days) elevated the density of opioid delta receptors in the cerebral cortex of the rat. Electroconvulsive shock treatment produced a similar effect in rats treated subchronically with reserpine or receiving intraventricularly 6-hydroxydopamine, but these manipulations of central catecholamines prevented the action of imipramine.

Animals↗
PubMed1989

Disruption of FR-40 by 5-HT agonists. I. Effects of chronic imipramine or trazodone.

Doses of LSD, quipazine, 8-OHDPAT and TFMPP were established that prominently disrupted FR-40 operant response pattern in two groups of rats. Subsequently, one group received daily intraperitoneal (IP) injections of imipramine, 2.5 mg/kg, for 4 weeks, then 10 mg/kg for 2 additional weeks. The second group received 5 mg/kg/day, IP, of trazodone for the first 4 weeks, then 20 mg/kg/day for the next two weeks. For these periods and the 3 weeks after discontinuing the chronic drug treatments (washout), test doses of the 4 agonists were evaluated twice weekly in random order for their effects to decrease FR-40 reinforcements and increase pauses. No consistent, systematic changes in sensitivity to the agonist effects on FR-40 behavior were observed during chronic drug treatments, although significant effects were at times observed. However, during the washout period in the imipramine group, both LSD and 8-OHDPAT effects on reinforcements were reversed to baseline levels. The effect of 5-OHDPAT on pauses during washout in this group was also attenuated. During washout in the trazodone group, the 8-OHDPAT-induced pausing and loss of reinforcements was reduced so as to be not significantly different from baseline values. Previous studies have demonstrated antagonism of LSD- and quipazine-induced disruption of FR-40 by pretreating with the 5-HT2-selective antagonist pirenperone (28). Since chronic antidepressants down-regulate brain 5-HT2 binding sites, the effects of LSD and quipazine were expected to be attenuated, which was not the case.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Chronic imipramine does not block cocaine-induced increases in brain stimulation reward.

Self-stimulating rats implanted with ventral tegmental area electrodes were tested with 15 mg/kg cocaine HCl before and after chronic imipramine treatment. Chronic imipramine had no influence on cocaine's ability to lower brain stimulation reward thresholds, suggesting that tricyclic antidepressant treatment does not block cocaine-induced euphoria.

Animals↗
PubMed1991

Down-regulation of dopamine1 (D1) receptors by chronic imipramine is species-specific.

Chronic treatment with imipramine (15 mg/kg, twice daily for 14 days) induces a down-regulation of limbic D1 receptors in rats but not in mice. In this mouse strain, both chronic and acute imipramine treatment have been shown to produce clear behavioral effects in the forced swim test. While the data presented here are consistent with previously reported findings in rats, they demonstrate that the down-regulation of D1 receptors by chronic antidepressant treatment is species-specific. This phenomenon indicates that D1 receptor down-regulation is not critical to the therapeutic mechanism of action of antidepressants.

Animals↗
PubMed1993

Effects of indeloxazine HCl on kindled amygdaloid seizures in rats: comparison with the effects of phenytoin, diazepam, ethanol, and imipramine.

The anticonvulsant effect of [(+/-)-2-[(inden-7-yloxy)methyl]morpholine (indeloxazine) HCl, a new cerebral activator, was investigated in rats against kindled seizures from the amygdala, an assumed model of secondarily generalized seizures in human. Indeloxazine (0.25-10 mg/kg, IP) dose-dependently depressed the kindled seizure and shortened the evoked amygdaloid afterdischarge. A high dose of indeloxazine (40 mg/kg, IP), however, induced generalized seizures. Comparison of the effects on the kindled seizures of indeloxazine to those of phenytoin, diazepam, ethanol, and imipramine revealed that the anticonvulsant actions of indeloxazine are similar to those of imipramine but not to those of phenytoin, ethanol, and diazepam. The results suggest that indeloxazine may exert its action through the monoaminergic system in the brain.

