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Pupillary effects of neurotensin: Structure- activity relationships
Authors:Daniel E. Hernandez   Kenneth B. Simons   Domenico Spampinato   Francis Rioux  Serge St-Pierre
Affiliation:1. School of Veterinary Medicine, North Carolina State University, Raleigh, NC USA;2. Jules Stein Eye Institute, UCLA Medical Center, Los Angeles, CA USA;3. Department of Pharmacology, University of Catania Medical School, Catania, Italy;4. Department of Pharmacology, Sherbrooke University, Quebec, Canada
Abstract:We have previously reported that intracameral (I.C.) administration of neurotensin (NT) potently induces a time- and dose-dependent miosis in rabbits. This study was designed to determine structure-function relationships for NT-induced miosis. NT and twelve different fragments and analogs of NT, and the structurally-unrelated peptides beta-endorphin (beta-end), somatostatin (SRIF) and thyrotropin-releasing hormone (TRH) were tested in a dose equimolar to 30 micrograms of NT for their effects on pupillary diameter (PD) in rabbits. In confirmation of previous findings, NT produced significant miosis. Followed in order of duration of effect were D-Trp11-NT, D-Tyr11-NT, the N-terminal fragment NT1-12, [Gln4] - NT and NMe-NT. The N-terminal fragment NT1-8, D-Arg8-NT, and D-Phe11-NT were weakly active. In addition, the initial N-terminal fragment NT1-6 and the C-terminal fragments NT8-13 and NT9-13 did not affect PD. D-Pro10-NT, beta-end, SRIF, and TRH were totally ineffective. The results of this investigation contribute to support a role for NT on regulation of pupillary function, and suggest that the midportion of NT appears to be critical for the expression of NT-induced miosis.
Keywords:neurotensin   miosis   neurotensin fragments and analogs
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