Clinical Commentary| Volume 80, ISSUE 7, e47-e49, October 01, 2016

Modern Microglia: Novel Targets in Psychiatric Neuroscience

  • Jennifer B. Dwyer
    Yale University Department of Psychiatry, Yale University, New Haven, Connecticut

    Yale University Child Study Center, Yale University, New Haven, Connecticut
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  • David A. Ross
    Address correspondence to: David A. Ross, M.D., Ph.D., Yale University Department of Psychiatry, 300 George Street, Suite 901, New Haven, CT 06511; .
    Yale University Department of Psychiatry, Yale University, New Haven, Connecticut
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      Much of psychiatric neuroscience has focused on studying neurons, with their relative health or dysfunction considered the key to mental health or disease. There are good reasons for this focus: neurons are the primary communicators of the central nervous system. Neurons form the most basic structure of synapses, exchanging information predominantly via chemical transmission. These synapses are the primary targets in psychiatry, with medications either interfering with synaptic communication (e.g., antipsychotics that antagonize dopaminergic transmission at D2 receptors) or augmenting it (e.g., benzodiazepines that allosterically enhance the function of gamma-aminobutyric acid receptors, or selective serotonin reuptake inhibitors, which prolong the actions of serotonin by preventing its reuptake and clearance). While the existence of other cells in the brain has long been known, their importance to neuronal functioning and their potential roles in psychiatric disorders is only now being fully appreciated.
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      Linked Article

      • Microglial Acid Sensing Regulates Carbon Dioxide-Evoked Fear
        Biological PsychiatryVol. 80Issue 7
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          Carbon dioxide (CO2) inhalation, a biological challenge and pathologic marker in panic disorder, evokes intense fear and panic attacks in susceptible individuals. The molecular identity and anatomic location of CO2-sensing systems that translate CO2-evoked fear remain unclear. We investigated contributions of microglial acid sensor T cell death–associated gene-8 (TDAG8) and microglial proinflammatory responses in CO2-evoked behavioral and physiological responses.
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