Abstract:
:Treatment of either crude or purified preparations of the gamma-aminobutyrate (GABA)/benzodiazepine receptor complex with arginine-specific reagents resulted in a time- and concentration-dependent loss of [3H]muscimol binding activity. Following exposure to either 2,3-butanedione or phenylglyoxal (less than or equal to 20 mM), [3H]muscimol binding was inhibited by up to 80%. [3H]Flunitrazepam binding was much less sensitive to the effects of the reagents. Scatchard analysis of the binding data indicated that treatment with butanedione resulted in a loss of [3H]muscimol binding sites with little effect on binding affinity. Considerable protection against inactivation was provided by arginine and by the endogenous receptor ligand, GABA. These results indicate that arginine residues play a critical role in maintaining the GABA receptor in a conformation capable of ligand binding, possibly by participating in the binding site through interaction with the carboxylate moiety of GABA.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Widdows KB,Kirkness EF,Turner AJdoi
10.1016/0014-5793(87)80204-1subject
Has Abstractpub_date
1987-09-28 00:00:00pages
125-8issue
1eissn
0014-5793issn
1873-3468pii
0014-5793(87)80204-1journal_volume
222pub_type
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