“…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 ;…”