[Early complications following resection of pulmonary tissue in the radiological picture].
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Biomedical subjects
Publications and source records attributed to K Ossowska.
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The aim of the present study was to investigate the influence of chronic treatment with haloperidol on the striatal N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxasole-propionic acid (AMPA) and dopamine D2 receptors using a quantitative autoradiography in rats. Haloperidol was given to animals in a dose of ca. 1 mg/kg/day in drinking water for 6 weeks or 3 months and was afterwards withdrawn for 5 days. Haloperidol increased by 20-50% the binding of [3H]spiperone in different regions of the caudate-putamen. Haloperidol decreased by ca. 30% the binding of [3H]AMPA in the ventrolateral region of intermediate part of the caudate-putamen, but did not influence the binding of [3H]MK-801. The present results suggest that, apart from supersensitivity to dopamine, chronic treatment with haloperidol also induces subsensitivity of striatal AMPA receptors.
The aim of this study was to examine the role of cortical NMDA receptors in the antipsychotic action of neuroleptics. Haloperidol (1 mg/kg/day) and clozapine (30 mg/kg/day) were administered to rats in drinking water. Autoradiographic and saturation binding analyses showed that a 3-month treatment with both haloperidol and clozapine increased the density of NMDA receptors labelled with [3H]CGP 39653 (a competitive antagonist) in the parietal and insular cortices. Haloperidol additionally increased the binding of that ligand in the frontal cortex. None of those neuroleptics influenced the binding of [3H]MK-801, an uncompetitive antagonist of NMDA receptors, in the frontal, parietal or insular cortices. A 6-week and a 3-month treatment with haloperidol antagonized the deficit of prepulse inhibition induced by phencyclidine (5 mg/kg s.c.). In contrast, short-term (4-day) administration of that neuroleptic was ineffective. The present study suggests that the increased density of cortical NMDA receptors, induced by long-term neuroleptic administration, may overcome the deficit of sensorimotor gating induced by phencyclidine. However, contribution of such an effect to the antipsychotic activity needs to be established.
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The effect of imipramine (10mg/kg) and mianserin (5 or 10mg/kg) on EEG epileptiform discharges, induced by a single amygdala stimulation in rabbits was studied. Imipramine reduced the duration of EEG afterdischarges, while mianserin prolonged it in leads from both amygdala complexes and from the motor cortex.
NMDA (100, 250 and 500 ng/0.5 microliters), kainic acid (50 and 100 ng/0.5 microliters) and AMPA (500 and 1000 ng/0.5 microliters), injected unilaterally into the ventrolateral part of the intermediate region of the caudate-putamen of rats, induced contralateral rotations. It is proposed that stimulation of NMDA, kainate and AMPA receptors present on strionigral neurons evokes an "antiparkinsonian effect".