Journal club 2014.02.13.

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Cortical GluK1 kainate receptors modulate scratching in adult mice

Journal of Neurochemistry | 2013 | 126 | 636-650

Kaori Yamada and Min Zhuo

jnc12351

Abstract

Recent investigations into the mechanisms mediating itch transmission have focused on spinal mechanisms, whereas few studies have investigated the role of the cerebral cortex in itch-related behaviors. Human imaging studies show that several cortical regions are active in correspondence with itch, including the anterior cingulate cortex (ACC). We present here evidence of cortical modulation of pruritogen-induced scratch- ing behavior. We combine pharmacological, genetic, and electrophysiological approaches to show that cortical GluK1- containing kainate (KA) receptors are involved in scratching

induced by histamine and non-histamine-dependent itching stimuli. We further show that scratching corresponds with enhanced excitatory transmission in the ACC through KA receptor modulation of inhibitory circuitry. In addition, we found that inhibiting GluK1-containing KA receptors in the ACC also reduced behavioral nociceptive responses induced by forma- lin. Our results reveal a new role of the cortex in pruritogen- induced scratching.

Keywords: cortex, glutamatergic transmission, inhibitory trans- mission, itch, kainate receptors, scratching.
J. Neurochem. (2013) 126, 636–650.

Journal club 2014.01.29.

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Distinct Expression of Mas1-Related G-Protein-Coupled Receptor B4 in Dorsal Root and Trigeminal Ganglia—Implications for Altered Behaviors in Acid-Sensing Ion Channel 3-Deficient Mice

Ya-Han Huang & Chin-Yu Chang & Chih-Cheng Chen & Chih-Dong Yang & Wei-Hsin Sun

Received: 26 February 2013 / Accepted: 8 July 2013 / Published online: 31 July 2013 # Springer Science+Business Media New York 2013

art%3A10.1007%2Fs12031-013-0070-0

Abstract

Mas1-related G-protein-coupled receptors (Mrgprs), comprising more than 50 distinct members, are specifically expressed in primary sensory neurons. Reflecting the diversity and specificity of stimuli they detect, Mrgprs are involved in pain, touch, and itch-related behaviors. Sensory–neuron-specif- ic acid-sensing ion channel 3 (ASIC3) is essential for touch and inflammatory pain, but mice lacking ASIC3 have complex behavioral alterations in various modalities of pain and touch. To understand whether Mrgprs are involved in complex behav- ioral alterations found in ASIC3-deficient mice, we examined Mrgpr gene expression in ASIC3−/− mice. Only MrgprB4 expression has shown significant change. MrgprB4 expression was increased in ASIC3−/− dorsal root ganglia (DRG) but decreased in ASIC3−/− trigeminal ganglia. The distinct alter- ations in DRG and trigeminal ganglia imply that MrgprB4 could have multiple functions. Given that MrgprB4 is expressed in neurons that may detect gentle touch and that ASIC3−/− mice have altered sensitivity of mechanoreceptors for light touch, the expression change of MrgprB4 is more likely related to the altered touch behaviors of ASIC3−/− mice.

Keywords

Dorsal root ganglion . Trigeminal ganglion . Mas1-related G-protein-coupled receptor B4 . ASIC3 . Nociceptors

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