Utilize este identificador para referenciar este registo:
https://hdl.handle.net/10316/108592
Título: | Depression as a Glial-Based Synaptic Dysfunction | Autor: | Rial, Daniel Lemos, Cristina Pinheiro, Helena Duarte, Joana M. Gonçalves, Francisco Q. Real, Joana I. Prediger, Rui D. Gonçalves, Nélio Gomes, Catarina A. Canas, Paula M. Agostinho, Paula |
Palavras-chave: | depression; synapse; astrocytes; microglia; purines | Data: | 2015 | Editora: | Frontiers Media S.A. | Projeto: | NARSAD PTDC/NEUNMC/ 4154/2014 UID/NEU/04539/2013 |
Título da revista, periódico, livro ou evento: | Frontiers in Cellular Neuroscience | Volume: | 9 | Número: | JAN2016 | Resumo: | Recent studies combining pharmacological, behavioral, electrophysiological and molecular approaches indicate that depression results from maladaptive neuroplastic processes occurring in defined frontolimbic circuits responsible for emotional processing such as the prefrontal cortex, hippocampus, amygdala and ventral striatum. However, the exact mechanisms controlling synaptic plasticity that are disrupted to trigger depressive conditions have not been elucidated. Since glial cells (astrocytes and microglia) tightly and dynamically interact with synapses, engaging a bi-directional communication critical for the processing of synaptic information, we now revisit the role of glial cells in the etiology of depression focusing on a dysfunction of the "quad-partite" synapse. This interest is supported by the observations that depressive-like conditions are associated with a decreased density and hypofunction of astrocytes and with an increased microglia "activation" in frontolimbic regions, which is expected to contribute for the synaptic dysfunction present in depression. Furthermore, the traditional culprits of depression (glucocorticoids, biogenic amines, brain-derived neurotrophic factor, BDNF) affect glia functioning, whereas antidepressant treatments (serotonin-selective reuptake inhibitors, SSRIs, electroshocks, deep brain stimulation) recover glia functioning. In this context of a quad-partite synapse, systems modulating glia-synapse bidirectional communication-such as the purinergic neuromodulation system operated by adenosine 5'-triphosphate (ATP) and adenosine-emerge as promising candidates to "re-normalize" synaptic function by combining direct synaptic effects with an ability to also control astrocyte and microglia function. This proposed triple action of purines to control aberrant synaptic function illustrates the rationale to consider the interference with glia dysfunction as a mechanism of action driving the design of future pharmacological tools to manage depression. | URI: | https://hdl.handle.net/10316/108592 | ISSN: | 1662-5102 | DOI: | 10.3389/fncel.2015.00521 | Direitos: | openAccess |
Aparece nas coleções: | FFUC- Artigos em Revistas Internacionais I&D CNC - Artigos em Revistas Internacionais |
Ficheiros deste registo:
Ficheiro | Descrição | Tamanho | Formato | |
---|---|---|---|---|
Depression as a glial-based synaptic dysfunction.pdf | 971.87 kB | Adobe PDF | Ver/Abrir |
Visualizações de página
74
Visto em 24/jul/2024
Downloads
36
Visto em 24/jul/2024
Google ScholarTM
Verificar
Altmetric
Altmetric
Este registo está protegido por Licença Creative Commons