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The cell biology of acute itch

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ABSTRACT

Itch, the irritation we feel and the relief that comes from scratching, is an evolutionary warning system and defense against harmful environmental agents. Although once considered a subtype of pain, itch is now recognized as a unique sense, with its own distinct physiology and cell receptors. Here, we discuss recent advances in our understanding of itch and the molecular players that mediate this sensory modality.

No MeSH data available.


Related in: MedlinePlus

Spinal circuits regulate itch signals. Pruriceptors transmitting itch signals terminate in the spinal dorsal horn. Here, a complex circuit made up of inhibitory and excitatory interneurons (EIs) controls itch transmission to the brain. Histamine and nonhistaminergic pathways are regulated downstream of Nppa+ interneurons (Mishra and Hoon, 2013), gated by Bhlhb5 inhibitory interneurons, and converge in the dorsal horn on GRPR+ (Sun et al., 2009) and TR4+ excitatory interneurons. Mechanical itch is gated via excitatory input under the control of NPY+ interneurons (Bourane et al., 2015).
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fig3: Spinal circuits regulate itch signals. Pruriceptors transmitting itch signals terminate in the spinal dorsal horn. Here, a complex circuit made up of inhibitory and excitatory interneurons (EIs) controls itch transmission to the brain. Histamine and nonhistaminergic pathways are regulated downstream of Nppa+ interneurons (Mishra and Hoon, 2013), gated by Bhlhb5 inhibitory interneurons, and converge in the dorsal horn on GRPR+ (Sun et al., 2009) and TR4+ excitatory interneurons. Mechanical itch is gated via excitatory input under the control of NPY+ interneurons (Bourane et al., 2015).

Mentions: Interestingly, ablation of BNP neurons did not affect GRP-induced itch, and BNP KO mice still displayed normal itch behavior when GRP was injected intrathecally (Mishra and Hoon, 2013). Antagonist blockade of GRPR reduced both BNP- and GRP-induced itch. These results, along with data revealing dorsal horn interneuron expression of GRPR (Wang et al., 2013), indicate that GRP acts downstream of BNP in the spinal cord and identify a new itch circuit in the dorsal horn (Fig. 3). However, later studies from Liu et al. (2014) using in situ hybridization and real-time RT-PCR demonstrated that GRP is expressed in the DRG. These discrepancies could be caused by the low expression of the proteins being studied and the differences in detection methods used by each laboratory. Moreover, it is possible that the expression levels of these peptides and receptors become altered by changes in physiology or alterations from abnormal pathological conditions.


The cell biology of acute itch
Spinal circuits regulate itch signals. Pruriceptors transmitting itch signals terminate in the spinal dorsal horn. Here, a complex circuit made up of inhibitory and excitatory interneurons (EIs) controls itch transmission to the brain. Histamine and nonhistaminergic pathways are regulated downstream of Nppa+ interneurons (Mishra and Hoon, 2013), gated by Bhlhb5 inhibitory interneurons, and converge in the dorsal horn on GRPR+ (Sun et al., 2009) and TR4+ excitatory interneurons. Mechanical itch is gated via excitatory input under the control of NPY+ interneurons (Bourane et al., 2015).
© Copyright Policy - openaccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4862869&req=5

fig3: Spinal circuits regulate itch signals. Pruriceptors transmitting itch signals terminate in the spinal dorsal horn. Here, a complex circuit made up of inhibitory and excitatory interneurons (EIs) controls itch transmission to the brain. Histamine and nonhistaminergic pathways are regulated downstream of Nppa+ interneurons (Mishra and Hoon, 2013), gated by Bhlhb5 inhibitory interneurons, and converge in the dorsal horn on GRPR+ (Sun et al., 2009) and TR4+ excitatory interneurons. Mechanical itch is gated via excitatory input under the control of NPY+ interneurons (Bourane et al., 2015).
Mentions: Interestingly, ablation of BNP neurons did not affect GRP-induced itch, and BNP KO mice still displayed normal itch behavior when GRP was injected intrathecally (Mishra and Hoon, 2013). Antagonist blockade of GRPR reduced both BNP- and GRP-induced itch. These results, along with data revealing dorsal horn interneuron expression of GRPR (Wang et al., 2013), indicate that GRP acts downstream of BNP in the spinal cord and identify a new itch circuit in the dorsal horn (Fig. 3). However, later studies from Liu et al. (2014) using in situ hybridization and real-time RT-PCR demonstrated that GRP is expressed in the DRG. These discrepancies could be caused by the low expression of the proteins being studied and the differences in detection methods used by each laboratory. Moreover, it is possible that the expression levels of these peptides and receptors become altered by changes in physiology or alterations from abnormal pathological conditions.

View Article: PubMed Central - HTML - PubMed

ABSTRACT

Itch, the irritation we feel and the relief that comes from scratching, is an evolutionary warning system and defense against harmful environmental agents. Although once considered a subtype of pain, itch is now recognized as a unique sense, with its own distinct physiology and cell receptors. Here, we discuss recent advances in our understanding of itch and the molecular players that mediate this sensory modality.

No MeSH data available.


Related in: MedlinePlus