Substance P-driven feed-forward inhibitory activity in the mammalian spinal cord

• Main Authors: King Christopher (Author), Takeda Daisuke (Author), Chen Meng (Author), Nakatsuka Terumasa (Author), Ling Jennifer (Author), Xing Hong (Author), Ataka Toyofumi (Author), Vierck Charles (Author), Yezierski Robert (Author), Gu Jianguo G (Author)
• Format: Book
• Published: SAGE Publishing, 2005-06-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

<p>Abstract</p> <p>In mammals, somatosensory input activates feedback and feed-forward inhibitory circuits within the spinal cord dorsal horn to modulate sensory processing and thereby affecting sensory perception by the brain. Conventionally, feedback and feed-forward inhibitory activity evoked by somatosensory input to the dorsal horn is believed to be driven by glutamate, the principle excitatory neurotransmitter in primary afferent fibers. Substance P (SP), the prototypic neuropeptide released from primary afferent fibers to the dorsal horn, is regarded as a pain substance in the mammalian somatosensory system due to its action on nociceptive projection neurons. Here we report that endogenous SP drives a novel form of feed-forward inhibitory activity in the dorsal horn. The SP-driven feed-forward inhibitory activity is long-lasting and has a temporal phase distinct from glutamate-driven feed-forward inhibitory activity. Compromising SP-driven feed-forward inhibitory activity results in behavioral sensitization. Our findings reveal a fundamental role of SP in recruiting inhibitory activity for sensory processing, which may have important therapeutic implications in treating pathological pain conditions using SP receptors as targets.</p>

Item Description

10.1186/1744-8069-1-20
1744-8069