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1
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
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Pharmacological profile and mechanism of action of antidepressant drugs

100%
Maj J.
Acta Physiologica Polonica
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1987
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tom 38
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nr 4
2

Ifenprodil and NMDA ligands

88%
Wosko S., Szopa A., Serefko A., Poleszak E.
Acta Neurobiologiae Experimentalis
|
2013
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tom 73
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nr 1
Depression is one of the most common affective disorders. According to the World Health Organization (WHO), it is currently the fourth major global health problem (Kessler et al. 2003). The growing number of people suffering from depression has motivated the scientists to search for new antidepressant drugs. Since numerous studies revealed that NMDA receptor may be involved in the mechanism of action of the antidepressant agents, modulation of the NMDA receptor function by different ligands has been taken into consideration. There are some promising results demonstrating the antidepressant activity of the antagonists binding to the polyamine site of the NMDA receptor complex. Ifenprodil belongs to a family of the selective, atypical non-competitive antagonists of the NMDA receptors. It acts via inhibition of the polyamine binding site of the NR2B subunit (Williams 1993). An antidepressantlike effect of ifenprodil was observed in several behavioral studies, for example in the forced swimming test (Carter et al. 1990, Williams 1993, Layer et al. 1995, Scolnik 1999, Paoletti and Neyton 2007). It was shown that its antidepressant-like activity is increased by other antidepressant drugs (imipramine and fluoxetine). The aim of our work was to evaluate the antidepressant activity of the joint administration of ifenprodil and NMDA ligands in the mouse forced swimming test (FST). The experiments were carried out on male Albino Swiss mice. In order to avoid the risk of obtaining the false positive/negative effects in the FST test caused by a possible influence of the tested substances on the locomotor activity, the spontaneous locomotor activity was measured. The obtained results demonstrated that ifenprodil at the dose of 10 mg/ kg enhances the antidepressant-like effect of the following NMDA receptor ligands: a competitive NMDA receptor antagonist – CGP 37849 (0.312 mg/kg), an antagonist at glycine site – L-701,324 (1 mg/kg) and a non-competitive antagonist at phencyclidyne – MK801 (0.05 mg/kg). However, it did not potentiate the antidepressant activity of the inorganic modulators of the NMDA receptor complex, such as Zn2+ (2.5 mg/kg) and Mg2+ (10 mg/kg). Treatment with the tested agents did not influence the locomotor activity. In conclusion, our findings indicated that antidepressant-like activity of ifenprodil is connected with serotoninergic and glutamatergic system.
3
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Adaptive changes in functions of brain neurotransmitter receptors, evoked by repeated administration of antidepressant drugs

75%
Przegalinski E.
Acta Physiologica Polonica
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1987
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tom 38
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nr 5
4

Embryotoxic effects of B-193 in mouse

75%
Anasiewicz A.
Folia Morphologica
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1996
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tom 55
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nr 4
5
Content available remote

Effect of tianeptine and fluoxetine on the levels of met-enkephalin and mRNA encoding proenkephalin in the rat

75%
Dziedzicka-Wasylewska M., Dlaboga D., Pierzchala-Koziec K., Rogoz Z.
Journal of Physiology and Pharmacology
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2002
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tom 53
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nr 1
The purpose of the present study was to evaluate the effects of acute and repeated treatment with two antidepressant drugs (ADs)of opposite pharmacological profile,i.e. tianpetine (TIA,serotonin reuptake enhancer)and fluoxetine (FLU,serotonin reuptake inhibitor)on the levels of Met-Enkephalin,(Met-Enk,a member of opioid peptide family, which has been suggested to play a role in the mechanism of action ADs)as well as on mRNA coding for proenkephalin (mRNA PENK)in various regions of the rat brain, pituitary,adrenal glands and plasma.Male Wistar rats were treated acutely or repeatedly (10 mg/kg p.o.,twice daily for 14 days)with TIA or FLU.Tissue for biochemical experiments was taken 2 h after last dose of appropriate drug.The levels of Met-Enk were estimated by radioimmunoassay,mRNA PENK was measured using in situ hybridization.From the results obtained in the present study it may be concluded that repeated administration of TIA or FLU induced similar changes in the levels of Met- Enk in the rat hippocampus,striatum,hypothalamus and neurointermediate lobe of pituitary.Such an effect is interesting,especially if one takes into account the differences in pharmacological profile between these two antidepressant drugs.It may be suggested that serotonin level might not be crucial for inducing the alterations in the content of Met-Enk.Since we did not observe any changes in the levels of PENK mRNA in the studied rat brain regions after repeated administration of TIA or FLU,it seems that the observed changes in the levels of Met-Enk do not result from effects of these antidepressants on biosynthesis of PENK,but rather from alterations in the peptide release.Another interesting finding of the present study was that in the anterior lobe of pituitary,adrenal glands and plasma,repeated administration of TIA induced alterations in the contents of Met-Enk,while repeated administration of FLU remained without any effect.It is tempting to speculate that such a differentiation between the effects of these two antidepressants might be linked to the well known feature of TIA (but not FLU)which has been shown to reduce both basal and stress-evoked activity of the hypothalamic-pituitary-adrenal (HPA)axis.
6
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Repeated treatment with mirtazapine induces brain-derived neurotrophic factor gene expression in rats

