Wyniki wyszukiwania

1

The antidepressant- and anxiolytic-like effects following co-treatment with escitalopram and risperidone in rats

100%

Kaminska K., Rogoz Z.

Journal of Physiology and Pharmacology

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2016

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tom 67

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nr 3

2

Antidepressants enhanced the antipsychotic-like effect of aripiprazole in the tests used for evaluaion of some positive and cognitive symptoms of schizophrenia in mice

100%

Rogoz Z., Lorenc-Koci E.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

INTRODUCTION: Schizophrenia is a devastating psychiatric disorder that impairs mental and social functioning and affects approximately 1% of the world’s population. It is known that in contrast to pharmacotherapy with typical antipsychotics, atypical antipsychotics alleviate not only the positive symptoms of schizophrenia but also the cognitive ones, however those effects are small and the mechanisms of this action are still unknown. A few clinical reports have suggested that antidepressants (ADs) are able to augment the activity of atypical antipsychotics. AIM(S): In the present study, we aimed to evaluate the effect of ADs escitalopram (ESC) or mirtazapine (MIR) and aripiprazole (ARI, an atypical antipsychotic drug) given separately or jointly, on the MK-801-induced positive and cognitive symptoms of schizophrenia in mice. METHOD(S): The experiments were conducted on male Albino Swiss mice (25–27 g). ADs and ARI were given 30 min before MK-801 injection. Locomotor hyperactivity induced by MK-801 (0.3 mg/kg) was measured for 30 min, starting 30 min after MK-801 administration. In the novel object recognition test, MK-801 (0.2 mg/kg) was given 30 min before the first introductory session. Memory retention was evaluated for 5 min, starting 90 min after the introductory session. RESULTS: ARI (0.3 mg/kg) decreased locomotor hyperactivity induced by MK-801 (0.3 mg/kg). Co-treatment with an inactive dose of ARI (0.01 mg/kg) and ESC (5 or 10 mg/kg) or MIR (2.5 and 5 mg/kg) inhibited the effect of MK‑801. Moreover, MK-801 (0.2 mg/kg) decreased the memory retention. ARI (0.3 mg/kg) reversed that effect. Co‑treatment with an inactive dose of ARI (0.03 mg/kg) and ESC (5 and 10 mg/kg) or MIR (2.5 and 5 mg/kg) abolished the deficit of object recognition memory induced by MK-801. CONCLUSIONS: The obtained results suggest that ADs may enhance the antipsychotic‑like effect of ARI in the animal tests used for evaluation of some positive and cognitive symptoms of schizophrenia. FINANCIAL SUPPORT: This study was financially supported by statutory funds of the Institute of Pharmacology Polish Academy of Sciences, Krakow, Poland.

3

The synergistic effect of selective sigma receptor agonists and uncompetitive NMDA receptor antagonists in the forced swim test in rats

100%

Skuza G., Rogoz Z.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 2

Data acquired to date show that some sigma receptor ligands reveal "antidepressant-like" activity in the forced swim test in mice and rats. Moreover, our preliminary results suggested that joint administration of sigma receptor ligands and amantadine (AMA, a glutamatergic/NMDA receptor antagonist) caused a positive interaction in the Porsolt test in rats, as had already been observed in the case of co-treatment with clinically active antidepressants and AMA. The aim of the present study was to examine the effect of combined administration of sigma1 or sigma2 receptor agonists, SA4503 or siramesine, respectively, and AMA or memantine (MEM) (uncompetitive NMDA receptor antagonist). SA4503 or siramesine given jointly with MEM (as well as with AMA) decreased the immobility time in rats. The effect of SA4503 and AMA co-administration was antagonized by progesterone, a sigma1 receptor antagonistic neurosteroid. Combined treatment with siramesine and AMA was modified by neither progesterone nor BD1047 (a novel sigma antagonist with preferential affinity for sigma1 sites); but it was counteracted by sulpiride and prazosin (a dopamine D2- and an alpha1-adrenergic receptor antagonist, respectively). The "antidepressant-like" effect induced by siramesine and MEM was not antagonized by progesterone, but was attenuated by BD1047, sulpiride and prazosin. The obtained results give support to the hypothesis that sigma (particularly sigma1) receptors may be one of the possible mechanisms by which drugs induce antidepressant-like activity in the forced swim test, and that this effect may be enhanced by NMDA receptor antagonists. Combined treatment with sigma ligands and AMA or MEM (applied in the clinic) may be an alternative to the treatment of antidepressant-resistant depressive patients in the future.

