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Agonist‐induced morphologic decrease in cellular d 1A dopamine receptor staining
Author(s) -
Ariano Marjorie A.,
Sortwell Caryl E.,
Ray Mikelene,
Altemus Katharine L.,
Sibley David R.,
Levine Michael S.
Publication year - 1997
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(199712)27:4<313::aid-syn5>3.0.co;2-f
Subject(s) - agonist , dopamine , chemistry , dopamine receptor , dopamine receptor d1 , receptor , staining , pharmacology , microbiology and biotechnology , endogenous agonist , neuroscience , biology , medicine , biochemistry , pathology
The distribution of D 1A dopamine (DA) receptor proteins was assessed by using subtype specific antireceptor antisera after acute DA exposure. The immunofluorescent staining of D 1A DA receptor protein expression was examined in (1) stably transfected Chinese hamster ovary (CHO) cells, (2) primary striatal cell cultures, and (3) rat striatal brain slices. After agonist exposure as brief as 2 min and as long as 60 min, profound loss of immunofluorescent D 1A receptor protein staining occurred in each paradigm. Additionally in the tissue slice, immunofluorescent neuropil staining for the receptor protein also was attenuated. The DA‐induced alteration in receptor protein staining was blocked by the antagonist (+)‐butaclamol and by the selective D1‐family antagonist SCH 23390. Receptor staining patterns reverted back to the control immunofluorescent distribution within 15 min after removing the agonist from the bath. Immunofluorescence for the second‐messenger cyclic AMP increased at all DA exposure times in the three experimental paradigms, was blocked by D1‐family antagonists, and decreased to basal staining after brief recovery periods. This demonstrated the functional integrity of the D 1A receptor in target cells. Pretreatment with the mitogenic plant lectin concanavalin A blocked the immunofluorescent decrease in receptor staining but not the elevation of the second messenger, indicating a morphologic distinction in these two events, parallel to other biochemical reports. The data suggested that a morphologic basis of acute homologous D 1A DA receptor desensitization may be transposition of membrane‐surface receptors to a transiently unavailable, intracellular compartment. This finding is supported by specific fluorescence incorporation of FM1‐43, used as a marker of endocytosis, in CHO cells treated with DA. Synapse 27:313–321, 1997. © 1997 Wiley‐Liss, Inc.