The Effect of Development on the Pattern of A1 and A2a-Adenosine Receptor Gene and Protein Expression in Rat Peripheral Arterial Chemoreceptors

Abstract

The peripheral arterial chemoreceptors in the carotid body (CB) are the first step in a closed–loop feedback control system that acts to normalize arterial oxygen and carbon dioxide levels by rapidly modulating ventilation. Type I cells in the CB are excitable and contain O₂ - sensitive K⁺ channels (Gonzalez et al., 1995; Montoro et al., 1996; Wyatt et al., 1995). Reduction of K⁺ conductance in response to hypoxia is the signal that triggers Type I cell depolarization, Ca²⁺ entry, and secretion of neurotransmitters that bind to receptors on the first order sensory nerve endings of the carotid sinus nerve with cell bodies in the petrosal ganglion {(Gonzalez et al., 1994;Gonzalez et al., 1992). These first order sensory neurons (chemoafferents) project to second order neurons within the nucleus tractus solitarii (nTS), which send projections to the muscles of respiration. While the cascade of molecular and cellular events occurs in multiple CB preparations from multiple mammalian species, key aspects of the cascade are still unknown, particularly identification of the specific oxygen sensor within the Type I cell that initiates the cascade and the specific excitatory neurotransmitter systems that are involved in chemoexcitation. Furthermore, in multiple immature mammalian species, including human infants, hypoxic chemosensitivity matures during the first several weeks of postnatal life. Specific mechanisms mediating that maturation are unknown.