4

Effect of repeated administration of venlafaxine on the level of mRNA coding for dopamine D1 and D2 receptors in rat brain

81%

Rogoz Z., Dziedzicka-Wasylewska M., Goralska M., Maj J.

Acta Neurobiologiae Experimentalis

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1999

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tom 59

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nr 3

5

Some behavioural effects of GYKI 52466, a non-competitive AMPA receptor antagonist

81%

Maj J., Kolodziejczyk K., Rogoz Z., Skuza G.

Acta Neurobiologiae Experimentalis

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1995

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tom 55

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nr 5

6

Effect of acute treatment with antidepressant drugs on the reactivity of D3 dopaminergic and beta-adrenergic receptors in the rat brain

81%

Dziedzicka-Wasylewska M., Rogoz Z., Dlaboga D., Margas W.

Acta Neurobiologiae Experimentalis

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1999

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tom 59

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nr 3

7

Porównawcze badania działania kwasów rozmarynowego i chlorogenowego na ośrodkowy układ nerwowy

81%

Borkowski B., Skuza G., Rogoz Z.

Herba Polonica

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1999

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tom 45

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nr 3

192-197

Badano wpływ kwasów rozmarynowego i chlorogenowego, związków wyizolowanych z surowców roślinnych, na ośrodkowy układ nerwowy u myszy, pod kątem ich ewentualnego działania sedatywno-nasennego, przeciwlękowego i przeciwdrgawkowego. Oba związki osłabiały aktywność lokomotoryczną oraz hiperaktywność wywołaną d-amfetaminą. Kwas rozmarynowy przedłużał narkozę heksobarbitalową, podczas gdy kwas chlorogenowy pozostawał bez wpywu. Badane kwasy były nieaktywne w testach hiperaktywności nomifenzynowej, czterech płytek oraz drgawek elektrycznych. Wyniki wskazują, że kwas rozmarynowy, a w mniejszym stopniu chlorogenowy, mogą odpowiadać za sedatywne działanie niektórych surowców roślinnych.

8

Two antidepressant drugs, taneptine and fluoxetine influence the rat central dopaminergic receptorsautoradography and in situ hybridization study

81%

Dlaboga D., Rogoz Z., Maj J., Dziedzicka-Wasylewska M.

Acta Neurobiologiae Experimentalis

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2001

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tom 61

|

nr 3

9

Chronic co-administration of iinipramine and amantadine induces liippocampal BDNF gene expression in rats

81%

Rogoz Z., Skuza G., Legutko B.

Acta Neurobiologiae Experimentalis

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2005

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tom 65

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nr 3

10

Antidopaminergic activity of EMD 57445, a new selective ligand of sigma receptors

81%

Maj J., Skuza G., Rogoz Z.

Acta Neurobiologiae Experimentalis

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1995

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tom 55

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nr 5

11

The effect of co-treatment with aripiprazole and antidepressants on the MK-801-induced deficits in the social interaction test in rats

81%

Rogoz Z., Kaminska K., Lorenc-Koci E.

Acta Neurobiologiae Experimentalis

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2015

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tom 75

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nr Supl.

BACKGROUND AND AIMS: Schizophrenia is a devastating psychiatric disorder that impairs mental and social functioning and affects approximately 1% of the world’s population. Although the atypical antipsychotics have some efficacy in alleviating social dysfunction in schizophrenic patients, this effect is small and mechanisms of this action are still unknown. Moreover, preclinical and clinical studies have suggested that the antidepressant-induced augmentation of atypical antipsychotics activity may efficiently improve the treatment of negative and some cognitive symptoms of schizophrenia. In the present study, we aimed to evaluate the effect of the atypical antipsychotic drug aripiprazole (ARI) and the antidepressant mirtazapine (MIR) or escitalopram (ESC), given separately or jointly, on the MK-801 (a NMDA receptor antagonist)-induced deficits in the social interaction test (an animal test modeling some negative symptoms of schizophrenia). METHODS: The experiments were conducted on male Wistar rats (185–200 g). The social interaction was measured 4 h after the subcutaneously administration of MK-801 (0.1 mg/kg), and 60 or 30 min after injection of the antidepressant and ARI, respectively. RESULTS: The present results showed that MK-801 (0.1 mg/kg) induced deficits in both parameters studied, i.e. the number of episodes and the time of interactions. ARI at a higher dose (0.3 mg/ kg) reversed that effect. Co-treatment with an ineffective dose of ARI (0.03 mg/kg) and MIR or ESC (5 mg/kg) abolished the deficits evoked by MK-801, and this effect was partly blocked by a 5-HT1A receptor antagonist (WAY 100635, 0.1 mg/kg) or a dopamine D1 receptor antagonist (SCH23390, 0.5 mg/kg). CONCLUSIONS: The obtained results suggest that the enhancement of antipsychotic-like effect of ARI by antidepressants on the MK-801-induced deficits in the social interaction test may be associated with serotonin 5-HT1A and dopamine D1 receptors.

