Cholinergic EPSCs and their potentiation by bradykinin in single paratracheal ganglion neurons attached with presynaptic boutons

Abstract

We have found that bradykinin (BK) potentiates the nicotine-induced currents in airway paratracheal/parabronchial ganglia (PTG) neurons. In this study, we investigated if BK affects the cholinergic synaptic transmission in rat PTG neurons attached with synaptic buttons. Excitatory postsynaptic currents (EPSCs) were recorded in acutely dissociated PTG neurons attached with presynaptic boutons. EPSC frequency was increased in the high-K(+) external solution without affecting their amplitude. Activation and deactivation kinetics also did not change in the high-K(+) solution. Cd(2+) inhibited the EPSC frequency at 10(-7) M and also amplitude at higher concentrations without changing the kinetics. Mecamylamine inhibited both the amplitude and frequency of EPSCs and reduced the activation and deactivation kinetics. 10(-8) M BK potentiated the EPSC amplitude to 1.37 ± 0.19 times of preapplication control. In addition, its frequency was increased to 2.04 ± 0.41 times. BK did not affect the activation and deactivation kinetics. The effects of BK were mimicked by [Hyp(3)]-BK, a B2 kinin receptor agonist, whereas HOE 140, a B2 kinin receptor antagonist, abolished the effects of BK. In conclusion, BK potentiates the cholinergic synaptic transmission via B2 kinin receptors in the PTG. Since predominant control of airway function is thought to be exerted by cholinergic nerves arising from the PTG, the present findings might underlie at least partly the inflammatory pathological conditions of the lower airway.