Robert W Boal1, Richard G Gillette. 1. Basic Science Department, Western States Chiropractic College, Portland, Ore 97230, USA. bboal@wschiro.edu
Abstract
OBJECTIVE: Recent experimental evidence demonstrating neuronal/synaptic plasticity and, in particular, long-term potentiation (LTP) and long-term depression (LTD) in spinal neurons is reviewed. The implications of these studies for possible mechanistic explanations of low back pain and its remediation by spinal manipulative therapy (SMT) are explored. Brief descriptions of LTP and LTD and elaboration of the key roles of calcium, glutamate, and glutamate receptors in LTP/LTD are provided as separate appendices. DATA SOURCES: The referenced articles regarding LTP/LTD in spinal cord neurons and neuronal plasticity, in general, were identified from accumulated review of the neuroscience literature. Publications cited from chiropractic sources relevant to central neuronal plasticity and LTP/LTD were identified using the Index to Chiropractic Literature and informal review. STUDY SELECTION: Experimental studies examining LTP/LTD mechanisms in spinal neurons and more general references useful as an introduction to central neuronal plasticity and LTP/LTD are included.Data Extraction Experimental evidence presented in this review has been previously published and illustrates neuronal plasticity from an animal model for low back pain. DATA SYNTHESIS: Both in vitro and in vivo evidence identifying LTP and LTD in dorsal horn nociceptive neurons is reviewed. Of special interest are studies showing LTP in response to intense noxious stimulation and reports that Adelta-mechanosensitive afferent activation can reverse an existing LTP condition in dorsal horn neurons. CONCLUSIONS: The potential involvement of LTP in low back pain is discussed and a role for LTD in spinal manipulative therapy is proposed. The need for future studies is identified in the areas of spatial and temporal changes in symptomatology post-SMT of the low back; combining, sequencing, and comparing several therapeutic approaches; and demonstrating LTD in spinal cord neurons post-SMT-like stimulation.
OBJECTIVE: Recent experimental evidence demonstrating neuronal/synaptic plasticity and, in particular, long-term potentiation (LTP) and long-term depression (LTD) in spinal neurons is reviewed. The implications of these studies for possible mechanistic explanations of low back pain and its remediation by spinal manipulative therapy (SMT) are explored. Brief descriptions of LTP and LTD and elaboration of the key roles of calcium, glutamate, and glutamate receptors in LTP/LTD are provided as separate appendices. DATA SOURCES: The referenced articles regarding LTP/LTD in spinal cord neurons and neuronal plasticity, in general, were identified from accumulated review of the neuroscience literature. Publications cited from chiropractic sources relevant to central neuronal plasticity and LTP/LTD were identified using the Index to Chiropractic Literature and informal review. STUDY SELECTION: Experimental studies examining LTP/LTD mechanisms in spinal neurons and more general references useful as an introduction to central neuronal plasticity and LTP/LTD are included.Data Extraction Experimental evidence presented in this review has been previously published and illustrates neuronal plasticity from an animal model for low back pain. DATA SYNTHESIS: Both in vitro and in vivo evidence identifying LTP and LTD in dorsal horn nociceptive neurons is reviewed. Of special interest are studies showing LTP in response to intense noxious stimulation and reports that Adelta-mechanosensitive afferent activation can reverse an existing LTP condition in dorsal horn neurons. CONCLUSIONS: The potential involvement of LTP in low back pain is discussed and a role for LTD in spinal manipulative therapy is proposed. The need for future studies is identified in the areas of spatial and temporal changes in symptomatology post-SMT of the low back; combining, sequencing, and comparing several therapeutic approaches; and demonstrating LTD in spinal cord neurons post-SMT-like stimulation.
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