12

Effects of olanzapine, risperidone and fluoxetine in the forced swimming and elevated plus-maze tests in rats

81%

Rogoz Z., Kabzinski M., Sadaj W.

Acta Neurobiologiae Experimentalis

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2011

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tom 71

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nr S

Several clinical reports have suggested a beneficial effect of the addition of a low dose of an atypical antipsychotic drug, e.g., olanzapine (OLA), risperidone (RIS) to the ongoing treatment with antidepressant drugs, particularly of the selective serotonin reuptake inhibitors (e.g., fluoxetine, fluvoxamine and paroxetine) in the treatment of drug-resistant depression. In anxiety disorders, like post-traumatic stress disorder, some studies found that atypical antipsychotics improved certain symptoms, while others failed to reach the same conclusion. Preclinical evidence on the intrinsic anxiolytic-like property of atypical antipsychotics is also inconclusive. In the present study we examined the effect of treatment with OLA or RIS, given separately or jointly with fluoxetine (FLU) in the forced swimming test (FST, an animal model of depression) and in the elevated plus-maze test (an animal model of anxiety) in male Wistar rats. The obtained results showed that treatment with OLA or RIS (0.05 and 0.1 mg/kg) and FLU (10 mg/kg) did not change the immobility time of rats in the FST. Moreover, co-treatment with OLA or RIS and FLU produced antidepressant-like activity in the FST, and that serotonin 5-HT1A receptors might play some role in these effects. RIS (0.1 and 0.3 mg/kg), OLA (1 mg/kg) and FLU (5 and 10 mg/kg) induced anxiolytic-like effect in the elevated plus-maze test. In contrast, co-administration with OLA or RIS and FLU was ineffective in that test. This finding indicates that low doses of OLA or RIS enhances the action of FLU in an animal model of depression, and they may be of particular importance to the pharmacotherapy of drug-resistant depression. In contrast, OLA or RIS and FLU may each be clinically effective in treating anxiety disorders, but their effects may be attenuated in the combination treatment with both medications. This study was supported by grant POIG 01.01.02-12-004/09-00 from European Regional Development Fund.

13

A relationship between glutathione deficiency during the early postnatal life and schizophrenia-like behavior in adulthood of sprague-dawley rats

81%

Lorenc-Koci E., Gorny M., Kaminska K., Rogoz Z.

Acta Neurobiologiae Experimentalis

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2017

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tom 77

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nr Suppl.1

INTRODUCTION: A growing body of evidence implicates glutathione (GSH) deficiency and dysregulation of redox state in the pathophysiology of schizophrenia. AIM(S): The aim of the present study was to examine the effects of buthionine-S,R-sulfoximine (BSO)-mediated inhibition of glutamate cysteine ligase (GCL; an enzyme contributing to the GSH synthesis), during the early postnatal life on the GSH and cysteine (Cys) levels in the liver and kidney of 16-days old Sprague-Dawley rats and on the rat performance in the behavioral tests that were evaluated in the adulthood. METHOD(S): Male Sprague-Dawley pups between the postnatal day p5 and p16 were treated sc with the selective inhibitor of GCL, compound BSO (3.8 mmol/kg) and the dopamine reuptake inhibitor GBR 12909 (5 mg/kg every second day), alone or in combination. Biochemical parameters, i.e. GSH and cysteine (Cys) levels were determined in the rat liver and kidney 4h after the last doses of the drugs. Other groups of rats treated with BSO and GBR 12909 were examined during adulthood in the social interaction test (p42, p60, p90), novel object recognition test (p43, p61, p91) and in the open field test (p44, p63, p93). RESULTS: BSO alone or especially with GBR 12909 significantly decreased GSH level measured 4h after its last doses both in the liver and kidney. However, Cys concentration was distinctly reduced only in the kidney. Treatment with BSO and GBR 12909 induced deficits in both parameters of the social interaction test (number and time of interactions) assessed in the defined time points in adulthood. Such treatment also evoked a decrease in the memory retention in the novel object recognition test and an increase in exploratory activity in the open field test. CONCLUSIONS: Our results suggest that the inhibition of GSH synthesis and the dopamine reuptake during the early postnatal development induces in rats long-term behavioral changes that correspond to negative and positive symptoms of schizophrenia. FINANCIAL SUPPORT: Partially supported by statutory funds of the Institute of Pharmacology Polish Academy of Sciences, Krakow, Poland.