Animals↗
PubMedDate not supplied

Leu-enkephalin content in rat brain during prolonged treatment with imipramine or amitriptyline.

Male Wistar rats were treated with imipramine /IMI/ /2 or 10 mg/kg, p.o./ or amitriptyline /AMI/ 10 mg/kg, p.o./ by drinking water. Each drug was given once or over periods of 1, 3, 4, 6 and 9 months. Leu-enkephalin /LENK/ content was measured by radioimmunoassay in the striatum, hypothalamus and brain perfusates after different periods of the treatment with antidepressants. A single 10 mg/kg dose of IMI increased the level of LENK in the striatum and decreased it in the hypothalamus. Six months after IMI treatment the level of LENK in the striatum was decreased after a 2 mg/kg dose and increased after 10 mg/kg; in the hypothalamus a dose-dependent increase of LENK content was observed. In brain perfusates the level of LENK was decreased 3 months after IMI treatment, but highly increased after a 9-month administration. This indicates that during prolonged treatment with imipramine the central enkephalinergic activity is dynamically changed and can affect the psychopharmacological effects of IMI. After the prolonged treatment with AMI a decrease of LENK level in the striatum was observed only after 4 months of the drug administration, and no changes were seen in the hypothalamus. It is suggested that both antidepressants studied have different action on the central enkephalinergic system.

Administration, Oral↗
PubMed1995

The effect of chronic treatment with imipramine on the immunoreactivity of animals subjected to a chronic mild stress model of depression.

A depression-like state was induced in Wistar rats by chronic (3-week) exposure to very mild, unpredictable stress, which led to diminished food consumption and diminished preference for sweet drinks (anhedonia). Anhedonia was then abolished by 5 weeks of daily administration of imipramine to the continually stressed animals. One day after the last drug injection and stressful event, a statistically significant decrease in the proliferative activity of splenocytes to Con A stimulation in vitro was observed in those animals. Eight weeks of stress (without antidepressant therapy) affected likewise, but in a less potent and non-significant manner, the activity of splenocytes. Administration of imipramine alone for a period of 5 weeks did not modify the activity of these cells.

Animals↗
PubMed1980

A re-examination of the clinical effects of imipramine and amitriptyline in depressive illness.

A double-blind trial of amitriptyline and imipramine was conducted in patients suffering from depressive illness. The results failed to confirm the prevalent belief that amitriptyline has a greater sedative effect and superior anxiolytic properties than imipramine. The therapeutic effect of these drugs was not shown to be related to their sedative properties and with regard to anxiety the reverse appeared to be true.

Amitriptyline↗
PubMed1984

Learned helplessness decreases [3H]imipramine binding in rat cortex.

Specific binding of [3H]imipramine decreased in frontal neocortex from rats demonstrating learned helplessness, an animal model of depression. The decrease was in maximal binding but not in affinity for the receptor site. No change in [3H]imipramine binding was found in septum or hippocampus. The receptor changes found in frontal neocortex parallel behavioral and neurochemical changes produced by learned helplessness in this region. These changes are also similar to those found in the frontal neocortex from suicides and in platelets of patients with depression.

Animals↗
PubMed1984

A double-blind comparison of fluvoxamine, imipramine and placebo in depressed patients.

In a placebo-controlled, double-blind study of 91 out-patient depressives, the anti-depressant effect of fluvoxamine, a selective serotonin uptake inhibitor was compared to that of imipramine. Overall drug effects were relatively weak but analyses in selected sub-groups showed both active drugs superior to placebo. Effects of fluvoxamine were more marked in non-situational depressives and it did not improve sleep while effects of imipramine were more marked in retarded depressives and on retardation ratings, suggesting that fluvoxamine may have a different pattern of clinical effects. Side effects of Fluvoxamine were predominantly gastrointestinal and it did not produce postural hypotension or anticholinergic side-effects.

Adult↗