Neonatal Environment and Neuroendocrine Programming of the Peripheral Respiratory Control System

Abstract

The carotid bodies are the main peripheral oxygen sensors involved in cardio-respiratory control under normoxic and hypoxic conditions. The present review briefly describes carotid body function during "normal" development and then presents recent results showing how environmental factors affect the trajectory of these developmental processes. This review then focuses on data obtained from our laboratories, which emphasise the shortterm modulation and long-term consequences of perinatal stress such as premature deprivation of placental steroids and neonatal disruption of mother-infant interactions on carotid body development and function. Our current data suggest that disturbances related to early deprivation of placental steroids, as it occurs with premature delivery, disrupt respiratory chemoreflexes attributed mainly to chemoreceptor cells' ability to respond to changes in oxygen levels during early life. Conversely, stress related to interference with normal mother-pup interactions during the neonatal period induces changes in carotid body function that persist well into adulthood. In both cases, changes in carotid body function are related (at least in part) to significant modification of dopaminergic neurotransmission within the carotid body as suggested by treatment-related changes in dopamine D 2 receptor gene expression level. Together, these data suggest that these environmental factors predispose to the occurrence of respiratory disease associated with respiratory control dysfunction such as sleep-disordered breathing during infancy.

Neonatal caffeine induces sex-specific developmental plasticity of the hypoxic respiratory chemoreflex in adult rats

“…The fact that systemic injection of adenosine accentuates the hypoxic ventilatory response in humans supports this interpretation (43,66). Adenosine A 2A receptors have been identified in the rat carotid body using either immunohistochemistry (13,25), Northern blot (2,5,35), or RT-PCR analysis (5,36). Since adenosine A 1 receptors were only detected using RT-PCR (2,5), this indicates that its expression level is very low in this structure.…”

“…Adenosine A 2A receptors have been identified in the rat carotid body using either immunohistochemistry (13,25), Northern blot (2,5,35), or RT-PCR analysis (5,36). Since adenosine A 1 receptors were only detected using RT-PCR (2,5), this indicates that its expression level is very low in this structure. However, given that NCT had no effect on A 1 receptor mRNA expression level, its potential involvement at the peripheral level will not be addressed in the following discussion.…”