Neuroscience letters
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Neuroscience letters · Oct 2008
Nociceptin/orphanin FQ causes non-quantal slowing of respiratory rhythm in brainstem-spinal cord preparation from newborn rat.
Nociceptin/orphanin FQ (N/OFQ) is the endogenous agonist of the N/OFQ peptide receptor, an inhibitory G protein-coupled receptor. N/OFQ acts as a neuromodulator to depress respiratory rhythm in the brainstem. Although the mechanisms of respiratory rhythm generation remain poorly understood, the pre-inspiratory neuron (Pre-I) and the pre-Bötzinger complex (preBötC) inspiratory neuron (Insp) network in the rostral ventrolateral medulla (RVLM) have been proposed to be essential for respiratory rhythm generation. ⋯ When superfusate K(+) was elevated from 6.2 to 11.2mM, Pre-I activity was increasingly uncoupled from C4 bursts. After the application of N/OFQ in a high [K(+)] superfusate, the 1:1 coupling of Pre-Is to C4 bursts was restored. We conclude that N/OFQ suppresses burst and spike generation of Pre-Is, and that suppression of Pre-Is activity with synchronous coupling to the Insps network contributes to N/OFQ-induced non-quantal slowing.
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Neuroscience letters · Oct 2008
Painful facet joint injury induces neuronal stress activation in the DRG: implications for cellular mechanisms of pain.
The cervical facet joint is implicated as one of the most common sources of chronic neck pain, owing to its rich nociceptive innervation and susceptibility to injurious mechanical loading. Injuries to the facet joint and its ligament can induce inflammation in the joint and spinal cord. Inflammatory molecules which are known to have a role in pain can also stimulate the integrated stress response (ISR). ⋯ BiP was significantly higher (p<0.001) in the DRG after injury than sham and was expressed predominantly in neurons. Similarly, quantification of BiP by immunoblot demonstrated a significant 2.1-fold increase (p=0.03) in injury compared to sham at day 7. Findings suggest neuronal stress activation is associated with painful facet joint injury, and that joint loading may directly mediate the behavior of DRG neurons in this class of injury.
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Neuroscience letters · Oct 2008
Contrasting genetic effects of major histocompatibility complex on ischemic peripheral nerve and spinal cord injury in female rats.
We have recently shown that the major histocompatibility complex (MHC) exerts a regulatory influence on the development of neuropathic pain-like behaviors after partial sciatic nerve injury in male rats. In the present study, we assessed the role of the MHC in peripheral nerve injury-induced pain as well as central pain following spinal cord injury in female rats using the following inbred strains: Dark Agouti (DA; RT1(av1)), Piebald Virol Glaxo (PVG; RT1(c)) and in the MHC-congenic strain PVG-RT1(av1). ⋯ Interestingly, the DA-RT1(av1) strain displayed significantly more severe allodynia than both PVG strains and this difference was not explained by the extent of spinal cord injury. These results suggest that there are differences in the genetic mechanisms for neuropathic pain development following peripheral or central nervous system injury, both in regarding to the role of the MHC complex as well as non-MHC genes.