14

Reboxetine administered repeatedly influences the central dopaminergic system in the rat

81%

Margas W., Rogoz Z., Maj J., Dziedzicka-Wasylewska M.

Acta Neurobiologiae Experimentalis

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2001

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tom 61

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nr 3

15

Repeated co-treatment with imipramine and amantadine induces hippocampal brain-derived neurotrophic factor gene expression in rats

81%

Rogoz Z., Skuza G., Legutko B.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 2

The problem of drug-resistant depression indicates a strong need for alternative antidepressant therapies. In our earlier papers we described synergistic, antidepressant-like effects of a combination of imipramine (IMI) and amantadine (AMA) in the forced swimming test in rats, an animal model of depression. Moreover, preliminary clinical data showed that the above-mentioned combination had beneficial effects in treatment-resistant patients. In addition, a number of studies predicted a role of the brain-derived neurotrophic factor (BDNF) in the mechanism of action of antidepressant drugs (ADs). 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 with IMI (5 or 10 mg/kg) and AMA (10 mg/kg), given separately or jointly (twice daily for 14 day), on mRNA level (the Northern blot) in the hippocampus and cerebral cortex. The experiment was carried out on male Wistar rats. The tissue for biochemical assays was dissected 24 h after the last dose of IMI and AMA. We also studied the effect of repeated treatment with IMI and AMA on the action of 5-HT1A- and 5-HT2A receptor agonists (8-OH-DPAT and (±)DOI, respectively) in behavioral tests. The obtained results showed that in the hippocampus IMI (10 mg/kg), and in the cerebral cortex IMI (5 and 10 mg/kg) and AMA (10 mg/kg) significantly elevated BDNF mRNA level. Joint administration of IMI (5 or 10 mg/kg) and AMA (10 mg/kg) induced a more potent increase BDNF gene expression in the hippocampus (but not in cerebral cortex) and either inhibited the behavioral syndrome induced by (±)DOI or did not change the action of 8-OH-DPAT (compared to treatment with either drug alone). The obtained results suggest that the enhancement of BDNF gene expression may be essential for the therapeutic effect of co-administration of IMI and AMA to drug-resistant depressed patients, and that among other mechanisms, 5-HT2A receptors possibly play some role in this effect.

16

Effect of combined treatment with imipramine and amantadine on the central dopamine D2 and D3 receptors in rats

81%

Rogoz Z., Dlaboga D., Dziedzicka-Wasylewska M.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 2

In spite of intensive research, the problem of treating antidepressant-resistant depressive patients has not yet been solved. Our previous studies demonstrated that joint administration of a tricyclic antidepressant drug, imipramine (IMI) with the uncompetitive antagonist of NMDA receptors, amantadine (AMA), produced stronger "antidepressant" effect in the forced swimming test (Porsolt's test) than the treatment with either drug alone given. Since it has been suggested that dopamine receptors, among others, may play a role in anti-immobility effect of IMI, in the present study we examined the effect of AMA (10 mg/kg) and IMI (5 and 10 mg/kg) given separately or jointly, as a single dose or repeatedly (twice daily for 14 days) on the dopamine D2 and D3 receptors in the rat brain, using receptor autoradiography. Following repeated administration of AMA alone or given in combination with IMI (5 mg/kg), the binding of [3H]quinpirole (dopamine D2/D3 receptors agonist) was increased, and similar changes were observed at the level of mRNA encoding dopamine D2 receptors. We used [3H]7-OH-DPAT to selectively label the dopamine D3 receptors. This experiment has shown that AMA given repeatedly did not induce statistically significant changes in the D3 receptor binding, while IMI at both used doses, increased the [3H]7-OH-DPAT binding, and this effect was still observed after repeated joint administration of AMA with both doses of IMI. However, using both radioligands, we did not observe any synergistic or even additive effects in the binding studies after joint administration of AMA and IMI. Nevertheless, we can conclude that repeated administration of AMA, given together with IMI, induces the up-regulation of dopamine D2 and D3 receptors in the rat brain, and this effect may explain their synergistic action observed in the behavioral studies involving dopaminergic transmission.

