Material and methods periods. Feeding behavior was assessed by counting the
126 H
naturally occurring fragment isolated from ovine hypo- pellets Moore Clark, St. Andrews, NB, Canada. Fish
thalamus [40] appears to be the most potent fragment. The were acclimated under these standard conditions for ap-
numbers in the fragments derive from the predicted signal proximately 2 weeks before the start of an experiment.
peptide cleavage site in the long form of CART [14]. Other Forty-eight hours prior to experimentation, two fish were
CART fragments including CART 54–105, CART 60– moved into an observation tank and starved.
105, CART 61–105 [43], CART 55–76 and CART 62–76 [32] have also been shown to cause a dose-
2.2. Intracerebroventricular i.c.v. injections dependent feeding inhibition in rats. Immunoneutralization
of CART by administration of rabbit anti-CART 55–102 Brain i.c.v. injections were administered following
results in higher food intake in rats, suggesting that CART
.
procedures described by Peter and Gill [37] Briefly,
is an endogenous satiety factor [32,42]. following deep anesthesia, a three-sided flap was cut in the
NPY-containing terminals are present around CART roof of the skull using a dentist drill equipped with a
peptide-positive cell bodies in the paraventricular nucleus circular saw. The flap was then folded to the side, exposing
of the hypothalamus [3,9,32] suggesting a regulation of the brain. Fish were then placed in a specially designed
NPY on CART output. Decreased levels of the adipocyte stereotaxic apparatus. The needle of a 5-ml microsyringe
hormone leptin, as seen during fasting or in obese rats with was stereotaxically placed in the preoptic region of the
impaired leptin action, cause a fall in the expression of brain third ventricle according to coordinates 11.0, M, D
CART mRNA [2,48] which can be restored by peripheral 1.2 taken from the stereotaxic atlas of the goldfish brain
administration of leptin [29]. Leptin treatment activates [37]. Following injection of 2 ml of test solution, the
CART hypothalamic neurons [16]. In turn, intracereb- needle was withdrawn and the space in the cranial cavity
roventricular injection of recombinant CART inhibits filled with teleost physiological saline [4]. The skull flap
NPY-induced feeding [32]. was put back in place, and secured by surgical thread. Fish
In fish, there is limited information on the neural control were then returned to their tanks, and normally recovered
of feeding behavior. Recent studies show that orexigenic from anesthesia within 2–5 min. All experiments were
peptides such as NPY [33,35], galanin [10], and orexins carried out in accordance with the principles published in
[46], and anorexigenic peptides such as corticotropin-re- the Canadian Council on Animal Care’s ‘‘guide to the care
leasing factor Bernier, Andrusky, Volkoff and Peter, and use of experimental animals’’.
unpublished; [11], cholecystokinin [20], serotonin [12] and bombesin [19] are involved in the regulation of
feeding in goldfish. 2.3. Observational experiments
To determine if CART peptides are involved in feeding in goldfish, we tested the effects of different doses of two
Fish were tested in random order in terms of treatment recombinant CART fragments, CART 62–76 and CART
and days. For each experiment, two fish were placed in a 55–102, on the feeding behavior of food-restricted fish
single observation tank to avoid stress due to isolation and and in fish subjected to NPY- or orexin A OXA-induced
to allow for an accurate observation of feeding behavior feeding. As CART peptides might have various physiolog-
and food consumption. Observations were made for each ical functions and influence other behaviors besides feed-
individual fish. An approximate 4 bw ration of pellets ing, we also examined the effects of CART fragments on
per fish was administered at 15 min post-injection. Be- behavioral activity.
havioral observations and measurement of food consump- tion commenced upon entry of pellets into the tank, and
were made for 1 h. Observations were divided in 15-min