Deletion of tachykinin NK1 receptor gene in mice does not alter respiratory network maturation but alters respiratory responses to hypoxia.

摘要: The aim of this study was to shed some light on the role Substance Ρ (SP) and its neurokinin NK1 receptors (NK1R) in respiratory network maturation function. On one hand, as SP is detected early during development (Tsuchida et al., 1990; Beresford 1992; Taoka 1996; St John al, 1997), assumed play a organization CNS (Quirion Dam, 1986) therefore that network. other compelling evidence exists activation NK1R affects ventilation. First, are expressed within pre-Botzinger complex, region containing putative rhythm generating neurons (Gray 1999; Wang 2001) increases activity (Hedner 1984; Chen Yamamoto Monteau Ptak 1999, 2000a, b) whereas destruction NK1R-positive cells alters breathing 2001). Second, may be implicated central transmission inputs from carotid bodies (CB) which detect peripheral hypoxia since contained CB afferent nerves (Liebstein 1985; Lindefors fiber terminals nucleus tractus solitarius (Lipski 1977; Mantyh 1989). concentration hypoxia, but not after denervation (Srinivasan 1991). Furthermore, lack degradation enzyme enhances response (Grasemann 1999).