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PubMed1991

Simultaneous determination of imipramine and amitryptiline by derivative spectrophotometry.

Three methods are proposed for the simultaneous determination of imipramine and amitryptiline by derivative spectrophotometry, one of them using both first- and second-derivative spectra, and the others using the first- and second-derivative spectra, respectively, obtained from a "diode array" spectrophotometer. The methods allow the determination of 0.62-10.14 micrograms ml-1 of imipramine, and 0.63-10.04 micrograms ml-1 of amitryptiline, and have been applied to their determination in blood serum.

Amitriptyline↗
PubMedDate not supplied

Determination of carbamazepine by HPLC electrochemical detection and application for estimation of imipramine desipramine, doxepin and nordoxepin.

A simple analytical procedure for the estimation of carbamazepine in serum is presented. The procedure utilizes high pressure liquid chromatography with an electrochemical detection technique. The assay was also found applicable for the simultaneous separation of imipramine from desipramine or doxepin from nordoxepin. The procedure does not require the use of UV detection, is less time consuming and provides sensitivity at ng and microgram level for the tricyclic antidepressants studied and carbamazepine, respectively. This sensitivity is within the therapeutic range required for drug monitoring. The method is useful for the separation and quantitation of carbamazepine from imipramine and desipramine which is useful in cases where one of these drugs is given concurrently with carbamazepine.

Carbamazepine↗
PubMed1995

Effect of long-term in vivo treatment with imipramine on the oxidative energy metabolism in rat brain mitochondria.

The effects of long-term administration of the tricyclic antidepressant imipramine on energy metabolism of rat brain mitochondria were examined. Intraperitoneal administration of the drug resulted in significant stimulation of the state 3 respiration rates with glutamate, pyruvate+malate, beta-hydroxybutyrate and succinate as the substrates. The effect was evident within a week of imipramine administration and was sustained through the second week of the drug treatment. State 4 respiration rates were also found to be increased in general. However, the respiration with ascorbate+TMPD as the electron donor system decreased. The intramitochondrial content of cytochrome b and c+c1 increased in the first week of the drug treatment; that of aa3 cytochrome increased only in the second week.

Animals↗
PubMed1986

Rapid reductive-carboxylation of secondary amines, one pot synthesis of N'-(4-11C-methyl)imipramine.

A new rapid high yield synthesis of radiolabeled N'-(4-11C-methyl)imipramine has been developed using a reductive-carboxylation approach, in which 11CO2 is reacted with either N'-trimethylsilyldesimipramine or N'-lithium derivative of desimipramine, followed by lithium aluminum hydride reduction, to give no carrier added or carrier added 11C-labeled imipramine respectively. The final product is characterized by chromatographic and spectroscopic methods.

Carbon Radioisotopes↗
PubMed1992

Disruption of female rat vaginal cyclicity by daily treatment with imipramine.

Intact, adult female rats were injected for 21 days with 10 mg/kg of the tricyclic antidepressant imipramine. During this time, there was almost total suppression of reproductive cyclicity as indicated by the absence of vaginal proestrus and by the absence of sexual receptivity. However, there was no evidence for a permanent disturbance in the female reproductive system. When treatment with imipramine was terminated, vaginal cyclicity resumed within the next 2 to 8 days. The generality of the current findings to other antidepressants or to the human female is currently unknown. However, since human females are the primary consumers of antidepressants, caution should be exercised when females are given antidepressant therapy.

Animals↗
PubMed1993

Adaptation of the NMDA receptor in rat cortex following chronic electroconvulsive shock or imipramine.

Chronic (14 days) administration of either imipramine or electroconvulsive shock effected significant changes in the ligand binding properties of the NMDA (N-methyl-D-aspartate) receptor complex in rat cortex. These changes were manifested as: (1) a reduction in the potency of glycine to inhibit the binding of 5,7-dichloro[3H]kynurenic acid to strychnine-insensitive glycine receptors; and (2) a reduction in the proportion of high affinity, glycine-displaceable [3H]CGP-39653 binding to NMDA receptors. Chronic electroconvulsive shock, but not imipramine treatment also reduced the density of [3H]CGP-39653 binding sites in cortical membranes. These findings demonstrate that the ability of chronic antidepressant treatments to induce adaptive changes in the glycine and glutamate regulatory sites of the NMDA receptor is not species specific, since it obtains in rats as well as mice.

2-Amino-5-phosphonovalerate↗
PubMed1993

Brofaromine in elderly major depressed patients--a comparative trial versus imipramine.

