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1.
Glia ; 71(8): 1791-1803, 2023 08.
Artigo em Inglês | MEDLINE | ID: mdl-36866453

RESUMO

Zika virus (ZIKV) is a strongly neurotropic flavivirus whose infection has been associated with microcephaly in neonates. However, clinical and experimental evidence indicate that ZIKV also affects the adult nervous system. In this regard, in vitro and in vivo studies have shown the ability of ZIKV to infect glial cells. In the central nervous system (CNS), glial cells are represented by astrocytes, microglia, and oligodendrocytes. In contrast, the peripheral nervous system (PNS) constitutes a highly heterogeneous group of cells (Schwann cells, satellite glial cells, and enteric glial cells) spread through the body. These cells are critical in both physiological and pathological conditions; as such, ZIKV-induced glial dysfunctions can be associated with the development and progression of neurological complications, including those related to the adult and aging brain. This review will address the effects of ZIKV infection on CNS and PNS glial cells, focusing on cellular and molecular mechanisms, including changes in the inflammatory response, oxidative stress, mitochondrial dysfunction, Ca2+ and glutamate homeostasis, neural metabolism, and neuron-glia communication. Of note, preventive and therapeutic strategies that focus on glial cells may emerge to delay and/or prevent the development of ZIKV-induced neurodegeneration and its consequences.


Assuntos
Infecção por Zika virus , Zika virus , Humanos , Zika virus/fisiologia , Infecção por Zika virus/complicações , Infecção por Zika virus/tratamento farmacológico , Infecção por Zika virus/patologia , Neuroglia/metabolismo , Sistema Nervoso Central/metabolismo , Encéfalo/metabolismo
2.
Philos Trans R Soc Lond B Biol Sci ; 370(1672)2015 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-26009760

RESUMO

Papers in this issue concern extrasynaptic transmission, namely release of signalling molecules by exocytosis or diffusion from neuronal cell bodies, dendrites, axons and glia. Problems discussed concern the molecules, their secretion and importance for normal function and disease. Molecules secreted extrasynaptically include transmitters, peptides, hormones and nitric oxide. For extrasynaptic secretion, trains of action potentials are required, and the time course of release is slower than at synapses. Questions arise concerning the mechanism of extrasynaptic secretion: how does it differ from the release observed at synaptic terminals and gland cells? What kinds of vesicles take part? Is release accomplished through calcium entry, SNAP and SNARE proteins? A clear difference is in the role of molecules released synaptically and extrasynaptically. After extrasynaptic release, molecules reach distant as well as nearby cells, and thereby produce long-lasting changes over large volumes of brain. Such changes can affect circuits for motor performance and mood states. An example with clinical relevance is dyskinesia of patients treated with l-DOPA for Parkinson's disease. Extrasynaptically released transmitters also evoke responses in glial cells, which in turn release molecules that cause local vasodilatation and enhanced circulation in regions of the brain that are active.


Assuntos
Corpo Celular/metabolismo , Dendritos/metabolismo , Exocitose/fisiologia , Neurônios/metabolismo , Neurotransmissores/metabolismo , Neurônios/citologia
3.
Philos Trans R Soc Lond B Biol Sci ; 370(1672)2015 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-26009775

RESUMO

Serotonin, a modulator of multiple functions in the nervous system, is released predominantly extrasynaptically from neuronal cell bodies, axons and dendrites. This paper describes how serotonin is released from cell bodies of Retzius neurons in the central nervous system (CNS) of the leech, and how it affects neighbouring glia and neurons. The large Retzius neurons contain serotonin packed in electrodense vesicles. Electrical stimulation with 10 impulses at 1 Hz fails to evoke exocytosis from the cell body, but the same number of impulses at 20 Hz promotes exocytosis via a multistep process. Calcium entry into the neuron triggers calcium-induced calcium release, which activates the transport of vesicle clusters to the plasma membrane. Exocytosis occurs there for several minutes. Serotonin that has been released activates autoreceptors that induce an inositol trisphosphate-dependent calcium increase, which produces further exocytosis. This positive feedback loop subsides when the last vesicles in the cluster fuse and calcium returns to basal levels. Serotonin released from the cell body is taken up by glia and released elsewhere in the CNS. Synchronous bursts of neuronal electrical activity appear minutes later and continue for hours. In this way, a brief train of impulses is translated into a long-term modulation in the nervous system.


Assuntos
Corpo Celular/metabolismo , Sistema Nervoso Central/fisiologia , Exocitose/fisiologia , Sanguessugas/fisiologia , Modelos Neurológicos , Neurônios/metabolismo , Serotonina/metabolismo , Animais , Transporte Biológico Ativo/fisiologia , Cálcio/metabolismo , Sistema Nervoso Central/citologia , Sistema Nervoso Central/metabolismo , Estimulação Elétrica , Retroalimentação Fisiológica/fisiologia , Vesículas Transportadoras/metabolismo
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