Figure 3.

Second-hand tobacco smoke (SHS) exposure effects on endogenous substance P contribution to spiking response in delayed-onset spiking (DS) neurons. A. Example spiking traces of DS neurons in the absence and presence of NK₁ receptor antagonist from both filtered air (FA)- and SHS-exposed animals. In FA-exposed animals, the NK₁ receptor antagonist left only one action potential in response to 100 pA depolarizing current injection which could evoke 65 action potentials per 2 s in the absence of antagonist. However, the antagonist hardly changed spiking response in SHS-exposed animal. B. The antagonism did not change the input resistance in FA-exposed animals (P = 0.425) but did increase that in SHS-exposed animals (*P = 0.034). C. Group data confirmed that spiking response was markedly reduced by NK₁ receptor antagonist in FA-exposed animals (*P < 0.001), but the antagonism did not change spiking response in SHS exposure group (P = 0.837). Note that spiking responses in the absence or presence of NK₁ receptor antagonist in SHS exposure group were closely overlapped each other. D. NK₁ receptor sensitive spiking response to depolarizing current injection. The antagonist effects on spiking responses were significantly different between FA and SHS exposure groups (anova interaction, *P < 0.001). aCSF, artificial cerebrospinal fluid.