In an 8-week controlled double-blind clinical trial with a total of 189 elderly patients brofaromine showed comparable efficacy to imipramine (Hamilton Depression Scale, von Zerssen self-rating scale, global evaluation). The numbers of adverse events were the same in both groups, but the spectrum differed distinctly. In the global evaluation of tolerability, there was an advantage for brofaromine. Mean daily doses were 85 mg/day in the brofaromine group and 87 mg/day in the imipramine group. Long-term efficacy and tolerability also proved to be good in the open follow-up of the patients treated with brofaromine.

Aged↗
PubMed1994

Lack of association between platelet tritiated imipramine binding and clinical status of depressed patients on chronic antidepressant treatment.

Platelet tritiated imipramine binding (Bmax) was studied in 33 depressed patients, before and after 1 and 4 weeks of antidepressant treatment, and in 34 healthy volunteers. The Bmax was significantly lower (-21%) in drug-free depressed patients than in controls and increased significantly as early as the first week of treatment to reach the control value, in parallel with a 38% decrease in the Hamilton depression rating scale (HDRS) score. After 4 weeks of treatment, the Bmax was still normal and remained significantly higher than the baseline value, while the clinical state of the patients had greatly improved (a 63% decrease in the HDRS score). However, an increase in the Bmax also occurred in non-responders to treatment. In addition, we observed that the ability of the treatment to increase the Bmax depended on the pharmacological profile of the drug used. The present results show that, in patients on antidepressant medication, platelet tritiated imipramine binding normalization cannot be considered as a marker of clinical remission.

Adult↗
PubMed2005

Quantitative analysis of immunolabeling for serotonin and for glutamate transporters after administration of imipramine and citalopram.

Serotonin (5-hydroxytryptamine, 5-HT) is an amine neurotransmitter derived from tryptophan and is important in brain systems regulating mood, emotional behavior, and sleep. Selective serotonin reuptake inhibitor (SSRI) drugs are used to treat disorders such as depression, stress, eating disorders, autism, and schizophrenia. It is thought that these drugs act to prolong the action of 5-HT by blocking reuptake. This may lead to decreased 5-HT content in the nerve fibers themselves; however, this has not previously been directly demonstrated. We have studied the effects of administration of two drugs, imipramine and citalopram, on levels of 5-HT in nerve fibers in the murine brain. Quantitative analysis of the areal density of 5-HT fibers throughout the brain was performed using ImageJ software. While a high density of fibers was observed in mid- and hind-brain regions and areas such as thalamus and hypothalamus, densities were far lower in areas such as cortex, where SSRIs might be thought to exert their actions. As anticipated, imipramine and citalopram produced a decline in 5-HT levels in nerve fibers, but the result was not uniform. Areas such as inferior colliculus showed significant reduction whereas little, if any, change was observed in the adjacent superior colliculus. The reason for, and significance of, this regionality is unclear. It has been proposed that serotonin effects in the brain might be linked to changes in glutamatergic transmission. Extracellular glutamate levels are regulated primarily by glial glutamate transporters. Qualitative evaluation of glutamate transporter immunolabeling in cortex of control and drug-treated mice revealed no discernable difference in intensity of glutamate transporter immunoreactivity. These data suggest that changes in intracellular and extracellular levels of serotonin do not cause concomitant changes in astroglial glutamate transporter expression, and thus cannot represent a mechanism for the delayed efficacy of antidepressants when administered clinically.

Amino Acid Transport System X-AG↗
PubMed2005

Repeated administration of citalopram and imipramine alters the responsiveness of rat hippocampal circuitry to the activation of 5-HT7 receptors.

The effects of a selective serotonin reuptake inhibitor, citalopram, and a tricyclic antidepressant drug, imipramine, administered repetitively for 14 days, were investigated ex vivo in rat hippocampal slices. Spontaneous epileptiform bursts were recorded from the CA3 area in nominally Mg(2+)-free incubation conditions. 5-carboxamidotryptamine (5-CT) dose-dependently increased bursting frequency in the presence of N-[2-[4-(2-methoxyphenyl)-1 piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide (WAY 100635). This effect could be dose-dependently blocked by (2R)-1-[(3-Hydroxyphenyl)sulfonyl]-2-[2-(4-methyl-1-piperidinyl)ethyl]pyrrolidine hydrochloride (SB 269970), thus implicating the involvement of 5-HT(7) receptors. Repeated treatment with citalopram or imipramine resulted in an attenuation of the excitatory effects of the activation of hippocampal 5-HT(7) receptor.

