A pain-relaying ion channel on a hypersensitive population of sensory neurons can instead elicit sensations of itch in both fish and mice when directly activated, providing a novel model of itch transduction.
Circuit and transcriptional analysis shows that genetically defined central amygdala neurons and their projections to the ventral periaqueductal gray mediate behavioral and affective responses to pruritus.
Type I interferon and interferon-γ signaling redundantly protects mice from the tick-borne pathogen Rickettsia parkeri in the skin, and interferon receptor-deficient mice are a tractable model for investigating rickettsiosis.
An ento-epidemiological model reveals that what made the Zika virus a public health problem in Feira de Santana, Brazil, was a surprisingly high attack rate coupled with a low risk of Microcephaly per challenged pregnancy.
MRGPRD and MRGRPX1 are co-expressed in primate DRG neurons, but β-alanine and BAM8-22, preferentially activate CMH-subclasses, and co-activating different cutaneous nociceptors by pruritogens does not change itch sensation to pain.
Although primary sensory neuron-derived calcitonin gene-related peptide (CGRP) contributes to the processing of pain messages, an understudied population of dorsal horn CGRP-expressing interneurons also contributes to the processing of mechanical sensitivity.