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Vol. 289, Issue 2, 1031-1040, May 1999
Lilly Neuroscience, Lilly Research Laboratories, Eli Lilly and
Company, Lilly Corporate Center, Indianapolis, Indiana
The stimulation of food consumption after i.c.v. administration
of various neuropeptide Y (NPY) receptor agonists was examined in CD-1
mice. These agonists, including endogenous peptides NPY, peptide
YY (PYY), and pancreatic polypeptide, as well as several N-terminal
truncated and synthetic peptides that are prototypic receptor
agonists at Y1-Y6 NPY receptors
([Leu31Pro34]NPY, NPY2-36,
NPY3-36, NPY13-36, PYY3-36, Pro34PYY, and D-Trp32NPY), showed
varying abilities to elicit food consumption such that PYY > NPY2-36 = NPY = PYY3-36 > Pro34PYY > NPY3-36 
[Leu31Pro34]NPY > NPY13-36 = D-Trp32NPY = pancreatic polypeptide.
Published reports have suggested that NPY-induced feeding is mediated
via the Y1 or the Y5 receptor subtypes. However, the relative ability
of the various peptide analogs to elicit feeding differed from the
relative ability of these peptides to bind to cloned Y1-Y6 receptors.
The effects of prototypic Y1 receptor antagonists on NPY-induced
feeding were also evaluated after i.c.v. administration. GR231118
(1229U91), a peptide Y1 antagonist, did not block NPY-induced feeding
at the doses tested. BIBP3226, a nonpeptide Y1 receptor antagonist, as
well as its opposite enantiomer, BIBP3435, which is inactive at Y1
receptors, blocked feeding elicited by NPY,
[Leu31Pro34], or PYY at doses that did not
cause overt behavioral dysfunction. The lack of effects with GR231118
and the nonstereoselective effects of BIBP3226 suggested that
NPY-induced feeding in mice was not mediated via the Y1 receptor. Thus,
by using currently available prototypic peptide NPY receptor agonists
for Y1-Y6 receptors and peptide and nonpeptide Y1 receptor antagonists
GR231118 and BIBP3226, the mediation of NPY-induced feeding cannot be
unequivocally attributed to any one of the known NPY receptors. It is
possible that NPY-induced feeding is mediated either by a combination
of more than one NPY receptor subtype or by a unique NPY receptor
subtype. Additional subtype-selective receptor antagonists, when
available, will help to clarify this issue further.
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