Analysis of Variance↗
PubMed2006

Neonatal citalopram exposure produces lasting changes in behavior which are reversed by adult imipramine treatment.

Neonatal exposure to antidepressants, including selective serotonin reuptake inhibitors such as citalopram, induces behavioral disturbances which persist in mature rats. These disturbances have been proposed to model the symptoms of endogenous depression. However, to date there is scant evidence for the predictive validity of any of these behaviors in response to adult antidepressant treatments. In order to directly assess the predictive validity of the early antidepressant exposure paradigm, the present study examined whether the behavioral abnormalities observed in adult animals exposed as neonates to citalopram can be reversed by adult antidepressant treatment with the prototypic antidepressant, imipramine. As noted earlier, neonatal citalopram exposure robustly increased locomotor activity and impaired male sexual behavior in adult rats. These behavioral changes were reversed following chronic adult imipramine treatment. No such reversal was observed in handled, saline treated rats. The present data support the hypothesis that some of the lasting behavioral abnormalities induced by early antidepressant exposure are sensitive to clinically relevant antidepressant treatments thus adding a measure of predictive validity to this paradigm as a model of these depressive symptoms.

Adrenergic Uptake Inhibitors↗
PubMed2004

Chronic treatment with imipramine reverses immobility behaviour, hippocampal corticosteroid receptors and cortical 5-HT(1A) receptor mRNA in prenatally stressed rats.

Prenatal stress in the rat induces enhanced reactivity of the hypothalamus-pituitary-adrenal (HPA) axis, disturbances in a variety of circadian rhythms and increased anxiety-like behaviour. Such abnormalities parallel those found in human depressed patients. Prenatally stressed (PS) rats could represent, therefore, an interesting animal model for the evaluation of the efficacy of pharmacotherapeutic intervention in psychiatric disorders that has often been addressed using control animals. In the present study, PS and non-stressed rats were chronically treated with the tricyclic antidepressant imipramine (10 mg/kg i.p. for 21 days) and assessed in the forced swim test. Glucocorticoid receptor binding sites in the hippocampus were measured and 5-HT(1A) receptor mRNA levels in the frontal cortex were also assessed. PS rats were characterised by increased immobility in the forced swim test, reduced hippocampal corticosteroid receptor binding and increased levels of cortical 5-HT(1A) mRNA. All these parameters were significantly reversed by chronic imipramine treatment. Conversely, no significant effects were observed for non-stressed rats. All these effects are consistent with the expected pharmacotherapy of depression-like abnormalities in PS rats. These results further indicate that PS rats are a relevant animal model of depression.

Animals↗
PubMed1987

Depletion of cellular beta-hexosaminidase by imipramine is prevented by dexamethasone; implications for treating psychotic hexosaminidase-A deficient patients.

Normal human skin fibroblasts secrete most of their hexosaminidase (Hex) into the medium upon incubation with 10(-4) imipramine, while preincubation with 2.5 X 10(-9) M dexamethasone prevents this effect. These results support the hypotheses that 1) treatment of psychotic Hex A deficient patients with amphiphilic antidepressants (such as imipramine) aggravates the patients' disease through depletion of their residual cellular Hex A, and 2) concomitant medication with dexamethasone may mitigate this drug-induced deleterious effect.

Cells, Cultured↗
PubMed1997

Long-term stress degenerates, but imipramine regenerates, noradrenergic axons in the rat cerebral cortex.

Exposed to a forced walking stress for 2 weeks, some rats became persistently inactive (depression-model rats), whereas others gradually recovered from exhaustion (spontaneous recovery rats). We also studied rats exposed to short-term stress, rats without stress, and the model rats treated with imipramine or saline. We examined the density of noradrenergic axons in the frontal cortex using retrograde labeling of the locus coeruleus with horseradish peroxidase injected into the cortex and immunohistochemical staining of cortical axons with dopamine beta-hydroxylase antiserum. The density was significantly lower in the depression-model rats, but tended to be higher in the recovery rats and short-term stressed rats. Chronic treatment with imipramine significantly increased the density in the model rats. There was also a correlation between the density of noradrenergic axons and the recovery rate of activity. Our results suggest that cortical noradrenergic degeneration is involved in the pathogenesis of depression.

Adrenergic Uptake Inhibitors↗
PubMed2003

Effects of chronic exercise and imipramine on mRNA for BDNF after olfactory bulbectomy in rat.

