Pinealectomy and reserpine advanced the reorganization of the circadian rhythm of motor activity of rats following a ten-hour shift in the photoperiod. Bilateral electrolytic lesion of the hypothalamic suprachiasmatic nuclei and administration of the antidepressant drug, imipramine, on the contrary, delayed the rhythm change. The results suggest a possible antagonistic reciprocal relationship between the pineal gland and the main pacemaker, whose balance causes a gradual adaptation of animals to the changing environment. Fast reorganization of motor activity at pineal dysfunction or under the influence of depressogenic drugs could cause desynchronization and psychiatric disorders in a form of depression.
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The effects of imipramine (single dose of 100 mg orally) and lofepramine (single dose of 140 mg orally) in comparison to placebo on the EEG power spectra were examined in 24 non-selected healthy male volunteers. All subjects received the three drugs in a completely counterbalanced sequence. On the basis of their relative alpha-intensity the Ss were divided in two groups of 12 Ss each (high and low alpha-intensity). Two-way analyses of variance were computed for the absolute power in the alpha-, beta-, delta- and theta-frequency-bands. Imipramine increased the intensity of the delta-, theta- and beta-frequency-bands and decreased the power in the alpha-band. Lofepramine increased the intensity of the beta-band. The effects of imipramine and lofepramine are dependent on the relative power in the alpha-band of the Ss.
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The cardiovascular effects and toxicity of tricyclic antidepressants (TCAs) have been well documented in medical literature. The most common manifestation of such effects is slowing of intraventricular conduction, manifested by prolonged PR, QRS and QT intervals on the standard electrocardiogram (ECG) and postural hypotension. In contrast to TCAs, selective serotonin reuptake inhibitors (SSRIs), including fluoxetine and citalopram, are considered to cause less effect on cardiac impulse conduction. In addition, these compounds induced significantly less anticholinergic, antihistaminergic and cardiotoxic side-effects than TCAs. However, there is an increasing number of case reports on dysrhythmias, like atrial fibrillation or bradycardia and syncope associated with fluoxetine and another SSRI treatment and overdose. Although such reports have not been common, they do raise concerns. In cardiac tissues isolated from canine, rabbit, rat and guinea pig hearts we have found that fluoxetine and citalopram inhibited cardiac Na+ and Ca2+ channels. These direct cardiac electrophysiological effects were similar to those of observed for tricyclic antidepressants clomipramine and imipramine. The inhibition of cardiac Ca2+ and Na+ channels by fluoxetine may explain most cardiac side-effects observed occasionally with the drug and mild but significant bradycardia reported during chronic treatment. Our results suggest that fluoxetine and citalopram may have antiarrhythmic (class I + IV type), as well as proarrhythmic properties (due to impairment of atrioventricular or intraventricular conduction and shortening of repolarization). Taking all these into consideration, in depressed patients having also severe cardiac disorders, ECG control may be suggested during fluoxetine and probable another SSRI therapy. The primary goal of this review is to compare these direct cardiac effects of fluoxetine and citalopram to those of previously reported for TCAs. This paper also summarizes the recently observed effects of fluoxetine apparently not related to the blockage of 5-HT transporter based on literature.
