Pacemaker Neurons and the Development of Nociception

Abstract

Spontaneous activity is known to be essential for the proper formation of sensory networks in the developing CNS. This activity can be produced by a variety of mechanisms including the presence of “pacemaker” neurons, which can be defined by their intrinsic ability to generate rhythmic bursts of action potential discharge. Recent work has identified pacemaker activity within lamina I of the neonatal rodent spinal cord that emerges from a complex interaction between voltage-dependent and voltage-independent (“leak”) ionic conductances, including an important modulatory role for the inward-rectifying K+ (Kir) channels. The available evidence suggests that lamina I pacemakers are glutamatergic and project extensively throughout the dorsal-ventral axis of the spinal cord, although the identity of their postsynaptic targets has yet to be elucidated. A better understanding of this connectivity could yield valuable insight into the role of the lamina I pacemaker population in the maturation of spinal circuitry underlying nociceptive processing and/or sensorimotor integration.