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  • Glial cells have emerged as important


    Glial cells have emerged as important AMD3100 8HCl protagonists of the central nervous system (CNS) physiology (Chen and Swanson, 2003; Kettenmann and Verkhratsky, 2008; Parpura and Verkhratsky, 2012). As widely described in the literature, astrocytes regulate glutamatergic synapses by clearance of glutamate in the synaptic cleft (Currie and Kelly, 1981; Danbolt, 2001; Schousboe and Waagepetersen, 2005). Glutamate uptake and release are mediated by Na+-dependent and Na+-independent glutamate transporters present in neuronal and glial cells. The importance of these protein transporters in the maintenance of CNS homeostasis is evident in some neurodegenerative diseases which are associated with dysfunctions in glutamate transport (see King et al., 2011). Glial participation in the hypothalamic response to hypertonic stimuli has already been reported in the literature (Gamrani et al., 2011; Wang et al., 2006; Yuan et al., 2010). Previous studies have described that hypothalamic astrocytes show a neurochemical response to a hypertonic stimulus (Jiang et al., 2011). Cao et al. (2008) demonstrated that hypothalamic glial cells synthesize and release glutamate under hypertonic conditions. Several studies described that glutamate transport is modulated by different neurotransmitters, such as GABA (Héja et al., 2009), dopamine (Amara, 2014; Gainetdinov et al., 2001) and AMD3100 8HCl (Araque et al., 2002). Gliotransmitters such as ATP and adenosine can also regulate glutamate levels in the extracellular environment (Fellin et al., 2006; Fields and Burnstock, 2006; Jeremic et al., 2001; Paes-de Carvalho et al., 2005). Although previous studies have described that adenosine inhibits the glutamate release in brain preparations (Harvey and Lacey, 1997), it is not still clarified if the control of glutamate release induced by Na+-hypertonicity is controlled by purinergic system. The current study aimed to evaluate the mechanism by which glial cells control glutamate release when submitted to a hypertonic stimulus as well as the role of the adenosinergic system in this regulation.
    Material and methods
    Results Both hypothalamic and glial cell cultures presented high purity for astrocytes as observed in supplementary material (Supplementary Figs. 1A–G). Our data also have shown that hypertonic stimulation evoked evident decrease in the cell volume of hypothalamic astrocytes in culture. This phenomenon was not observed in astrocytes cultured from brain cortex (Supplementary Figs. 1A–D).
    Conclusions Taken together these results conclude that (1) hypothalamic glial cells respond to a hypertonic stimulus by the release of glutamate into the extracellular medium and (2) this phenomenon is followed by an increase of extracellular adenosine which (3) activates adenosine A1 receptors (4) blocking the initial glutamate release. The current study demonstrates for the first time that hypothalamic glial cells present a specialized neurochemistry that responds physiologically to hypertonic changes. They utilize the purinergic system to regulate Na+-dependent glutamate release induced by a hypertonic stimulus.
    Introduction As a top-ranking cause of many diseases and premature death, cigarette smoking is not only associated with cardiovascular disease, cancer and respiratory disease but is also associated with mental illness. Recent studies suggested that smokers had a higher risk for suffering from depression, anxiety and psychological distress (Degenhardt et al., 2017, Leung et al., 2012, Taylor et al., 2014). Nicotine is the main psychoactive component of tobacco responsible for its addictive properties, which rapidly reach the brain through the blood/brain barrier (Malkawi et al., 2009). Nicotine had many effects on brain circuits and behavior, and it stimulates neuronal systems involved in primary reinforcement, including glutamatergic neurons, dopaminergic neurons, cholinergic neurons and others (Cross et al., 2018, Picciotto and Mineur, 2014). Nicotine addiction is characterized by compulsive nicotine-seeking and -taking, relapsing to tobacco smoking. Accumulating lines of evidence suggested that glutamatergic neurons play critical roles in various aspects of nicotine addiction, including acquisition and maintenance of nicotine consumption, nicotine withdrawal and persistent nicotine-seeking even after prolonged abstinence (Cross et al., 2018).