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Paroxetine increases serotonergic neurotransmission by inhibiting presynaptic reuptake of serotonin (5-hydroxytryptamine; 5-HT) and thereby increasing the level of the neurotransmitter at the synaptic cleft. In vitro, it is a more potent inhibitor of serotonin uptake than the selective serotonin reuptake inhibitors (SSRIs) Citalopram, fluvoxamine and fluoxetine. Paroxetine was more potent than sertraline in one study that compared mean inhibition constants for serotonin uptake, but not in another study that compared the concentrations required to inhibit serotonin uptake by 50%. In contrast to the tricyclic antidepressants, paroxetine has little effect on the uptake of dopamine or noradrenaline (norepinephrine) in vitro. It has negligible affinity for αr(1-), αr(2-) and βr-adrenoceptors, dopamine D(1) and D(2) receptors, hi starnine H(1) receptors and serotonin 5-HT(1A), 5-HT(2A) and 5-HT(2C) receptors. However, paroxetine does have weak affinity for muscarinic cholinergic receptors. As shown in rats, paroxetine appears to indirectly activate somatodendritic 5-HT(1A) autoreceptors when initially administered, thereby inhibiting firing of 5-HT neurons and release of serotonin. This may explain why the onset of therapeutic effect of paroxetine is delayed. However, repeated administration of paroxetine causes adaptive changes in synaptic serotonergic receptors, including a decrease in the responsiveness of somatodendritic and terminal serotonin autoreceptors. Central βr-adrenoceptors are not down-regulated by administration of paroxetine to rats. Various studies in healthy volunteers without sleep disorders or volunteers reporting poor sleep have indicated that paroxetine disturbs normal sleep patterns by reducing rapid eye movement (REM) sleep time and lengthening REM latency. The effect of paroxetine on sleep in patients with panic disorder has not been determined, but in patients with depression the drug improves subjective quality of sleep. In electroencephalographic studies in healthy volunteers, administration of a single dose of paroxetine 30mg produced changes indicative of a sedative profile, whereas administration of 70mg produced changes indicative of activating properties. No significant impairment of psychomotor function was observed after administration of single or multiple doses of paroxetine 20 or 30mg to healthy volunteers or patients with depression. The sedation and impairment of psychomotor function caused by haloperidol, amobarbital, oxazepam or alcohol (ethanol) were not potentiated by the administration of paroxetine 30mg. In contrast to amitriptyline 150 mg/day or doxepin 150 mg/day, 2 to 6 weeks' treatment with paroxetine 20 or 30 mg/day did not produce clinically significant haemodynamic or electrophysiological effects on cardiac function in healthy volunteers or patients with depression. Fewer adverse cardiac effects were reported by paroxetine than nortriptyline recipients in a study in patients with depression and ischaemic heart disease. The anxiolytic activity of paroxetine has been demonstrated after 7 or 21 days' administration in several rodent models.
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A participation of neuronal and tissue uptake mechanism in responses to periarterial electrical sympathetic nerve stimulation (ES) and intra-arterial applications of norepinephrine (NE) was investigated in the isolated and perfused canine ophthalmic arteries (OA), using key pharmacological drugs such as imipramine, tyramine, cocaine, cortisol and diltiazem. Results were as follows: (1) NE, KCl and ES induced marked vasoconstrictions in a dose- and frequency-related manner, but tyramine induced only a slight constriction even at large doses; (2) cortisol, an uptake2 blocker, did not significantly modify KCl- and ES-induced vasoconstrictions, but significantly enhanced NE-induced responses; (3) small doses of imipramine, a neuronal uptake1 blocker, did not modify NE-induced vasoconstrictions, but large doses decreased them. On the other hand, the ES-induced response was slightly increased by a relative small dose of imipramine; (4) cocaine, another uptake1 blocker, slightly enhanced NE- and ES-induced responses; (5) ES-induced response was reduced by not only diltiazem, but also Ca2+-free solution with EGTA (1 mM l-1). The NE-induced response was not affected by diltiazem (Ohkubo and Chiba, 1987, Exp. Eye Res. 45, 263-70), and slightly but significantly depressed by Ca2+-free solution with EGTA. These results suggest that tissue and neuronal uptake mechanisms exist in responses to ES and NE1, the response to ES was markedly dependent on Ca2+ influx to the cell membrane2, and exogenous NE may induce Ca2+ movement mainly from the intracellular store site.
