Neurturin signalling via GFRα2 is essential for innervation of glandular but not muscle targets of sacral parasympathetic ganglion neurons

2004 ◽  
Vol 25 (2) ◽  
pp. 288-300 ◽  
Author(s):  
Y Wanigasekara ◽  
M.S Airaksinen ◽  
R.O Heuckeroth ◽  
J Milbrandt ◽  
J.R Keast
Keyword(s):  
Parasympathetic Ganglion ◽  
Ganglion Neurons

Effect of bradykinin on membrane properties of guinea pig bronchial parasympathetic ganglion neurons

2000 ◽  
Vol 278 (3) ◽  
pp. L485-L491 ◽  
Author(s):  
Radhika Kajekar ◽  
Allen C. Myers
Keyword(s):  
Guinea Pig ◽  
Sensory Nerve ◽  
Input Resistance ◽  
Inhibitory Effect ◽  
Membrane Properties ◽  
Alternative Mechanism ◽  
Induced Membrane ◽  
Parasympathetic Ganglion ◽  
Hoe 140 ◽  
Ganglion Neurons

The effect of bradykinin on membrane properties of parasympathetic ganglion neurons in isolated guinea pig bronchial tissue was studied using intracellular recording techniques. Bradykinin (1–100 nM) caused a reversible membrane potential depolarization of ganglion neurons that was not associated with a change in input resistance. The selective bradykinin B2 receptor antagonist HOE-140 inhibited bradykinin-induced membrane depolarizations. Furthermore, the cyclooxygenase inhibitor indomethacin attenuated bradykinin-induced membrane depolarizations to a similar magnitude (∼70%) as HOE-140. However, neurokinin-1 and -3 receptor antagonists did not have similar inhibitory effects. The ability of bradykinin to directly alter active properties of parasympathetic ganglion neurons was also examined. Bradykinin (100 nM) significantly reduced the duration of the afterhyperpolarization (AHP) that followed four consecutive action potentials. The inhibitory effect of bradykinin on the AHP response was reversed by HOE-140 but not by indomethacin. These results indicate that bradykinin can stimulate airway parasympathetic ganglion neurons independent of sensory nerve activation and provide an alternative mechanism for regulating airway parasympathetic tone.

Pharmacological properties of P2 receptors on rat otic parasympathetic ganglion neurons

Life Sciences ◽  
2008 ◽  
Vol 83 (5-6) ◽  
pp. 185-191 ◽  
Author(s):  
Bei Ma ◽  
Li-hua Yu ◽  
Juan Fan ◽  
Xin Ni ◽  
Geoffrey Burnstock
Keyword(s):  
P2 Receptors ◽  
Pharmacological Properties ◽  
Parasympathetic Ganglion ◽  
Ganglion Neurons

Antigen depolarizes guinea pig bronchial parasympathetic ganglion neurons by activation of histamine H1 receptors

1995 ◽  
Vol 268 (6) ◽  
pp. L879-L884 ◽  
Author(s):  
A. C. Myers ◽  
B. J. Undem
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
High Titer ◽  
Membrane Resistance ◽  
Dependent Manner ◽  
Immediate Hypersensitivity ◽  
Concentration Dependent Manner ◽  
Parasympathetic Ganglion ◽  
Histamine H1 Receptors ◽  
Ganglion Neurons

Studies were carried out to evaluate the mechanism by which neurotransmission through airway parasympathetic ganglia may be modulated during immediate hypersensitivity reactions. Guinea pigs were passively sensitized by injection of guinea pig serum containing high-titer anti-ovalbumin antibodies. Intracellular recordings were obtained from intrinsic parasympathetic ganglion neurons from the right mainstem bronchus in vitro. Ovalbumin (10 micrograms/ml) elicited a membrane potential depolarization and changes in membrane resistance in bronchial ganglion neurons from passively sensitized guinea pigs. Histamine mimicked the depolarizing effect of ovalbumin in a concentration-dependent manner (0.1–10 microM) and caused a transient increase and decrease in membrane resistance. Pyrilamine, a histamine H1-receptor antagonist, inhibited the histamine-induced membrane depolarization and decrease in resistance. By contrast, blocking histamine H2 and H3 receptors did not inhibit histamine-induced depolarization. Pyrilamine also reduced the antigen-induced depolarization of ganglion neurons, demonstrating a role for histamine H1 receptors in this response. The data provide evidence that the antigen-induced depolarization of airway ganglion neurons is secondary to an antigen-antibody interaction on intrinsic mast cells and the consequential effect of histamine on H1 receptors. These studies demonstrate that histamine released during an immediate hypersensitivity reaction has direct effects on airway parasympathetic nerves.

Bradykinin activates airway parasympathetic ganglion neurons by inhibiting M-currents

Neuroscience ◽  
2001 ◽  
Vol 105 (3) ◽  
pp. 785-791 ◽  
Author(s):  
T Mochidome ◽  
H Ishibashi ◽  
K Takahama
Keyword(s):  
Parasympathetic Ganglion ◽  
Ganglion Neurons

Role of cyclooxygenase activation and prostaglandins in antigen-induced excitability changes of bronchial parasympathetic ganglia neurons

2003 ◽  
Vol 284 (4) ◽  
pp. L581-L587 ◽  
Author(s):  
Radhika Kajekar ◽  
Bradley J. Undem ◽  
Allen C. Myers
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Synaptic Transmission ◽  
Cyclooxygenase Inhibitors ◽  
Antigen Challenge ◽  
Parasympathetic Nerve ◽  
Parasympathetic Ganglia ◽  
Parasympathetic Ganglion ◽  
Ganglion Neurons

In vitro antigen challenge has multiple effects on the excitability of guinea pig bronchial parasympathetic ganglion neurons, including depolarization, causing phasic neurons to fire with a repetitive action potential pattern and potentiating synaptic transmission. In the present study, guinea pigs were passively sensitized to the antigen ovalbumin. After sensitization, the bronchi were prepared for in vitro electrophysiological intracellular recording of parasympathetic ganglia neurons to investigate the contribution of cyclooxygenase activation and prostanoids on parasympathetic nerve activity. Cyclooxygenase inhibition with either indomethacin or piroxicam before in vitro antigen challenge blocked the change in accommodation. These cyclooxygenase inhibitors also blocked the release of prostaglandin D2 (PGD2) from bronchial tissue during antigen challenge. We also determined that PGE2 and PGD2 decreased the duration of the action potential after hyperpolarization, whereas PGF2α potentiated synaptic transmission. Thus prostaglandins released during antigen challenge have multiple effects on the excitability of guinea pig bronchial parasympathetic ganglia neurons, which may consequently affect the output from these neurons and thereby alter parasympathetic tone in the lower airways.

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