Neuroscience
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Trigeminal neuropathic pain (TGN) is an attacking, abrupt, electric-shock headache involving abnormal cortical activity. The neural mechanism underlying TGN remains elusive. In this study, we explored the role of microglia in the primary somatosensory barrel cortex (S1BF), which is a critical region for TGN, of a mouse model of TGN that displayed significant pain-related behaviors. ⋯ In addition, we found that microglia in the S1BF (microgliaS1BF) were significantly activated, with density and morphology changes. Intraperitoneal administration of minocycline, a microglia inhibitor, attenuated pain sensitization, and decreased GluS1BF neuronal activity. Together, these findings demonstrate the putative importance of microglia as a key regulator in TGN through actions on GluS1BF neuronal adaptation.
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Mesolimbic dopamine has been implicated in reward learning. Fischbach-Weiss and Janak (this issue) use optogenetics to attenuate dopamine signaling and study its role in cue-driven motivated behavior.