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Beyond the current hypothesis of depression, several new biological substrates have been proposed for this disorder. The present study investigated whether the anti-inflammatory drugs celecoxib and piroxicam have antidepressant activity in animal models of depression. After acute administration, we observed antidepressant-like effects of celecoxib (10 mg/kg) and piroxicam (10 mg/kg) in the modified forced swim test in rats. Piroxicam increased serotonin and norepinephrine levels in the hippocampus. Prolonged (21-day) treatment with celecoxib (10 mg/kg) and piroxicam (10 mg/kg) rescued sucrose preference in a chronic mild stress model of depression. Additionally, the chronic mild stress-induced reduction of hippocampal glutathione was prevented by treatment with celecoxib and piroxicam. Superoxide dismutase in the hippocampus was increased after chronic mild stress compared with the non-stressed saline group. The non-stressed celecoxib and piroxicam groups and stressed piroxicam group exhibited an increase in hippocampal superoxide dismutase activity compared with the stressed saline group. Lipid hydroperoxide was increased in the stressed group treated with vehicle and non-stressed group treated with imipramine but not in the stressed groups treated with celecoxib and piroxicam. These results suggest that the antidepressant-like effects of anti-inflammatory drugs might be attributable to enhanced antioxidant defenses and attenuated oxidative stress in the hippocampus.
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This paper describes a procedure for the synthesis and application of a citalopram-derived affinity resin in purifying the 5HT-reuptake system from human blood platelets. A two-step scheme has been developed for partial purification, based on wheat germ agglutinin-lectin (WGA) affinity and citalopram affinity chromatographies. Upon solubilization of the carrier with 1% digitonin, a 50-70-fold increase in specific [3H]imipramine binding activity with a 70% recovery could be accomplished through WGA-lectin chromatography. The WGA pool was then subjected to affinity chromatography on citalopram-agarose. At least 90% of the binding capacity adsorbed to the column. Specific elution using 10 microM citalopram resulted in a 22% recovery of binding activity. A 10,000-fold overall purification was obtained by using this two-step procedure. Analysis of the fractions on SDS-PAGE after 125I labeling revealed specific elution of 78- and 55-kDa proteins concomitant with the appearance of [3H]imipramine binding activity. The pharmacological profile of the partially purified reuptake system correlated well with that derived from the crude membrane-bound reuptake system, suggesting a copurification of the 5HT binding activity and [3H]imipramine binding activity.
D-cycloserine (DCS), a partial N-methyl-D-aspartate (NMDA) agonist, facilitates the extinction of conditioned fear in animals and promotes the efficacy of exposure-based therapies in humans. The current study examined whether pre-exposure to the antidepressant imipramine affects the enhancement of extinction by DCS.
The effects of tricyclic antidepressants drugs (TCA) amitriptyline, imipramine and nortriptyline, on purified Electrophorus electricus (L.) acetylcholinesterase (AChE; acetylcholine hydrolase, EC 184.108.40.206) were studied using kinetic methods and specific fluorescent probe propidium. The antidepressants inhibited AChE activity by a non-competitive mechanism. Inhibition constants range from 200 to 400 microM. Dimethylated amitriptyline and imipramine were more potent inhibitors than the monomethylated nortriptyline. Fluorescence measurements using bis-quaternary ligand propidium were used to monitor ligand-binding properties of these cationic antidepressants to the AChE peripheral anionic site (PAS). This ligand exhibited an eight-fold fluorescence enhancement upon binding to the peripheral anionic site of AChE from E. electricus (L.) with K(D)=7 x 10(-7)M. It was observed that TCA drugs displaced propidium from the enzyme. On the basis of the displacement experiments antidepressant dissociation constants were determined. Similar values for the inhibition constants suggest that these drugs have similar affinity to the peripheral anionic site. The results also indicate that the catalytic active center of AChE does not participate in the interaction of enzyme with tricyclic antidepressants. These studies suggest that the binding site for tricyclic antidepressants is located at the peripheral anionic site of E. electricus (L.) acetylcholinesterase.
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To improve a gas chromatography/electron impact ionization mass spectrometry (GC/MS) method for determining the concentration of procaterol in human plasma.
For a rational treatment approach, further studies are needed, particularly in depression and conduct disorder; psychosocial-environment contributions and possible biological markers should be investigated in order to identify children who require psychopharmacological treatments and those who will respond to psychosocial interventions or the combination of both. Symptoms targeted to require pharmacotherapy and symptoms targeted to respond to psychosocial interventions have to be identified.
