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Ultrastructural localization of β‐Arrestin‐1 and ‐2 in rat lumbar spinal cord
Author(s) -
Kittel Agnes,
Komori Naoka
Publication year - 1999
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/(sici)1096-9861(19991004)412:4<649::aid-cne6>3.0.co;2-4
Subject(s) - spinal cord , postsynaptic potential , biology , anatomy , lumbar spinal cord , neuroscience , receptor , biochemistry
β‐arrestins play significant roles in agonist‐mediated desensitization of G protein‐coupled receptors. Although the presence of β‐arrestin subtypes, β‐arrestin‐1 and ‐2, in rat brain has been studied extensively, their existence in the spinal cord has not been described. In the current study, we performed immunohistochemical analyses of β‐arrestins at both light and electron microscopic levels using rat lumbar 1–2 spinal cord segments. Intense immunoreactivity for β‐arrestin‐1 was found in the motoneurons in lamina IX of the ventral horn and elongated cells in the dorsal nucleus of Clarke. Modest immunoreactivity was detected among the neurons of laminae V and VII/VIII, and weaker immunoreactivity in laminae III, IV, and X. β‐arrestin‐2 immunoreactivity was also distributed through laminae III–X in the order of IX > dorsal nucleus of Clarke > V > VII/VIII > IV > III > X. Laminae I and II did not show immunoreactivity. At the electron microscopic level, both β‐arrestin‐immunoreactive and nonimmunoreactive dendrites were observed, whereas axons and terminal boutons were devoid of immunoreactivity. In immunoreactive dendrites most β‐arrestin immunoreactivity was distributed throughout the cytoplasm, demonstrating their association with microtubules. In addition, strong immunoreactivity was often found at postsynaptic densities. Our results thus suggest β‐arrestins' possible involvement in both motor and sensory mechanisms at the postsynaptic level in rat lumbar spinal cord. J. Comp. Neurol. 412:649–655, 1999. © 1999 Wiley‐Liss, Inc.