title: Distribution and localization of 5-HT(1A) receptors in the rat lumbar spinal cord after transection and deafferentation.
abstract: The serotonergic system is highly plastic, capable of adapting to changing afferent information in diverse mammalian systems. We hypothesized that removing supraspinal and/or peripheral input would play an important role in defining the distribution of one of the most prevalent serotonergic receptors, the 5-HT(1A) receptor (R), in the spinal cord. We investigated the distribution of this receptor in response to a complete thoracic (T7-T8) spinal cord transection (eliminating supraspinal input), or to spinal cord isolation (eliminating both supraspinal and peripheral input) in adult rats. Using two antibodies raised against either the second extracellular region (ECL(2)) or the third intracellular region (ICL(3)) of the 5-HT(1A)R, we compared the 5-HT(1A)R levels and distributions in specific laminae of the L3-L5 segments among the control, spinal cord-transected, and spinal cord-isolated groups. Each antibody labeled different populations of 5-HT(1A)R: ECL(2) labeled receptors in the axon hillock, whereas ICL(3) labeled receptors predominantly throughout the soma and proximal dendrites. Spinal cord transection increased the number of ECL(2)-positive cells in the medial region of laminae III-IV and lamina VII, and the mean length of the labeled axon hillocks in lamina IX. The number of ICL(3)-labeled cells was higher in lamina VII and in both the medial and lateral regions of lamina IX in the spinal cord-transected compared to the control group. In contrast, the length and number of ECL(2)-immunolabeled processes and ICL(3)-immunolabeled cells were similar in the spinal cord-isolated and control groups. Combined, these data demonstrate that the upregulation in 5-HT(1A)R that occurs with spinal cord transection alone is dependent on the presence of sensory input.
authors.affiliation: Department of Physiological Science, University of California-Los Angeles, Los Angeles, California 90095-1606, USA.
authors.forename: Chad K
authors.initials: CK
authors.lastname: Otoshi
authors.forename: Wendy M
authors.initials: WM
authors.lastname: Walwyn
authors.forename: Niranjala J K
authors.initials: NJ
authors.lastname: Tillakaratne
authors.forename: Hui
authors.initials: H
authors.lastname: Zhong
authors.forename: Roland R
authors.initials: RR
authors.lastname: Roy
authors.forename: V Reggie
authors.initials: VR
authors.lastname: Edgerton
mesh_terms: D000818:Animals; D000906:Antibodies; D000918:Antibody Specificity / Q000276:immunology; D001369:Axons / Q000378:metabolism / Q000473:pathology; D002452:Cell Count; D003712:Dendrites / Q000378:metabolism / Q000473:pathology; D003714:Denervation / Q000009:adverse effects*; D004195:Disease Models, Animal; D005260:Female; D007150:Immunohistochemistry / Q000379:methods; D008159:Lumbar Vertebrae / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology; D020671:Posterior Horn Cells / Q000378:metabolism / Q000473:pathology; D017434:Protein Structure, Tertiary / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D044282:Receptor, Serotonin, 5-HT1A / Q000378:metabolism*; D019051:Rhizotomy / Q000009:adverse effects*; D012677:Sensation / Q000502:physiology; D012701:Serotonin / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000503:physiopathology; D013131:Spine / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D015854:Up-Regulation / Q000502:physiology
chemical_list: D000906:Antibodies; D044282:Receptor, Serotonin, 5-HT1A; D012701:Serotonin