Lennon and Carnegie have proposed that the clinical symptomatology of experimental allergic encephalitis (EAE), an acute autoimmune demyelinating disease, may be due, at least in part, to an immune response directed against CNS serotonin receptors. To test this hypothesis we treated strain 13 guinea pigs, which had been immunized with guinea pig basic protein (GPBP) in complete Freund's adjuvant (CFA), with drugs known to affect central nervous system (CNS) serotonin levels. These drugs included imipramine hydrochloride, tryptophan and carbidopa which increase CNS serotonin and reserpine which decreases it. Five experiments were conducted in which all immunized animals treated with saline only died, as expected, as did all animals treated with reserpine which died even more quickly. A significant proportion of animals treated with the other three drugs, alone or in combination, survived or lived longer than controls. We conclude that survival of animals with EAE is enhanced by treatment with these drugs. We suggest that further evaluation of a possible blockade in serotonin transmission in EAE and multiple sclerosis (MS) is warrented, since, if such a blockade were demonstrated, it is possible that these drugs may have potential for therapeutic efficacy in patients with MS.
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The effects of several neurotransmitters on prostaglandin (PG) D2-induced cataleptic behavior in rats were investigated by the high bar test. Intracerebroventricular administration of PG D2 elicited cataleptic behavior in a dose-dependent manner without producing a marked change in spontaneous motor activity. The incidences of cataleptic behavior were 20% and 100% at doses of 2 nmol and 50 nmol of PG D2, respectively. Intraperitoneal pretreatment with L-DOPA (100 mg/kg), apomorphine (1 mg/kg), amantadine (0.2 mg/kg), atropine (0.5 mg/kg) or p-chlorophenylalanine (300 mg/kg) significantly decreased the cataleptic behavior induced by 50 nmol of PG D2. Conversely, simultaneous treatment with 5-hydroxy-L-tryptophan (30 mg/kg), 5-methoxy-N,N-dimethyltryptamine (5 mg/kg), imipramine (20 mg/kg) or clomipramine (10 mg/kg) markedly increased the cataleptic behavior induced by 2 nmol of PG D2. Propranolol (10 mg/kg) and phenoxybenzamine (10 mg/kg) did not affect the induction of cataleptic behavior by either 2 nmol or 50 nmol of PG D2. These results suggest that PG D2 might be involved in inducing cataleptic behavior by modulating serotonergic, cholinergic and dopaminergic systems.
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New uses are still being discovered for a number of psychotropic agents that have been available for some time. Among the more important recent discoveries are the efficacy of the tricyclic antidepressants for panic disorder and agoraphobia with panic attacks; the use of the monoamine oxidase inhibitors for the above disorders and for atypical depression and hysteroid dysphoria; the use of propranolol for anxiety disorders and for uncontrollable violent outbursts; the antianxiety and antipanic effects of clonidine; and the usefulness of lithium in treating schizophrenia and schizoaffective disorder and for emotionally unstable character disorders. In addition to strengthening the therapeutic armamentarium, the author says, the discovery of new drug response patterns helps generate or strengthen hypotheses about the pathophysiology of various psychiatric disorders.
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We investigated the incidence of convulsions observed during treatment with antidepressants. Among the patients observed in this department, 582 cases received the antidepressants for more than 2 months were selected. 8 cases (1. 4%) of these patients showed convulsions. Detailed evaluation revealed a high incidence of convulsions occurred in patients who were administered more than two kinds of antidepressants. Among tetracyclic antidepressants, viz. maprotiline and clomipamine, and tricyclic antidepressants, viz. amitriptyline indicated a high incidence rate of convulsions. On the contrary, mianserin and imipramine tended to show a lower incidence. In 4 cases, acute toxic symptoms were seen before the convulsion, and the serum concentration of antidepressants in these patients was high. If toxic symptoms and elevated level of serum concentration are useful indicator for prediction of convulsion by treatment with antidepressants, these might be a noteworthy clinical findings. At present, if doctors are required to administer more than moderate amounts of more than two antidepressants, careful administration is desirable. With the accumulation of such cases, it is necessary to obtain further evaluation of the relationship between toxic symptoms and serum concentration of antidepressants.
