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.

Chemosensitivity of Phox2b‐expressing retrotrapezoid neurons is mediated in part by input from 5‐HT neurons

“…; Zhou et al . ). These boutons could possibly still respond to acidosis by releasing neurotransmitters, so that even some of the residual pH response seen in dissociated RTN neurons (Wang et al .…”

Effects of suplatast tosilate on acutely dissociated sensory and paratracheal ganglia neurons

“…We also found that bradykinin, a potent inflammatory peptide, depolarized the membrane potential via inhibition of M-type K ϩ channels and induced action-potential generation in acutely dissociated paratracheal ganglia neurons (27). Furthermore, bradykinin potentiated the nicotinic current and cholinergic excitatory postsynaptic currents (EPSCs) in the neurons (47,48). Thus the paratracheal ganglia may serve as critical sites for the pathogenesis of airway inflammation associated with cough.…”

Acute Cocaine Reduces Excitatory Synaptic Transmission in Pyramidal Neurons of the Mouse Medial Prefrontal Cortex

“…The cocaine-induced reduction of sEPSCs observed in this study may be at least partly account for the reduced activity of mPFC neurons recorded after cocaine administration in rats in vivo. 12) The reduction of mPFC neuronal activity may be related to cocaine-induced hypofrontality, in which mPFC neuronal responses to cocaine and cocaine-associated cues are amplified. 12) Thus, our finding might be one of the mechanisms for generating hypofrontality, which is critically involved in the development of cocaine addiction.…”

“…11) In support of this finding, acute cocaine administration decreases neuronal activity in the rat mPFC. 12) These cocaine-induced changes, so-called hypofrontality, may contribute to the development of cocaine addiction. However, the mechanism(s) underlying these inhibitory effects of cocaine remains unclear.…”