17

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

81%

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.

18

Repeated treatment with mirtazapine induces brain-derived neurotrophic factor gene expression in rats

81%

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.

19

Opposite influence of MPEP, an mGluR5 antagonist, on the locomotor hyperactivity induced by PCP and amphetamine

81%

Pietraszek M., Rogoz Z., Wolfarth S., Ossowska K.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 3

Potential antipsychotic effects of a selective non-competitive antagonist of metabotropic glutamate receptor 5 (mGluR5), 2-methyl-6-phenylethynylpyridine (MPEP), was examined in two commonly used screening tests: (1) the hyperactivity induced by an NMDA receptor antagonist phencyclidine (PCP), and (2) the hyperactivity induced by an indirect dopamine agonist, D-amphetamine. PCP was administered at a dose of 2.5 mg/kg s.c. and D-amphetamine was given at a dose of 1 mg/kg s.c. MPEP (5 mg/kg i.p.) significantly enhanced the locomotor activity increased by PCP, but inhibited amphetamine-induced hyperactivity. The opposite effect of MPEP in the two above-mentioned models questions significance of the blockade of mGluR5 receptors to antipsychotic effects.

20

Brain-derived neurotrophic factor gene expression in rats following repeated treatment with mirtazapine

71%

Rogoz Z., Skuza G., Dudys D., Ciszek M., Legutko B.

Acta Neurobiologiae Experimentalis

|

2005

|

tom 65

|

nr 3

Ograniczanie wyników

The antidepressant- and anxiolytic-like effects following co-treatment with escitalopram and risperidone in rats

Antidepressants enhanced the antipsychotic-like effect of aripiprazole in the tests used for evaluaion of some positive and cognitive symptoms of schizophrenia in mice

The synergistic effect of selective sigma receptor agonists and uncompetitive NMDA receptor antagonists in the forced swim test in rats

Effect of repeated administration of venlafaxine on the level of mRNA coding for dopamine D1 and D2 receptors in rat brain

Some behavioural effects of GYKI 52466, a non-competitive AMPA receptor antagonist

Effect of acute treatment with antidepressant drugs on the reactivity of D3 dopaminergic and beta-adrenergic receptors in the rat brain

Porównawcze badania działania kwasów rozmarynowego i chlorogenowego na ośrodkowy układ nerwowy

Two antidepressant drugs, taneptine and fluoxetine influence the rat central dopaminergic receptorsautoradography and in situ hybridization study

Chronic co-administration of iinipramine and amantadine induces liippocampal BDNF gene expression in rats

Antidopaminergic activity of EMD 57445, a new selective ligand of sigma receptors

The effect of co-treatment with aripiprazole and antidepressants on the MK-801-induced deficits in the social interaction test in rats

Effects of olanzapine, risperidone and fluoxetine in the forced swimming and elevated plus-maze tests in rats

A relationship between glutathione deficiency during the early postnatal life and schizophrenia-like behavior in adulthood of sprague-dawley rats

Reboxetine administered repeatedly influences the central dopaminergic system in the rat

Repeated co-treatment with imipramine and amantadine induces hippocampal brain-derived neurotrophic factor gene expression in rats

Effect of combined treatment with imipramine and amantadine on the central dopamine D2 and D3 receptors in rats

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

Repeated treatment with mirtazapine induces brain-derived neurotrophic factor gene expression in rats

Opposite influence of MPEP, an mGluR5 antagonist, on the locomotor hyperactivity induced by PCP and amphetamine

Brain-derived neurotrophic factor gene expression in rats following repeated treatment with mirtazapine