The binding characteristics of [3H]-imipramine in slide mounted tissue sections of rat forebrain have been studied to ascertain the optimal binding conditions for labeling the sites prior to autoradiographic localization. The conditions for the experiments and the kinetics of the imipramine binding correspond reasonably well with those used in membrane preparations to initially define the imipramine binding site. Subsequent labeling of sections, using these parameters, allowed the autoradiographic localization of high concentrations of imipramine binding sites in such areas as the cerebral cortex, striatum, and several limbic and visual system structures. In addition, there was a marked overlap between regions demonstrating imipramine binding and areas known to be innervated by serotonergic neurons. This study outlines the potential sites of action of imipramine in the brain and defines areas for future investigations which attempt to localize brain regions involved in the etiology of depression and areas involved in the side effects of antidepressant drug therapy.
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We found 19 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
Ethanolic- and isopropanolic-aqueous extracts of Cimicifuga racemosa are used for the treatment of climacteric complaints. As hot flushes and psychic complaints seem to be special targets for Cimicifuga extracts in clinical studies, these parameters were studied in experimental animals. Hot flush equivalents were measured in castrated rats as a quick increase in peripheral temperature with the aid of a transmitter implanted subcutaneously on the ventral side. The hot flush equivalents proved to respond to estrogen and the antidopaminergic drug veralipride but they were also reduced very effectively by Cimicifuga extract BNO 1055 (which is contained in Klimadynon/Menofem). In addition, an ethanolic-aqueous extract of C. racemosa was studied in the tail suspension test (TST), a behavioural test indicative for antidepressant activity. A significant decrease of the period of immobility was observed after treatment with 30 mg/kg body weight (bw) imipramine or with 50 or 100 mg/kg bw Cimicifuga extract. These findings in pharmacological tests-a reduction of the frequency of hot flush equivalents and hints on antidepressant activity of Cimicifuga extracts-are in good agreement with the therapeutical responses in climacteric women.
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Tests conducted on isolated and denervated preparations of the rat seminal duct brought evidence that tricyclic antidepressants (melipromine, noverile and azaphen) when employed in low concentrations (1-10(-9) g/ml) produced an adrenosensitizing effect. Denervation with the subsequent block by desoxycorticosterone (1-10(-5) g/ml) of exteraneuronal amine uptake did not alter the position, shape and inclination of the "concentration-effect" noradrenaline curves received in the presence of noverile and cocaine. It is believed that there exists a predominance of the postsynaptic mechanism of the aminosensitizing action of tricyclic antidepressants on the smooth muscle organ.
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The diffusional transport of a series of small drug molecules (<400 Da) in agarose gel with and without kappa-carrageenan (a negatively charged polysaccharide) is studied. The drug molecules have amphiphile character, the hydrophilic part being a tertiary amine which is the same in all six drugs. The difference in structure resides in the hydrophobic part which give these molecules different properties such as a difference in CMC-values (critical micelle concentration). The transport studies show that the apparent diffusion coefficients (Dapp) of all the drugs in 1% (w/w) agarose gel are almost identical and with a value similar to that in water. These results were anticipated because of the small size of the drugs, the low concentration of agarose, and the lack of interaction between the diffusant and the polymer. In agarose gels also containing 0.02% (w/w) kappa-carrageenan, however, the Dapp-values are significantly decreased for all drugs, except for lidocaine. This lowering of the Dapp is ascribed to the interaction between the drug molecules and kappa-carrageenan. The Dapp-values of the drugs in the gel system containing kappa-carrageenan correlate well with the adsorption isotherms of the same drugs in the drug/kappa-carrageenan/water system obtained previously  and the Dapp-values follow the order: chlorpromazine
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A number of epidemiological studies have established a link between insulin resistance and the prevalence of depression. The occurrence of depression was found to precede the onset of diabetes and was hypothesized to be associated with inherited inter-related insufficiency of the peripheral and central insulin receptors. Recently, dicholine succinate, a sensitizer of the neuronal insulin receptor, was shown to stimulate insulin-dependent H2O2 production of the mitochondrial respiratory chain leading to an enhancement of insulin receptor autophosphorylation in neurons. As such, this mechanism can be a novel target for the elevation of insulin signaling.
