NMDA glutamate receptor polymorphisms modulate antipsychotic-induced hyperprolactinemia in schizophrenia; Progress in Neuro-Psychopharmacology and Biological Psychiatry; Vol. 143
| Parent link: | Progress in Neuro-Psychopharmacology and Biological Psychiatry.— .— Amsterdam: Elsevier Science Publishing Company Inc. Vol. 143.— 2025.— Article number 111569, 9 p. |
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| Other Authors: | , , , , , , , , , |
| Summary: | Title screen Dopamine receptor inhibition underlies both the therapeutic and adverse effects of antipsychotics, but the mechanisms modulating these effects in patients with schizophrenia remain incompletely understood. Hyperprolactinemia (HPRL), a direct consequence of D2 dopamine receptor blockade, provides a unique clinical model to investigate how genetic variation in glutamatergic signaling influences the downstream effects of dopaminergic disruption. We hypothesized that polymorphisms in GRIN2A and GRIN2B, encoding NMDA glutamate receptor subunits, modify the neuroendocrine consequences of dopamine receptor inhibition. By studying antipsychotic-induced HPRL, we aimed to demonstrate that NMDA receptor genetic variants shape the functional outcomes of dopaminergic perturbation Текстовый файл AM_Agreement |
| Language: | English |
| Published: |
2025
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| Subjects: | |
| Online Access: | https://doi.org/10.1016/j.pnpbp.2025.111569 |
| Format: | Electronic Book Chapter |
| KOHA link: | https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=684627 |