We examined the effects of chronic activity wheel running and antidepressant treatment on brain-derived neurotrophic factor (BDNF) messenger RNA (mRNA) in multiple brain regions-hippocampal formation (HF), ventral tegmental area/substantia nigra (VTA/SN), nucleus accumbens (NAc), and piriform cortex (PFx)-after bilateral olfactory bulbectomy (OBX). Male, Long-Evans rats (n=72) underwent either sham or OBX surgery and were randomly divided into eight experimental groups in a 2 (sham vs. OBX) x 2 (sedentary vs. activity wheel)x2 (saline vs. imipramine) factorial design. Animals were killed after 21 days of treatment. Drug x exercise interaction effects were observed for HF (P=0.006-0.023) and VTA/SN (P=0.021); exercise increased BDNF mRNA in the saline treated animals but not in the imipramine treated animals. OBX did not affect BDNF mRNA in the HF or VTA/SN (P>0.05). BDNF mRNA levels in the PFx were not altered by exercise, drug, or OBX (P>0.05). These results suggest that the effect of exercise on BDNF mRNA extends beyond the HF to the mesolimbic ventral tegmental area and that the potentiation of BDNF mRNA by exercise and antidepressant pharmacotherapy, reported by other investigators, is time limited.

Animals↗
PubMed2000

Chronic lithium chloride fails to prevent imipramine-induced sensitization to the dopamine D(2)-like receptor agonist quinpirole.

Lithium salts, an effective antimanic treatment, are able to prevent the development of the dopaminergic behavioural supersensitivity induced by chronic treatment with neuroleptics, by denervation of the dopaminergic terminal fields and by rapid eye movements (REM) sleep deprivation, which is considered a model of mania. We have studied the effect of a lithium (LiCl) diet, inducing a lithium serum level in the range of therapeutic efficacy, on the development of the supersensitivity to the locomotor effect of the dopamine D(2)-like receptor agonist, quinpirole, induced by chronic treatment with the antidepressant drug, imipramine. The results show that lithium is not able to prevent the development of such behavioural supersensitivity. The present data suggest that antidepressant-induced dopaminergic supersensitivity might provide a useful model of those manic states induced by (or subsequent to) antidepressant treatments. Moreover, the finding is consistent with the view that antidepressant-induced dopaminergic supersensitivity might play a role in the therapeutic effect of these drugs (which is known to be augmented by lithium, and not antagonised). Finally, the results show that the dopaminergic supersensitivity induced by imipramine is qualitatively different from that induced by neuroleptics or denervation of the dopaminergic terminal fields.

Analysis of Variance↗
PubMed2001

Carbamazepine prevents imipramine-induced behavioural sensitization to the dopamine D(2)-like receptor agonist quinpirole.

Chronic treatment with antidepressants potentiates the behavioural sensitivity to the administration of dopamine receptor agonists. Such supersensitivity might be involved in the mechanism of action of antidepressant drugs, but it has also been suggested to play a role in the mechanisms underlying antidepressant treatment-related mania (i.e. antidepressant-induced mood switch and rapid cycling). Consistently to this hypothesis, we have recently shown that lithium salts, which are poorly effective in antidepressant-related mania, fail to prevent the development of imipramine-induced supersensitivity to the locomotor effect of the dopamine D(2)-like receptor agonist quinpirole. In the present paper, we report the ability of carbamazepine, an anticonvulsant with antimanic and mood stabiliser properties, to prevent the development of supersensitivity to the locomotor response to quinpirole induced by chronic treatment with imipramine. The present results, together with the results of our previous study, might contribute to explain the different responsiveness to lithium and carbamazepine observed in some manic patients, and are consistent with the clinical data suggesting that carbamazepine might be more effective than lithium in antidepressant-related mania.

Analysis of Variance↗
PubMed1998

Effects of imipramine and sertraline on protein kinase activity in rat frontal cortex.

Three-week administration of sertraline or imipramine to rats (10 mg/kg, intraperitoneally, twice a day) increased ex vivo cyclic AMP-dependent protein kinase activity in the soluble but not in the particulate fraction of the frontal cortex. However, cyclic AMP-dependent protein kinase activity was not affected in either fraction of the parietotemporal cortex and hippocampus. Neither antidepressant altered protein kinase C activity in the soluble and particulate fractions or Ca2+/calmodulin-dependent protein kinase II activity in the frontal cortex. Therefore, sertraline and imipramine both selectively enhance cyclic AMP-dependent protein kinase activity in the frontal cortex. This enhancement might be involved in their biochemical mechanisms.

1-Naphthylamine↗