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Liquid-liquid chromatography based on the ion-pair partition technique gives separation systems of high efficiency when silica micro-particles are used as the support for the stationary phase. With 10-mum particles, plate heights of the order of 40-70 mum have been achieved with a linear velocity of 0.25 cm/sec. The retention in ion-pair partition systems is determined by the nature and concentration of the counter ion, and the properties of the mobile phase also have a major influence. It is often possible to predict the selectivity, and this can be controlled by varying the composition of the mobile phase. This paper describes the application of ion-pair partition chromatography to the bioanalysis of drugs, drug metabolites and biogenic substances. Typical counter ions in the stationary phase were methanesulphonate and perchlorate for ammonium compounds and tetrabutylammonium for the separation of organic anions. Determinations by liquid chromatography were demonstrated for quinidine and dihydroquinidine, metanephrine and normetanephrine and for imipramine and its demethyl metabolite in plasma. A quaternary ammonium compound, QX-572, was determined in urine and chromatograms are shown for the isolation of indoleacetic and hydroxyindoleacetic acid in urine. The methods have been used in routine analysis. Ultraviolet detection has permitted the determination of highly absorbing compounds down to the 10-ng level in plasma and urine.
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Our findings suggest that Aβ metabolism may be affected in depression; these findings also possibly answer the question of why even early-onset depression is a risk factor for developing Alzheimer's disease.
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The present study investigated the potential of therapeutic drug monitoring data to document pharmacokinetic drug interactions with psychotropic medication, both in terms of methodology and applicability. It focused on 105 patients exposed to one of five agents known for their capacity to induce (phenytoine, phenobarbital, and carbamazepine) or to inhibit (thioridazine and levomepromazine) the metabolism of psychotropic drugs. These patients were matched by gender, age, and monitored psychotropic medication to 105 patients randomly selected from a pool of subjects nonexposed to target comedication. Such a paired approach was shown to be effective in reducing variability for a majority of substances. Power analysis suggested that eight to 10 pairs of exposed and nonexposed patients would effectively allow the detection of twofold effects of interacting substances. In keeping with the literature, analysis of the ratios of dose-normalized exposed to nonexposed concentrations indicated that phenothiazine comedication led to significantly higher concentrations of desmethylated metabolites but not parent compounds, when clomipramine, imipramine, or amitriptyline were administered. A similar, as yet undocumented interaction was observed for the tetracyclic antidepressant mianserine. In contrast, the present study revealed that maprotiline concentrations were increased, but its metabolite was largely unaffected by phenothiazine comedication. Increased concentrations were also observed for moclobemide, but not citalopram or its metabolite. In addition to its long recognized capacity to decrease haloperidol concentrations, carbamazepine was shown to induce the metabolism of clopenthixol and possibly flupenthixol. The consistency of such a picture substantiates the need to consider therapeutic drug monitoring databases as cost-effective and reliable tools for postmarketing surveillance.
