Review

Effects of general anesthetics on visceral pain transmission in the spinal cord

Yun Wang¹ , Jing Wu² , Qing Lin⁴ , HJ Nauta³ , Yun Yue¹ and Li Fang^3,4

¹  Department of Anesthesiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, PR China

²  Department of Neuro-Oncology, the University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA

³  Division of Neurosurgery, Department of Surgery, the University of Texas Medical Branch, Galveston, TX 77555-0517, USA

⁴  Department of Neuroscience and Cell Biology, the University of Texas Medical Branch, Galveston, TX 77555-0517, USA

author email corresponding author email

Molecular Pain 2008, 4:50doi:10.1186/1744-8069-4-50

Published:	30 October 2008

Abstract

Current evidence suggests an analgesic role for the spinal cord action of general anesthetics; however, the cellular population and intracellular mechanisms underlying anti-visceral pain by general anesthetics still remain unclear. It is known that visceral nociceptive signals are transmited via post-synaptic dorsal column (PSDC) and spinothalamic tract (STT) neuronal pathways and that the PSDC pathway plays a major role in visceral nociception. Animal studies report that persistent changes including nociception-associated molecular expression (e.g. neurokinin-1 (NK-1) receptors) and activation of signal transduction cascades (such as the protein kinase A [PKA]-c-AMP-responsive element binding [CREB] cascade)-in spinal PSDC neurons are observed following visceral pain stimulation. The clinical practice of interruption of the spinal PSDC pathway in patients with cancer pain further supports a role of this group of neurons in the development and maintenance of visceral pain. We propose the hypothesis that general anesthetics might affect critical molecular targets such as NK-1 and glutamate receptors, as well as intracellular signaling by CaM kinase II, protein kinase C (PKC), PKA, and MAP kinase cascades in PSDC neurons, which contribute to the neurotransmission of visceral pain signaling. This would help elucidate the mechanism of antivisceral nociception by general anesthetics at the cellular and molecular levels and aid in development of novel therapeutic strategies to improve clinical management of visceral pain.