Ashley Marie Moses

All Publications

• Projectomic Organization of the Serotonin System of the Mouse Brain. bioRxiv : the preprint server for biology Song, J. H., Friedmann, D., Wu, Y., Moses, A., Baruni, J. K., Yuan, Y., Rana, I., Zhao, K., Sten, T. H., Wang, Q., Xiao, S. A., Chen, X., Linderman, S. W., Luo, L. 2026

  Abstract

  The serotonin system innervates nearly the entire brain to support diverse functions, and its dysfunction is implicated in multiple psychiatric disorders. Although recent studies suggested that this anatomically diffuse system supports differentiated rather than uniform modulation, its overall organization is unclear. Here, using systematic whole-brain axon tracing and integrated analyses, we show that the serotonin projectome is organized by functional relatedness rather than physical proximity of its targets. Dorsal and median raphe serotonin neurons partition into five projectomic groups, each preferentially innervating the hippocampus, basal ganglia, cortex, medial interbrain, or brainstem/lateral thalamus, with within-group structure ranging from discrete subgroups to continuous variation. Spatial transcriptomic analyses reveal that each projectomic group corresponds to a distinct combination of transcriptomic clusters, with transcriptome and somatic position jointly predicting projectomic identity. Projection-specific serotonin depletion produces dissociable behavioral phenotypes. Together, projectomic identity emerges as a central axis linking axon collateralization, molecular diversity, and behavioral function.

  View details for DOI 10.64898/2026.07.15.738594

  View details for PubMedID 42523243

  View details for PubMedCentralID PMC13404724

• Teneurin-3 and latrophilin-2 are required for somatotopic map development and somatosensory topognosis. Current biology : CB Sangster, K. T., Zhang, X., Del Toro, D., Sarantopoulos, C., Moses, A. M., Mahasenan, S., Pederick, D. T., Perreault, S., Fallet-Bianco, C., Roome, R. B., Seiradake, E., Luo, L., Kania, A. 2026

  Abstract

  Somatotopy is a recurring organizational feature of the somatosensory system where adjacent neurons and their connections represent adjacent regions of the body. The molecular mechanisms governing the formation of such "body maps" remain largely unknown. Here, we demonstrate that the cell surface proteins teneurin-3 and latrophilin-2 are expressed in opposing gradients aligning with the somatotopic map in the dorsal horn of the mouse spinal cord. Genetic manipulation of these proteins in the spinal dorsal horn or sensory neurons distorts the somatotopy of neuronal connections and impairs the accurate localization of a noxious stimulus on the surface of the body. Our work provides the foundation for a molecular model of somatotopic map formation and insights into the role of somatotopic maps in the ability to accurately locate somatosensory stimuli, also known as topognosis.

  View details for DOI 10.1016/j.cub.2026.04.040

  View details for PubMedID 42105753

• Teneurin-3 and latrophilin-2 are required for somatotopic map formation and somatosensory topognosis. bioRxiv : the preprint server for biology Sangster, K. T., Zhang, X., Del Toro, D., Sarantopoulos, C., Moses, A. M., Mahasenan, S., Pederick, D. T., Perreault, S., Fallet-Bianco, C., Roome, R. B., Seiradake, E., Luo, L., Kania, A. 2025

  Abstract

  Somatotopy is a recurring organisational feature of the somatosensory system where adjacent neurons and their connections represent adjacent regions of the body. The molecular mechanisms governing the formation of such "body maps" remain largely unknown. Here we demonstrate that the cell surface proteins teneurin-3 and latrophilin-2 are expressed in opposing gradients in multiple somatotopic maps in the mouse, including within the dorsal horn of the spinal cord. Genetic manipulation of these proteins in spinal dorsal horn or sensory neurons distorts the somatotopy of neuronal connections and impairs accurate localisation of a noxious stimulus on the surface of the body. Our work provides the foundation for a molecular model of somatotopic map formation and insights into their function in the localisation of somatosensory stimuli or topognosis.

  View details for DOI 10.1101/2025.08.13.670179

  View details for PubMedID 40909519

  View details for PubMedCentralID PMC12407721

• Oxytocin receptor disruption in <i>Avil-</i>expressing cells results in blunted sociability and increased inter-male aggression PLOS ONE Tabbaa, M., Moses, A., Hammock, E. A. D. 2021; 16 (11): e0260199

  Abstract

  Social behaviors are foundational to society and quality of life while social behavior extremes are core symptoms in a variety of psychopathologies and developmental disabilities. Oxytocin (OXT) is a neuroactive hormone that regulates social behaviors through its receptor (OXTR), with all previously identified social behavior effects attributed to the central nervous system, which has developmental origins in the neural tube. However, OXTR are also present in neural crest-derived tissue including sensory ganglia of the peripheral nervous system. Avil encodes for the actin-binding protein ADVILLIN, is expressed in neural crest-derived cells, and was therefore used as a target in this study to knock out OXTR expression in neural-crest derived cells. Here, we tested if OXTRs specifically expressed in Avil positive neural crest-derived cells are necessary for species-typical adult social behaviors using a Cre-LoxP strategy. Genetically modified male and female mice lacking OXTR in Avil expressing cells (OXTRAvil KO) were tested for sociability and preference for social novelty. Males were also tested for resident intruder aggression. OXTRAvil KO males and females had reduced sociability compared to OXTRAvil WT controls. Additionally, OXTRAvil KO males had increased aggressive behaviors compared to controls. These data indicate that OXTRs in cells of neural crest origin are important regulators of typical social behaviors in C57BL/6J adult male and female mice and point to needed directions of future research.

  View details for DOI 10.1371/journal.pone.0260199

  View details for Web of Science ID 000735928900022

  View details for PubMedID 34847180

  View details for PubMedCentralID PMC8631681