Effects of urinary bladder distension on activity of T 3–T 4 spinal neurons receiving cardiac and somatic noxious inputs in rats

Abstract

The aims of this study were to examine effects of urinary bladder distension (UBD) on T 3–T 4 spinal neurons receiving cardiac and somatic noxious inputs and to determine the pathway involved in transmitting urinary bladder inputs to thoracic spinal segments. Extracellular potentials of single T 3–T 4 neurons were recorded in pentobarbital anesthetized male rats. Either bradykinin solution (10 −5 M) or an algogenic mixture (adenosine 10 −3 M, bradykinin, histamine, serotonin, prostaglandin E2 10 −5 M each) was administered intrapericardially. UBD was produced by saline inflation (0.5–2.0 ml, 20 s). Of 487 neurons tested for responses to UBD, 70 were inhibited and 37 were excited. Seventy-six out of 336 neurons received convergent input from UBD and heart; 69/76 viscerovisceral convergent neurons had somatic fields. Spinal transection at rostral C 1 abolished UBD inhibition in 5/9 neurons; whereas transections at L 1–L 2 abolished UBD inhibition in 3/3 cells tested. Results showed that T 3–T 4 spinal neurons processing cardiac and somatic nociceptive information were primarily inhibited by input from the urinary bladder through either supraspinal structures or direct intraspinal pathways.