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   <subfield code="a">A complex interaction between glycine/NMDA receptors and serotonergic/noradrenergic antidepressants in the forced swim test in mice</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Ewa Poleszak, Piotr Wlaź, Bernadeta Szewczyk, Aleksandra Wlaź, Regina Kasperek, Andrzej Wróbel, Gabriel Nowak]</subfield>
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   <subfield code="a">Both clinical and preclinical studies demonstrate the antidepressant activity of the functional NMDA receptor antagonists. In this study, we assessed the effects of two glycine/NMDA receptor ligands, namely L-701,324 (antagonist) and d-cycloserine (a partial agonist) on the action of antidepressant drugs with different pharmacological profiles in the forced swim test in mice. Swim sessions were conducted by placing mice individually in glass cylinders filled with warmed water for 6min. The duration of behavioral immobility during the last 4min of the test was evaluated. The locomotor activity of mice was measured with photoresistor actimeters. L-701,324 and d-cycloserine given with reboxetine (administered in subeffective doses) did not change the behavior of animals in the forced swim test. A potentiating effect was seen when both tested glycine site ligands were given concomitantly with imipramine or fluoxetine in this test. The lesion of noradrenaline nerve terminals produced by DSP-4 neither altered the baseline activity nor influenced the antidepressant-like action of L-701,324 or d-cycloserine. The depletion of serotonin by p-CPA did not alter baseline activity in the forced swim test. However, it completely antagonized the antidepressant-like action produced by L-701,324 and d-cycloserine. Moreover, the antidepressant-like effects of imipramine, fluoxetine and reboxetine were abolished by d-serine, a full agonist of glycine/NMDA receptors. The present study demonstrates that glycine/NMDA receptor functional antagonists enhance the antidepressant-like action of serotonin, but not noradrenaline-based antidepressants and such their activity seems to depend on serotonin rather than noradrenaline pathway.</subfield>
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   <subfield code="a">The Author(s), 2011</subfield>
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   <subfield code="a">NMDA receptor</subfield>
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   <subfield code="u">Chair and Department of Applied Pharmacy, Medical University of Lublin, Chodźki 1, 20-093, Lublin, Poland</subfield>
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   <subfield code="a">Wlaź</subfield>
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   <subfield code="u">Department of Animal Physiology, Institute of Biology, Maria Curie-Skłodowska University, Akademicka 19, 20-033, Lublin, Poland</subfield>
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