Effect of selective phosphodiesterase inhibitors on synaptic transmission in the guinea-pig ileum

1998 ◽  
Vol 357 (6) ◽  
pp. 677-681 ◽  
Author(s):  
A. A. Izzo ◽  
Nicola Mascolo ◽  
Francesco Capasso
Keyword(s):  
Guinea Pig ◽  
Synaptic Transmission ◽  
Phosphodiesterase Inhibitors ◽  
Guinea Pig Ileum

scholarly journals Effect of papaverine on synaptic transmission in the guinea-pig ileum

1997 ◽  
Vol 121 (4) ◽  
pp. 768-772 ◽  
Author(s):  
Angelo A. Izzo ◽  
Nicola Mascolo ◽  
Marcello Costa ◽  
Francesco Capasso
Keyword(s):  
Guinea Pig ◽  
Synaptic Transmission ◽  
Guinea Pig Ileum

Slow synaptic transmission in myenteric AH neurons from the inflamed guinea pig ileum

2009 ◽  
Vol 297 (3) ◽  
pp. G582-G593 ◽  
Author(s):  
Kulmira Nurgali ◽  
Trung V. Nguyen ◽  
Michelle Thacker ◽  
Louise Pontell ◽  
John B. Furness
Keyword(s):  
Guinea Pig ◽  
Synaptic Transmission ◽  
Intestinal Inflammation ◽  
Enteric Neurons ◽  
Type I ◽  
Type Ii ◽  
Guinea Pig Ileum ◽  
In Vitro Investigation ◽  
Lower Amplitude

We investigated the effect of inflammation on slow synaptic transmission in myenteric neurons in the guinea pig ileum. Inflammation was induced by the intraluminal injection of trinitrobenzene sulfonate, and tissues were taken for in vitro investigation 6–7 days later. Brief tetanic stimulation of synaptic inputs (20 Hz, 1 s) induced slow excitatory postsynaptic potentials (EPSPs) in 49% and maintained postsynaptic excitation that lasted from 27 min to 3 h in 13% of neurons from the inflamed ileum. These neurons were classified electrophysiologically as AH neurons; 10 were morphological type II neurons, and one was type I. Such long-term hyperexcitability after a brief stimulus is not encountered in enteric neurons of normal intestine. Electrophysiological properties of neurons with maintained postsynaptic excitation were similar to those of neurons with slow EPSPs. Another form of prolonged excitation, sustained slow postsynaptic excitation (SSPE), induced by 1-Hz, 4-min stimulation, in type II neurons from the inflamed ileum reached its peak earlier but had lower amplitude than that in control. Unlike slow EPSPs and similar to SSPEs, maintained excitation was not inhibited by neurokinin-1 or neurokinin-3 receptor antagonists. Maintained postsynaptic excitation was not influenced by PKC inhibitors, but the PKA inhibitor, H-89, caused further increase in neuronal excitability. In conclusion, maintained excitation, observed only in neurons from the inflamed ileum, may contribute to the dysmotility, pain, and discomfort associated with intestinal inflammation.

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