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 β-endorphin (β-end), somatostatin (SRIF) and thyrotropin-releasing hormone (TRH) were tested in a dose equimolar to 30 μg 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-Trp 11-NT, D-Tyr 11-NT, the N- terminal fragment NT 1–12, [Gln 4] - NT and NMe-NT. The N-terminal fragment NT 1–8, D-Arg 8-NT, and D-Phe 11-NT were weakly active. In addition, the initial N-terminal fragment NT 1–6 and the C-terminal fragments NT 8–13 and NT 9–13 did not affect PD. D-Pro 10-NT, β-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.
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