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Gastrin-releasing peptide receptor in the spinal cord mediates mechanical allodynia following nerve injury
Li C, Back S, Lee J, Baek SK, Na H (2010) Gastrin-releasing peptide receptor in the spinal cord mediates mechanical allodynia following nerve injury. Neuroscience 2010 Abstracts 176.2/OO4. Society for Neuroscience, San Diego, CA.
Summary: Gastrin-releasing peptide receptor (GRPR) has been suggested as an itch-specific gene in the spinal cord (Sun et al., Nature, 2009). They described that selective ablation of GRPR-expressing lamina I neurons led to deficits in itch-related scratching behaviors without any effects on pain behaviors including nerve injury-induced mechanical allodynia. It has been known that two types of mechanical allodynia, such as static and dynamic allodynia, can be detectable in neuropathic patients, and may be mediated by distinct mechanisms. In the present study, we investigated the role of spinal GRPR in each of static and dynamic allodynia using both rat- and mouse-tail models of neuropathic pain. Bombesin-saporin (bombesin-sap) was administered intrathecally to ablate spinal GRPR-expressing neurons. Scratching behaviors evoked by pruritogenic agents, such as serotonin and chloroquine, and physiological pain behaviors were analyzed before nerve injury. Static or dynamic allodynia was assessed by the application of von Frey filaments to the tail or brushing the tail with a filament, respectively. RC3095, a GRPR antagonist, was given intrathecally to see its effects on static and dynamic allodynia in neuropathic rats. Bombesin-sap treatment resulted in reduction of GRPR-immunoreactive cells in lamina I of spinal dorsal horn and scratching deficits. Physiological pain behaviors of these animals were not different from those of control animals. Following the partial injury of tail-innervating nerves, animals treated with bombesin-sap exhibited comparable dynamic allodynia to control one. However, they failed to manifest static allodynia during the entire experimental period. In addition, RC3095 relieved static, but not dynamic, allodynia. These findings suggest that spinal GRPR mediates nerve injury-induced static mechanical allodynia as well as itching sensation in normal state.
Related Products: Bombesin-SAP (Cat. #IT-40)
Featured Article: Ablation of GRPR+ neurons in the spinal cord by bombesin-saporin knocks out itch sensation in mice without affecting pain circuit
Chen ZF, Sun YG, Zhao ZQ, Meng XL, Yin J, Liu XY (2009) Featured Article: Ablation of GRPR+ neurons in the spinal cord by bombesin-saporin knocks out itch sensation in mice without affecting pain circuit. Targeting Trends 10(4)
Related Products: Bombesin-SAP (Cat. #IT-40), Blank-SAP (Cat. #IT-21)
Read the featured article in Targeting Trends.
See Also:
Cellular basis of itch sensation.
Sun YG, Zhao ZQ, Meng XL, Yin J, Liu XY, Chen ZF (2009) Cellular basis of itch sensation. Science 325:1531-1534. doi: 10.1126/science.1174868
Summary: Whether itch and pain use separate neuronal pathways has long been a subject of debate. The authors injected 400 ng of bombesin-SAP (Cat. #IT-40) into the intrathecal space of mice and examined itch and pain behavior. Lesioned mice had dramatic deficits in all itch behavior tested regardless of the histamine dependence of the itch. All pain behaviors, however, were left intact. These data indicate that the gastrin-releasing peptide receptor-expressing neurons are essential for itch transmission.
Related Products: Bombesin-SAP (Cat. #IT-40)