75%
Rogoz Z., Skuza G., Legutko B.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 4
Recent studies indicate a role of the brain-derived neurotrophic factor (BDNF) in the pathophysiology of depression, as well as in the mechanism of action of antidepressant drugs (ADs). It has been shown that serum BDNF levels are decreased in depressed patients. Moreover, antidepressant treatment increases serum BDNF levels and it is positively correlated with medication response. In addition, repeated administration of ADs induces an increase in rat hippocampal or cortical BDNF gene expression. Since the most potent effect of ADs on BDNF gene expression was found after prolonged treatment, in the present study we investigated the influence of repeated treatment (twice daily for 14 days) of the new AD mirtazapine (5 or 10 mg/kg) on BDNF mRNA level (the Northern blot) in rat hippocampus and cerebral cortex. Imipramine was used as a reference compound. The experiment was carried out on male Wistar rats. The tissue for biochemical assays was collected 24 h after the last doses of mirtazapine and imipramine. We also studied the effect of repeated mirtazapine on the action of the 5-HT2A receptor agonist (±)DOI in the behavioral test (head twitches induced by (±)DOI) in rats. The obtained results showed that, like imipramine (10 mg/kg), mirtazapine (10 mg/kg) increased BDNF gene expression in both the examined brain regions: in the hippocampus by 24.0 and 26.5%, in the cerebral cortex by 29.9 and 41.5%, respectively, compared with the vehicle-treated control. Neither mirtazapine nor imipramine administered repeatedly at a lower dose (5 mg/kg) significantly changed BDNF mRNA levels in the hippocampus and cerebral cortex. Repeated treatment with mirtazapine (10, but not 5 mg/kg) inhibited the behavioral syndrome induced by (±)DOI. This study provides first conclusive evidence that repeated mirtazapine administration increases BDNF mRNA levels; moreover, it indicates that the enhancement of BDNF gene expression may be essential for the clinical effect of mirtazapine.
7
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Effect of some antidepressants on the low corticosterone concentration-induced gene transcription in LMCAT fibroblast cells

75%
Otczyk M., Mulik K., Budziszewska B., Jaworska-Feil L., Basta-Kaim A., Kubera M., Jagla G., Nowak W., Lason W.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 1
The aim of the present study was to investigate effects of some classical and new antidepressants on functional activity of the glucocorticoid receceptor (GR) induced by low corticosterone concentration in mouse fibroblast cells stably transfected with mouse mammary tumor virus-chloramphenicol acetyltransferase plasmid (LMCAT cells). We found that the transcriptional activity of GR stimulated by 50 nM corticosterone was strongly attenuated by imipramine, desipramine, fluoxetine and tianeptine in a concentration-dependent way, whereas reboxetine had only a weak effect and venlafaxine was inactive. Further study revealed that the inhibitor of c-Jun N-terminal kinase - mitogen-activated protein kinase (JNK-MAPK), SP600125 (0.1 µM), reversed the imipramine-induced suppression of GR function, whereas the inhibitor of extracellular signal-regulated kinase (ERK)-MAPK, PD 98059 (15µM), potentiated the antidepressant action. No effect of selective inhibitors of p38-MAPK, phosphatidylinositol 3-kinase (PI3-K)/Akt, and glycogen synthase kinase (GSK-3) on the imipramine-induced inhibition of GR function was detected. These data indicate that the functional activity of GR evoked by low corticosterone concentration in LMCAT cells is efficiently inhibited by tricyclic antidepressants. Moreover, it was found that JNK- and ERK-MAPK were oppositely involved in the regulation of the imipramine-induced inhibition of the GR functional activity. Thus, the present study supports the notion that the interaction of antidepressants with GR may play a role in attenuating pathological hyperactivity of HPA axis in depression.
8
Content available remote

