William C. de Groat

Localization of P2X and P2Y Receptors in Dorsal Root Ganglia of the Cat

The distribution of P2X and P2Y receptor subtypes in upper lumbosacral cat dorsal root ganglia (DRG) has been investigated using immunohistochemistry. Intensity of immunoreactivity for six P2X receptors (P2X5 receptors were immuno-negative) and the three P2Y receptors examined in cat DRG was in the order of P2Y2 = P2Y4>P2X3>P2X2 = P2X7>P2X6>P2X1 = P2X4>P2Y1. P2X3, P2Y2, and P2Y4 receptor polyclonal antibodies stained 33.8%, 35.3%, and 47.6% of DRG neurons, respectively. Most P2Y2, P2X1, P2X3, P2X4, and P2X6 receptor staining was detected in small- and medium-diameter neurons. However, P2Y4, P2X2, and P2X7 staining was present in large- and small-diameter neurons. Double-labeling immunohistochemistry showed that 90.8%, 32.1%, and 2.4% of P2X3 receptor-positive neurons coexpressed IB4, CGRP, and NF200, respectively; whereas 67.4%, 41.3%, and 39.1% of P2Y4 receptor-positive neurons coexpressed IB4, CGRP, and NF200, respectively. A total of 18.8%, 16.6%, and 63.5% of P2Y2 receptor-positive neurons also stained for IB4, CGRP, and NF200, respectively. Only 30% of DRG neurons in cat were P2X3-immunoreactive compared with 90% in rat and in mouse. A further difference was the low expression of P2Y1 receptors in cat DRG neurons compared with more than 80% of the neurons in rat. Many small-diameter neurons were NF200-positive in cat, again differing from rat and mouse.

Autonomic Control of the Lower Urinary Tract

Publisher Summary This chapter focuses on the autonomic control of the lower urinary tract. Parasympathetic neuroeffector transmission in the bladder is mediated by ACh acting on postjunctional muscarinic (M) receptors. The sacral parasympathetic outflow, which in humans originates from S2 to S4 segments of the spinal cord, provides the major excitatory input the bladder. Histofluorescence microscopy in animals and humans has shown that adrenergic terminals richly innervate the smooth muscle of the bladder base, but the bladder body has a considerably weaker adrenergic innervation. Injuries to the neuraxis that interrupt connections between pontine micturition center and the lumbosacral spinal cord lead to complete loss of bladder function and in turn urinary retention. In most spinal cord injured patients, bladder reflexes slowly recover as a result of a reorganization of synaptic connections in the spinal cord and the emergence of sacral reflex mechanisms that initiate involuntary bladder contractions. Damage to peripheral neural pathways to the lower urinary tract or to the lumbosacral spinal causes a loss of bladder sensations as well as loss of voluntary and reflex voiding.