Induction of c-fos-like protein within the lumbar spinal cord and thalamus of the rat following peripheral stimulation
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Intermittent noxious stimulation following spinal cord contusion injury impairs locomotor recovery and reduces spinal brain-derived neurotrophic factor-tropomyosin-receptor kinase signaling in adult rats
2011, NeuroscienceCitation Excerpt :The first observation in support of this is the fact that c fos labeling was observed only in neurons. In addition to being an immediate early gene, c fos has been linked to nociceptive activity and the expression of pain for over two decades (e.g. Bullitt, 1989). Similarly, TrkB labeling was observed primarily in neurons, with no evidence of glial expression.
Transdural motor cortex stimulation reverses neuropathic pain in rats: A profile of neuronal activation
2011, European Journal of PainFormalin-induced c-fos expression in the brain of infant rats
2011, Journal of PainNociceptors, Pain, and Spinal Manipulation
2011, Pain Management, Second EditionDifferential microglial activation between acute stress and lipopolysaccharide treatment
2009, Journal of NeuroimmunologySeparation of A- versus C-nociceptive inputs into spinal-brainstem circuits
2008, NeuroscienceCitation Excerpt :In the present study, FLI induced prior to anesthesia was minimized by allowing a delay of 4 h between anesthetic induction and perfusion, as it has been reported that FLI in diencephalic neurons returns to near basal levels 3 h post stimulus (Bon et al., 1997). Our observation that the majority of neurons activated by a noxious heat stimulus are located in the superficial, compared with the deep, dorsal horn is consistent with previous reports from this (Koutsikou et al., 2007) and other laboratories that have used the expression of Fos protein as a marker of neuronal activity (Bullitt, 1989; Williams et al., 1990; Coggeshall, 2005). As reported previously (Koutsikou et al., 2007), there is a tendency for more neurons to be activated by slow compared with fast rates of skin heating and for there to be more Fos-positive neurons in lamina I compared with lamina II.
This work was supported by Research Grants 5K08NS01006 and 5P0INS14899 from the National Institutes of Neurologic and Communicative Disorders and Stroke of the United States Public Health Service.
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I am grateful to Dr. Alan Light, who first alerted me to the possibilities of c-