Developmental Changes in [3H]Lysergic Acid Diethylamide ([3H]LSD) Binding to Serotonin Receptors in the Human Brainstem
Journal of Neuropathology & Experimental Neurology – January 01, 1996
Source: OpenAlex
Summary
The highest levels of serotonin receptor binding in the human brainstem occur prenatally, highlighting serotonin's crucial role in neural development. Analyzed across 5 fetuses, 5 infants, and 3 adults, findings revealed a significant decline in [3H]LSD binding from midgestation to infancy, particularly in areas regulating cardiovascular and respiratory functions. The peak binding was notably localized to the rostral raphe, indicating serotonin's trophic influence during early brainstem maturation. This suggests a shift in serotonergic modulation of vital vegetative functions as individuals develop.
Abstract
The ontogeny of serotonin receptors in the human brainstem is largely unknown, despite the putative roles of serotonin in neural development, synaptic transmission, brainstem modulation of vegetative functions, and clinical disorders of serotonergic function. This study provides baseline information about the quantitative distribution of [3H]LSD binding to serotonergic receptors (5-HT1A-1D, 5-HT2) in the human brainstem, from midgestation through maturity, with a focus upon early infancy. Brainstems were analyzed from 5 fetuses (19-25.5 weeks postconception), 5 infants (42-55.5 weeks postconception), and 3 mature individuals (4, 20, and 52 years). Tissue autoradiography was used with [3H]LSD for total serotonergic receptor binding and [3H]LSD and serotonin for nonspecific binding; computer-based quantitation was applied. The highest levels of [3H]LSD binding occurred prenatally throughout the brainstem. At all ages, the highest relative binding localized to the rostral raphe. A marked decline in [3H]LSD binding occurred between the midgestation and infancy in brainstem regions involved in control of cardiovascular function, respiration, and pain. The fetal peak in [3H]LSD binding to 5-HT receptors is consistent with a trophic role of serotonin in immature human brainstem, and a decrease, between midgestation and infancy, in serotonergic modulation of vegetative functions controlled by the brainstem.