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Our experience of reinnervation of sole in diabetic sensorimotor polyneuropathy: A chance to change the natural history of disease
2021, Journal of Clinical Orthopaedics and TraumaInvestigating resting-state functional connectivity in the cervical spinal cord at 3 T
2017, NeuroImageCitation Excerpt :This has been discussed in detail previously (e.g. with regard to possible influences of central pattern generators on ventral correlations, input from the peripheral nervous system on dorsal correlations, and supra-spinal influences on both of these; see Barry et al. (2014), Eippert and Tracey (2014), and Kong et al., 2014) and we will only briefly discuss possible underlying factors not mentioned previously. With regard to the dorsal horn connectivity, there is some anatomical evidence for primary afferents that also cross to the contralateral side (Culberson et al., 1979; Light and Perl, 1979) and electrophysiological evidence for an interneuronal network that connects the two dorsal horns (Fitzgerald, 1982, 1983). This has been corroborated more recently with a number of studies identifying populations of dorsal commissural interneurons (Petkó and Antal, 2000; Bannatyne et al., 2006), though these mostly focussed on the lumbar spinal cord.
Spinal and Supraspinal Mechanisms of Placebo Analgesia
2013, Placebo and Pain: From Bench to BedsidePropriospinal pathways in the dorsal horn (laminae I-IV) of the rat lumbar spinal cord
2012, Brain Research BulletinSpinal glycinergic and GABAergic neurons expressing C-FOS after capsaicin stimulation are increased in rats with contralateral neuropathic pain
2011, NeuroscienceCitation Excerpt :Since glycinergic neurons are scarce in the superficial laminae (Hossaini et al., 2007; Todd and Sullivan, 1990; Zeilhofer et al., 2005), it seems likely that these activated neurons are GABAergic rather than glycinergic. Using electrophysiology it has been shown (Fitzgerald, 1983) that nociceptive stimulation activates neurons in lamina II on the contralateral side of the spinal cord, while neurons in the deep dorsal horn were inhibited (Fitzgerald, 1982), suggesting that the activated neurons in laminae I and II are responsible for the inhibition of neurons in the deep dorsal horn on that side. Our results are in line with this idea by showing not only that the activated neurons in lamina II are indeed GABAergic but also that an increase of activated (Gly/GABA) neurons in the deep dorsal horn is lacking.