Synaptic Dynamics of the Feed-forward Inhibitory Circuitry Gating Mechanical Allodynia in Mice

Conclusions ThePrkcg-P2A-tdTomato mice the authors constructed provide a useful tool for further analysis on how the spinal allodynia gate works. The current study indicated that nerve injury enhanced the excitability of spinal protein kinase C γ expressing interneurons due to disinhibition of the feed-forward inhibitory circuit, and enabled Aβ primary inputs to activate spinal protein kinase C γ expressing interneurons.Editor ’s PerspectiveWhat We Already Know about This TopicMechanical allodynia characteristic of neuropathic pain is caused by neuroplastic changes in the spinal cord dorsal hornA β primary afferent nerve fibers provide the required nociceptive input for allodyniaWhat This Article Tells Us That Is NewUsing the clustered regularly interspaced short palindromic repeats/clustered regularly interspaced short palindromic repeats-associated nuclease 9 technique, a novel mouse strain was created allowing study of a key set of spinal interneuronsThe data suggest hyperexcitability of spinal protein kinase C γ expressing interneurons facilitates allodynia after nerve injury

Source: Anesthesiology - April 15, 2020 Category: Anesthesiology Source Type: research