Expression of Fos protein in the rat central nervous system in response to noxious stimulation: effects of chronic inflammation of the superior cervical ganglion

Abstract

The aim of this study was to investigate the possible interactions between the nociceptive system, the sympathetic system and the inflammatory process. Thus, the superior cervical ganglion of rats was submitted to chronic inflammation and Fos expression was used as a marker for neuronal activity throughout central neurons following painful peripheral stimulation. The painful stimulus consisted of subcutaneously injected formalin applied to the supra-ocular region. Fos-positive neurons were identified by conventional immunohistochemical techniques, and analyzed from the obex through the cervical levels of the spinal cord. In the caudal sub-nucleus of the spinal trigeminal nuclear complex, the number of Fos-positive neurons was much higher in rats with inflammation of the superior cervical ganglion than in control rats, either sham-operated or with saline applied to the ganglion. There was a highly significant difference in the density of Fos-positive neurons between the inflamed and control groups. No significant difference was found between control groups. These results suggest that the inflammation of the superior cervical ganglion generated an increased responsiveness to painful stimuli, which may have been due to a diminished sympathetic influence upon the sensory peripheral innervation.

Loss of ganglioglomerular nerve input to the carotid body impacts the hypoxic ventilatory response in freely-moving rats

“…On the basis of the substantial evidence that GGNs innervate their ipsilateral carotid bodies ( Biscoe and Purves, 1967 ; Zapata et al, 1969 ; Bowers and Zigmond, 1979 ; Brattström, 1981a ; McDonald and Mitchell, 1981 ; McDonald, 1983a ; McDonald, 1983b ; Verna et al, 1984 ; Torrealba and Claps, 1988 ; Ichikawa, 2002 ; Asamoto, 2004 ; Savastano et al, 2010 ), we are working on the key assumption that bilateral transection of the GGN (GGNX) leads to alterations in the functions of primary (type 1) glomus cells and vasculature, and perhaps sustenacular (type 2) glomus cells and/or chemoafferent nerve terminals. A decrease in GGN input to the carotid bodies may result from a loss of function of pre-ganglion neurons and/or post-ganglionic cell bodies in the SCG as a result of physical insults and/or disease processes including inflammatory diseases ( Rudik, 1969 ; Camargos and Machado, 1988 ; Laudanna et al, 1998 ; Hanani et al, 2010 ), prion diseases ( Liberski, 2019 ), herpes simplex virus infection ( Price and Schmitz, 1979 ), acquired immunodeficiency syndrome ( Chimelli et al, 2002 ), metastatic states ( Moubayed et al, 2017 ), hyperthyroidism ( Matano et al, 2014 ); amyotrophic lateral sclerosis ( Kandinov et al, 2013 ), neuro-endocrine disorders in females ( Pirard, 1954 ); myocardial ischemia ( Liu et al, 2013 ; Cheng et al, 2018 ), obstructive jaundice ( Chen et al, 2021 ); Duchenne muscular dystrophy ( De Stefano et al, 2005 ), Alzheimer’s disease ( Jengeleski et al, 1989 ; Alzoubi et al, 2011 ), amyloid precursor protein deficiency ( Cai et al, 2016 ), Lewy body disease and Parkinson’s disease ( Del Tredici et al, 2010 ), Mecp2 deficiency ( Roux et al, 2008 ), lead exposure ( Zhu et al, 2019 ), hypercholesterolemia Chumasov et al, 1994 ), hypertension ( Tang et al, 1995a ; Tang et al, 1995b ; Tang et al, 1995c ), direct ischemic challenge ( Kilic et al, 2019 ), multiple systems neuropathy ( McGorum et al, 2015 ), diabetic neuropathy ( Minker et al, 1978 ; Bitar et al, 1997 ; Cameron and Cotter, 2001 ;…”