| Texto completo | |
| Autor(es): |
Ribeiro, Deidiane Elisa
;
Roncalho, Aline Lulho
;
Glaser, Talita
;
Ulrich, Henning
;
Wegener, Gregers
;
Joca, Samia
Número total de Autores: 6
|
| Tipo de documento: | Artigo Científico |
| Fonte: | INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES; v. 20, n. 11, p. 26-pg., 2019-06-01. |
| Resumo | |
Stress exposure is considered to be the main environmental cause associated with the development of depression. Due to the limitations of currently available antidepressants, a search for new pharmacological targets for treatment of depression is required. Recent studies suggest that adenosine triphosphate (ATP)-mediated signaling through the P2X7 receptor (P2X7R) might play a prominent role in regulating depression-related pathology, such as synaptic plasticity, neuronal degeneration, as well as changes in cognitive and behavioral functions. P2X7R is an ATP-gated cation channel localized in different cell types in the central nervous system (CNS), playing a crucial role in neuron-glia signaling. P2X7R may modulate the release of several neurotransmitters, including monoamines, nitric oxide (NO) and glutamate. Moreover, P2X7R stimulation in microglia modulates the innate immune response by activating the NLR family pyrin domain containing 3 (NLRP3) inflammasome, consistent with the neuroimmune hypothesis of MDD. Importantly, blockade of P2X7R leads to antidepressant-like effects in different animal models, which corroborates the findings that the gene encoding for the P2X7R is located in a susceptibility locus of relevance to depression in humans. This review will discuss recent findings linked to the P2X7R involvement in stress and MDD neuropathophysiology, with special emphasis on neurochemical, neuroimmune, and neuroplastic mechanisms. (AU) | |
| Processo FAPESP: | 18/08426-0 - Alcalóides indólicos, subprodutos do processamento de Maqui (Aristotelia chilensis) como aditivos alimentares no tratamento da Doença de Alzheimer |
| Beneficiário: | Alexander Henning Ulrich |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |
| Processo FAPESP: | 15/13345-1 - Doença de Huntington: envolvimento de Huntingtin no controle do comprometimento celular |
| Beneficiário: | Talita Glaser |
| Modalidade de apoio: | Bolsas no Brasil - Pós-Doutorado |
| Processo FAPESP: | 12/50880-4 - Células-tronco: dos papéis de receptores de cininas e purinas às aplicações terapêuticas |
| Beneficiário: | Alexander Henning Ulrich |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |