JURANYI ZSOLT PDF

Jurányi Zsolt is the author of Az alvilág zsoldjában ( avg rating, 16 ratings, 1 review, published ) and Az alvilág csapdájában ( avg rating. nov. Az alvilág csapdájában has 3 ratings and 1 review. Sándor said: Az első rész fényévekkel jobb volt, szerintem. Csak azért vergődtem végig. List of computer science publications by Zsolt Jurányi.

Author: Bagar Mokasa
Country: New Zealand
Language: English (Spanish)
Genre: Education
Published (Last): 15 December 2016
Pages: 50
PDF File Size: 5.57 Mb
ePub File Size: 8.89 Mb
ISBN: 685-9-81442-195-8
Downloads: 62368
Price: Free* [*Free Regsitration Required]
Uploader: Douzshura

AB – The most dominant hypotheses for the pathogenesis of schizophrenia have focused primarily upon hyperfunctional dopaminergic and hypofunctional glutamatergic neurotransmission in the central nervous system. The most dominant hypotheses for the pathogenesis of schizophrenia have focused primarily upon hyperfunctional dopaminergic and hypofunctional glutamatergic neurotransmission in the central nervous system.

Jurányi Zsolt

When risperidone and Org were added in combination, a decrease in extracellular dopamine concentrations was accompanied with sustained elevation of extracellular glycine levels. Org injection reduced extracellular dopamine concentrations and elevated extracellular glycine levels but the concentrations of serine and glutamate were not changed.

N-methyl-d-aspartate NMDA receptor hypofunction in schizophrenia can be reversed by glycine transporter type-1 GlyT-1 inhibitors, which regulate glycine concentrations at the vicinity of NMDA receptors.

  HOW P&G TRIPLED ITS INNOVATION SUCCESS RATE PDF

Link to publication in Scopus. The therapeutic efficacy of all atypical antipsychotics is explained in part by antagonism of the dopaminergic neurotransmission, mainly by blockade of D zolt dopamine receptors. Access to Document Our data indicate jursnyi coadministration of an antipsychotic with a GlyT-1 inhibitor may normalize hypofunctional NMDA receptor-mediated glutamatergic neurotransmission with reduced dopaminergic side effects characteristic for antipsychotic medication.

dblp: Zsolt Jurányi

Risperidone increased extracellular concentrations of dopamine but failed to influence those of zsolg or glutamate measured in microdialysis samples. T1 – Alterations in brain extracellular dopamine and glycine levels following combined administration of the glycine transporter type-1 inhibitor Org and risperidone.

Neurochemical ResearchVol. Abstract The most dominant hypotheses for the pathogenesis of schizophrenia have focused primarily upon hyperfunctional dopaminergic and hypofunctional glutamatergic neurotransmission in the central nervous system.

Neurochemical Research35 12 Alterations in brain extracellular dopamine and glycine levels following combined administration of the glycine transporter type-1 inhibitor Org and risperidone. Keywords Antipsychotic agents Extracellular glycine and dopamine Glycine transporter type-1 inhibitors Microdialysis Schizophrenia.

Loop | Zsolt Juranyi

To investigate this type of combined drug administration, rats were treated with the atypical antipsychotic risperidone together with the GlyT-1 inhibitor Org The therapeutic efficacy zso,t all atypical antipsychotics is explained in part by antagonism of the dopaminergic neurotransmission, mainly by blockade of D2 dopamine receptors. Interestingly, the extracellular concentrations of glutamate were also enhanced.

  INTOXICACION POR ISOPROPANOL PDF

Combined drug administration with D 2 dopamine receptor blockade and activation of hypofunctional NMDA receptors may be needed for a more effective treatment of positive and negative symptoms and the accompanied cognitive deficit in schizophrenia.

Link to citation list in Scopus.

N2 – The most dominant hypotheses for the pathogenesis of schizophrenia zsolr focused primarily upon hyperfunctional dopaminergic and hypofunctional glutamatergic neurotransmission in the central nervous system. Combined drug administration with D2 dopamine receptor blockade and activation of hypofunctional NMDA receptors may be needed for a more effective treatment of positive and negative symptoms and the accompanied cognitive deficit in schizophrenia.