Ultrastructural localization of ?-Arrestin-1 and -2 in rat lumbar spinal cord

Abstract

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.

Desensitization of G Protein–coupled Receptors and Neuronal Functions

“…Both arrestins were highly expressed in the cortex and hippocampus, but βarrestin-2 was particularly abundant in the medial habenular, in most hypothalamic nuclei, the extended amygdala, and, in the developing brain, in the subventricular zone . In the spinal cord, βarrestin-2 was found through laminae III-X in the order of IX > dorsal nucleus of Clarke > V > VII/VIII > IV > III > X (Kittel & Komori 1999).…”

“…Modest expression was detected in the neurons of laminae V and VII/VIII, and somewhat weaker immunoreactivity was observed in laminae III, IV, and X. Interestingly, in the spinal cord, both βarrestin-positive and -negative dendrites were observed, whereas axons and terminal boutons seem to be lacking βarrestins. Like in the brain, strong immunoreactivity for βarrestin-1 was mostly found at postsynaptic densities in the spinal cord (Kittel & Komori 1999). In transfected cellular systems, βarrestin-1 appears to regulate desensitization of numerous GPCRs (Oakley et al 2000), including D1 and D2 dopamine receptors (Kim et al 2001, Oakley et al 2000 and µORs (Oakley et al 2000, Schulz et al 1999; but see Cheng et al 1998).…”

β-arrestin-2 regulates NMDA receptor function in spinal lamina II neurons and duration of persistent pain

“…33), the expression pattern is not well characterized. In situ hybridization revealed that Arrb2 mRNA is widely expressed in SDH of WT mice, although the staining is stronger in the deep dorsal horn (laminae III–VI, Fig.…”

Ligands for Clathrin-Mediated Endocytosis Are Differentially Sorted into Distinct Populations of Early Endosomes

“…The extent to which the correlation between the final fate of an endocytic ligand (in terms of degradation and recycling) and their pre-early endosome sorting is general and applicable to other ligands remains to be addressed. This model also suggests an intriguing connection between certain endocytic adaptors and microtubule-dependent motility, the plausibility of which is supported by the microtubule-binding activity of several cargo-specific adaptor proteins (Kittel and Komori, 1999;Hussain et al, 2003).…”