Browsing by Author "Gomez, Gonzalo I."

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    Activation of Melanocortin-4 Receptor by a Synthetic Agonist Inhibits Ethanol-induced Neuroinflammation in Rats
    (2019) Flores Bastias, Osvaldo; Gomez, Gonzalo I.; Orellana Roca, Juan Andrés; Karahanian, Eduardo
    Background: High ethanol intake induces a neuroinflammatory response resulting in the subsequent maintenance of chronic alcohol consumption. The melanocortin system plays a pivotal role in the modulation of alcohol consumption. Interestingly, it has been shown that the activation of melanocortin-4 receptor (MC4R) in the brain decreases the neuroinflammatory response in models of brain damage other than alcohol consumption, such as LPS-induced neuroinflammation, cerebral ischemia, glutamate excitotoxicity, and spinal cord injury.
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    Astroglial Hemichannels and Pannexons: The Hidden Link between Maternal Inflammation and Neurological Disorders
    (2021) Prieto Villalobos, Juan Carlos; Alvear Soto, Tanhia Francheska; Liberona, Andres; Lucero, Claudia M.; Martinez Araya, Claudio J.; Balmazabal, Javiera; Inostroza, Carla A.; Ramírez Rojas, Gigliola; Gomez, Gonzalo I.; Orellana Roca, Juan Andrés
    Maternal inflammation during pregnancy causes later-in-life alterations of the offspring's brain structure and function. These abnormalities increase the risk of developing several psychiatric and neurological disorders, including schizophrenia, intellectual disability, bipolar disorder, autism spectrum disorder, microcephaly, and cerebral palsy. Here, we discuss how astrocytes might contribute to postnatal brain dysfunction following maternal inflammation, focusing on the signaling mediated by two families of plasma membrane channels: hemi-channels and pannexons. [Ca2+](i) imbalance linked to the opening of astrocytic hemichannels and pannexons could disturb essential functions that sustain astrocytic survival and astrocyte-to-neuron support, including energy and redox homeostasis, uptake of K+ and glutamate, and the delivery of neurotrophic factors and energy-rich metabolites. Both phenomena could make neurons more susceptible to the harmful effect of prenatal inflammation and the experience of a second immune challenge during adulthood. On the other hand, maternal inflammation could cause excitotoxicity by producing the release of high amounts of gliotransmitters via astrocytic hemichannels/pannexons, eliciting further neuronal damage. Understanding how hemichannels and pannexons participate in maternal inflammation-induced brain abnormalities could be critical for developing pharmacological therapies against neurological disorders observed in the offspring.
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    Connexin 43 Hemichannel Activity Promoted by Pro-Inflammatory Cytokines and High Glucose Alters Endothelial Cell Function
    (2018) Sáez, Juan Carlos; Contreras-Duarte, Susana; Gomez, Gonzalo I.; Labra, Valeria C.; Santibanez, Cristian A.; Gajardo Gómez, Rosario; Avendano, Beatriz C.; Diaz, Esteban F.; Montero, Trinidad D.; Velarde, Victoria; Orellana Roca, Juan Andrés
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    Heavy Alcohol Exposure Activates Astroglial Hemichannels and Pannexons in the Hippocampus of Adolescent Rats : Effects on Neuroinflammation and Astrocyte Arborization
    (2018) Gomez, Gonzalo I.; Falcon, Romina V.; Maturana, Carola J.; Labra, Valeria C.; Salgado Cortés, Nicole Andrea; Rojas Vidal, Consuelo Antonia; Oyarzun, Juan E.; Cerpa Nebott, Waldo Francisco; Quintanilla, Rodrigo A.; Orellana Roca, Juan Andrés