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Human SK-N-SH neuroblastoma cells accumulate and store the adrenal imaging agent metaiodobenzylguanidine (MIBG) with minor involvement of specialized cytoplasmic storage granules (Smets LA et al., Active uptake and extravesicular storage of meta-iodo-benzylguanidine in human neuroblastoma SK-N-SH cells. Cancer Res 49: 2941-2944, 1989). In the present study the mechanism of extravesicular MIBG retention was investigated and compared with granular storage of MIBG and norepinephrine (NE) in PC-12 pheochromocytoma cells. SK-N-SH cells concentrated both MIBG and NE by neuron-specific Uptake-1 but long-term retention was only observed with MIBG. Retention of accumulated NE was, however, promoted by inhibition of intracellular catecholamine degradation with pyrogallol. Drug release by controlled cell permeabilization and by KCl-induced exocytosis indicated that MIBG was mainly stored as freely diffusible, cytoplasmic molecules. SK-N-SH cells were depleted from stored MIBG by the Uptake-1 inhibitor imipramine but poorly so by the granule-depleting drug reserpine. Conversely, PC-12 cells were depleted by reserpine but insensitive to imipramine. The data suggest that extravesicular retention of MIBG in SK-N-SH cells is not based on intracellular sequestration but is solely due to efficient re-uptake of accumulated drug after leaking from the cells. The accumulation of MIBG in SK-N-SH cells, reflecting "pure" Uptake-1, appears to be a powerful system for exploring various cellular and molecular aspects of catecholamine uptake.
In this study, a platinum wire coated with poly(3,4-ethylenedioxythiophen) was used as an electro-assisted solid-phase microextraction fiber for the quantification of tricyclic antidepressant drugs in biological samples by coupling to GC employing a flame ionization detector. In this study, an electric field increased the extraction rate and recovery. The fiber used as a solid phase was synthesized by the electropolymerization of 3,4-ethylenedioxythiophen monomers onto a platinum wire. The ability of this fiber to extract imipramine, desipramine, and clomipramine by using the electro-assisted solid-phase microextraction technique was evaluated. The effect of various parameters that influence the extraction efficiency, which include solution temperature, extraction time, stirring rate, ionic strength, time and temperature of desorption, and thickness of the fiber, was optimized. Under optimized conditions, the linear ranges and regression coefficients of calibration curves were in the range of 0.5-250 and 0.990-0.998 ng/mL, respectively. Detection limits were in the range of 0.15-0.45 ng/mL. Finally, this method was applied to the determination of drugs in urine and wastewater samples and recoveries were 4.8-108.9%.
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Antidepressants (AD) need to be chronically administered (weeks to months) to provide beneficial effects. Evidence suggests that combined administration of inhibitors of monoamine reuptake and phosphodiesterase type 4 allows a highly effective therapeutic action. Also, this coadministration more rapidly boosts the cyclic adenosine monophosphate (cAMP) pathway, which is normally activated during chronic treatment of single compounds. Little is known, however, about how this augmentation therapy affects the core mechanism of glutamatergic plasticity. We therefore investigated how in vivo combinational subchronic rolipram and imipramine (scRI) treatment affects depressive behavior, cAMP-dependent transcription, and glutamatergic transmission in the hippocampus, a region critically implicated in depression.
3-Cyano-imipramine (cianopramine) is a potent and selective inhibitor of serotonin uptake into synaptosomes. In a double-blind trial, 60 patients with various types of depression fulfilling the DSM-III criteria of depressive episodes were treated with either cianopramine (n = 20, mean daily dose 3.3 +/- 0.6 mg) amitriptyline (n = 20, mean daily dose 86.4 +/- 21 mg) or placebo (n = 20) orally. According to the ratings of the Hamilton Scale of Depression and clinical global evaluations, both active drugs showed statistical superiority over placebo (P less than 0.02). The frequencies of anticholinergic side effects in the cianopramine group were comparable to those of the placebo group and were less than in the amitriptyline group. The findings suggest that cianopramine is a promising new antidepressant.
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Ziprasidone is a novel antipsychotic agent with a unique combination of pharmacological activities at human receptors. Ziprasidone has high affinity for human 5-HT receptors and for human dopamine D(2) receptors. Ziprasidone is a 5-HT(1A) receptor agonist and an antagonist at 5-HT(2A), 5-HT(2C) and 5-HT(1B/1D) receptors. Additionally, ziprasidone inhibits neuronal uptake of 5-HT and norepinephrine comparable to the antidepressant imipramine. This unique pharmacological profile of ziprasidone may be related to its clinical effectiveness as a treatment for the positive, negative and affective symptoms of schizophrenia with a low propensity for extrapyramidal side effects, cognitive deficits and weight gain.