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Abstract
Glucagonlike peptide-1 (7-36) amide (GLP-1) and its receptors are present in several
brain regions and may play a role in the physiological control of feeding. To investigate
the effect of GLP-1 on eating in the absence of postingestive food stimuli, rats were
implanted with gastric cannulas for sham feeding and lateral ventricular cannulas
for infusion of GLP-1. Rats (n = 10) sham fed 0.8 mol/L sucrose for 45 min, beginning
5 min after intracerebroventricular (icv) infusion of 2.5 microL of artificial cerebrospinal
fluid with 0-30 microg of GLP-1 . Behaviors were observed each minute using a time-sampling
technique. Additionally, lick-by-lick records of the microstructural pattern of sucrose
intake were made during the first 15 min of each test for five rats receiving 3 and
10 microg of GLP-1. GLP-1 decreased sham-fed intake by as much as 50%, but GLP-1 did
not terminate sham feeding. The frequency of observations of feeding was decreased,
but the frequency of resting, the terminal item in the behavioral sequence of postprandial
satiety in real feeding rats, did not reliably increase. No abnormal behaviors were
observed. Although GLP-I did not affect the latency to begin sham feeding, it significantly
reduced the initial rate of licking. GLP-I did not affect the motor aspects of licking,
because the interlick intervals within individual bursts of licking or overall lick
efficiency were normal. These data suggest that intracerebroventricular infusions
of GLP-1 inhibit sham feeding by decreasing the orosensory positive feedback that
drives licking, rather than by activating physiological satiating mechanisms or nonspecific
mechanisms such as aversion or motor incapacity.