Peripheral inflammation alters desensitization of substance P-evoked current in rat dorsal root ganglion neurons

2011 ◽  
Vol 670 (2-3) ◽  
pp. 495-499 ◽  
Author(s):  
Bihua Bie ◽  
Zhi-Qi Zhao
Keyword(s):  
Substance P ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Peripheral Inflammation ◽  
Ganglion Neurons

scholarly journals Noradrenaline regulates substance P release from rat dorsal root ganglion neurons in vitro

2011 ◽  
Vol 27 (5) ◽  
pp. 300-306 ◽  
Author(s):  
Yan-Jie Wang ◽  
Xing-Fu Li ◽  
Feng Ding ◽  
Qiang Shu ◽  
Li-Jun Song ◽  
...  
Keyword(s):  
Substance P ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
P Release ◽  
Ganglion Neurons ◽  
Substance P Release

Ventricular sensory neurons in canine dorsal root ganglia: effects of adenosine and substance P

1995 ◽  
Vol 269 (2) ◽  
pp. R318-R324 ◽  
Author(s):  
M. H. Huang ◽  
C. Sylven ◽  
M. Horackova ◽  
J. A. Armour
Keyword(s):  
Substance P ◽  
Dorsal Root Ganglion ◽  
Receptor Antagonist ◽  
Adenosine Receptor ◽  
Dorsal Root ◽  
Left Ventricular ◽  
Dorsal Root Ganglion Neurons ◽  
Adenosine Receptor Antagonist ◽  
Ganglion Neurons ◽  
Increased Activity

Effects elicited by adenosine and substance P on ventricular sensory endings of 14 dorsal root ganglion afferent neurons were studied in situ in anesthetized dogs. Sensory-field application of adenosine (1 microM) increased the activity of these neurons by 179%. Application of a nonspecific adenosine antagonist to epicardial sensory fields suppressed ongoing activity in all 14 neurons by 39%. Application of an A1- or A2-adenosine-receptor antagonist suppressed activity generated by 10 of these neurons by 44 and 59%, respectively. Adenosine applied after A1- or A2-receptor blockade increased activity in 10 neurons by 131 and 145%, respectively, indicating that A1- and A2-receptor effects were not additive. Application of substance P (1 microM) to identified sensory fields increased activity in 12 of these neurons by 169%, whereas application of a substance P-receptor antagonist reduced activity generated by these neurons by 75%. Myocardial ischemia increased activity of nine neurons associated with left ventricular sensory fields by 320%, an effect that was counteracted by the nonspecific adenosine-receptor antagonist. It is concluded that A1- and A2-adenosine receptors, as well as substance P receptors, are present on ventricular epicardial sensory nerve endings of dorsal root ganglion neurons that are tonically active during normal states, becoming further activated during ischemia.

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