Association of spinal lamina I projections with brainstem catecholamine neurons in the monkey.

Abstract

In addition to giving primary projections to the parabrachial and periaqueductal gray regions, ascending lamina I projections course through and terminate in brainstem regions known to contain catecholaminergic cells. For this reason, double-labeling experiments were designed for analysis with light and electron microscopy. The lamina I projections in the Cynomolgus monkey were anterogradely labeled with Phaseolus vulgaris leucoagglutinin (PHA-L) and catecholamine-containing neurons were labeled immunocytochemically for tyrosine hydroxylase (TH). Light level double-labeling experiments revealed that the terminations of the lamina I ascending projections through the medulla and pons strongly overlap with the localization of catecholamine cells in: the entire rostrocaudal extent of the ventrolateral medulla (A1 caudally, C1 rostrally); the solitary nucleus and the dorsomedial medullary reticular formation (A2 caudally, C2 rostrally); the ventrolateral pons (A5); the locus coeruleus (A6); and the subcoerulear region, the Kölliker-Fuse nucleus, and the medial and lateral parabrachial nuclei (A7). At the light microscopic level, close appositions between PHA-L-labeled lamina I terminal varicosities and TH-positive dendrites and somata were observed, particularly in the A1, A5 and the A7 cell groups on the contralateral side. At the electron microscopic level, examples of lamina I terminals were found synapsing on cells of the ventrolateral catecholamine cell groups in preliminary studies. The afferent input relayed by these lamina I projections could provide information about pain, temperature, and metabolic state as described previously. Lamina I input could impact interactions of the catecholamine system with higher brain centers modulating complex autonomic, endocrine, sensory, motor, limbic and cortical functions such as memory and learning. Nociceptive lamina I input to catecholamine cell regions with projections back to the spinal cord could form a feedback loop for control of spinal sensory, autonomic and motor activity.