Activation of endocannabinoid transmission induces antidepressant-like effects in rats

75%
Adamczyk P., Golda A., McCreary A. C., Filip M., Przegalinski E.
Journal of Physiology and Pharmacology
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2008
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tom 59
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nr 2
Recent reports indicate that endocannabinoid (eCB) system may be involved in depression and in the antidepressant-like activity demonstrated in experimental models. The present study examined the effects of the eCB uptake inhibitor 4-hydroxyphenyl-5Z,8Z,11Z,14Z-eicosatetraenamide (AM404; 0.1-3 mg/kg), the fatty acid amide hydrolase (FAAH) inhibitor cyclohexylcarbamic acid 3-carbamoylbiphenyl-3-yl ester (URB597; 0.03-0.3 mg/kg), the cannabinoid CB1 receptor agonist (–)-cis-3-[2-hydroxy-4-(1,1-dimethylheptyl) phenyl]-trans-4-(3-hydroxypropyl)-cyclohexanol (CP55,940; 0.03-0.3 mg/kg) and the CB1 receptor antagonist rimonabant (0.3-3 mg/kg) on immobility time in the forced swim test (FST) in rats. Moreover, the effects of AM404, CP55,940 and URB597 on the antidepressant-like activity of imipramine and citalopram in the FST were also examined. We found that AM404 (0.3-3 mg/kg), CP55,940 (0.1 mg/kg) and URB597 (0.1-0.3 mg/kg) reduced the immobility time of rats, while rimonabant (0.3-3 mg/kg) was inactive in this respect. We also observed that the anti-immobility effects of AM404 (1 mg/kg), CP55,940 (0.1 mg/kg) and URB597 (0.3 mg/kg), but not of imipramine (30 mg/kg), were blocked by rimonabant (3 mg/kg). In another set of experiments we showed that the inactive dose of AM404 (0.1 mg/kg) potentiated the effects of the inactive doses of imipramine (15 mg/kg) or citalopram (30 mg/kg), while CP55,940 (0.03 mg/kg) and URB597 (0.03 mg/kg) enhanced the effect of imipramine only. None of the drugs studied, given alone or in combination, increased the basal locomotor activity of rats. Our results indicate that activation of the eCB system induces antidepressant-like effects in the FST in rats, and that these effects are mediated by CB1 receptors. Moreover, they also indicate that agents activating eCB transmission enhance the anti-immobility responses to antidepressant drugs.
9
Content available remote

Brain region-dependent changes in the expression of endocannabinoid-metabolizing enzymes in rats following antidepressant drugs

63%
Smaga I., Gawlinski D., Brodowicz J., Filip M.
Journal of Physiology and Pharmacology
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2019
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tom 70
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nr 5
10
Content available remote

Combined chronic treatment with citalopram and lithium does not modify the regional neurochemistry of nitric oxide in rat brain

63%
Wegener G., Bandpey Z., Heiberg I. L., Volke V., Trabace L., Rosenberg R., Harvey B. H.
Journal of Physiology and Pharmacology
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2004
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tom 55
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nr 3
A substantial number of patients do not respond sufficiently to antidepressant drugs and are therefore often co-medicated with lithium as an augmentation strategy. Also inhibitors of nitric oxide synthase (NOS) have been used as an augmentation strategy, while inhibitors of NOS exhibit antidepressant-like properties in various animal models. Therefore, we hypothesized that modulation of NOS may be involved in the long-term effects of antidepressants and lithium, and studied the influence of acute and chronic administration of citalopram, alone or in combination with lithium, on NOS activity in hippocampus, cerebellum, and frontal cortex, by determination of L-citrulline being formed. We found that administration of acute or chronic citalopram (5 mg/kg and 20 mg/kg/24h, respectively) alone or in combination with subchronic lithium (60 mmol/kg chow pellet) did not influence the activity of NOS ex vivo in all regions compared to control. In contrast, high doses of lithium caused a significant decrease in NOS activity in vitro. We conclude that basal conditions are unsuitable for the study of antidepressant effects on NOS, and that the neurochemistry of nitric oxide remains unaltered following chronic citalopram or subchronic lithium under normal physiological conditions.
11
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The role of dopamine D2 receptor in the behavioral effects of imipramine - study with the use of antisense oligonucleotides

63%
Dziedzicka-Wasylewska M., Kolasiewicz W., Rogoz Z., Margas W., Maj J.
Journal of Physiology and Pharmacology
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2000
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tom 51
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nr 3
12
Content available remote

The decrease in JNK- and p38-MAP kinase activity is accompanied by the enhancement of PP2A phosphatase level in the brain of prenatally stressed rats

51%
Budziszewska B., Szymanska M., Leskiewicz M., Basta-Kaim A., Jaworska-Feil L., Kubera M., Jantas D., Lason W.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 2
Our previous study suggests that in prenatal stress model of depression glucocorticoid receptor (GR) function in adult rats is enhanced. However, the long-term consequences of stress, a causal factor in depression, on intracellular elements involved into the regulation of GR function is poorly examined. Mitogen-activated protein kinases (MAPKs), activity of which is disturbed in depression, are important regulators of GR action, so they can mediate the effect of stress on GR function. Therefore, the aim of the present study was to investigate the levels of active phosphorylated forms of extracellular signal-regulated kinases (ERK), Jun N-terminal kinases (JNK) and the p38 kinase in the hippocampus and frontal cortex in rats subjected to prenatal stress. The concentration of MAP kinase phosphatase (MKP-1, MKP-2) and protein phosphatase-2A (PP2A), which dephosphorylate all forms of MAP kinases, were also determined. During verification of the applied model of depression, we found that prenatally stressed rats displayed high level of immobility in the Porsolt test and that the administration of imipramine, fluoxetine, mirtazapine and tianeptine for 21 days normalized this parameter. Western blot study revealed that rats subjected to prenatal stress had decreased levels of p-JNK1 and p-JNK2 in the hippocampus and p-p38 in the frontal cortex, but the concentrations of p-ERK1 and p-ERK2 were not changed. Chronic treatment with imipramine inhibited the stress-induced decrease in p-JNK1/2, while imipramine, fluoxetine and mirtazapine blocked changes in p-p38. PP2A phosphatase level was higher in the hippocampus and frontal cortex in prenatally stressed animals than in control rats. Chronic treatment with antidepressant drugs attenuated the stress-induced increase in the level of this phosphatase, but had no effect on its concentration in control animals. There was no significant difference in MKP-1 and in MKP-2 levels in both brain structures between control and prenatally stressed rats. The obtained results showed that prenatal stress decreased the levels of active form of JNK and p38, but enhanced PP2A phosphatase expression and most of these changes were reversed by antidepressant drugs. Since p-JNK and p-p38 are known to inhibit GR function their lowered levels may enhance glucocorticoid action. Furthermore, the increased PP2A concentration may intensify GR action not only by inhibition of JNK and p38 phosphorylation, but also by a direct influence on the process of GR translocation.
13
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Content available

ACTH 4-9 analogue facilitates the antiimmobility effect of antidepressants and dopamine agonists in swimming rats

51%
Zebrowska-Lupina I., Pietrasiewicz T., Ossowska G., Lupina T., Klenk-Majewska B.
Journal of Physiology and Pharmacology
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1997
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tom 48
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nr 2
14
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

The effect of NMDA antagonists on footshock-induced fighting behavior in chronically stressed rats

51%
Ossowska G., Klenk-Majewska B., Szymczyk G.
Journal of Physiology and Pharmacology
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1997
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tom 48
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nr 1
15

Improve your mood

32%
Polish Food
|
1999
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nr 2
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