Neuropeptide Y stimulates feeding but inhibits sexual behavior in rats

JT CLARK, PS KALRA, SP KALRA - Endocrinology, 1985 - academic.oup.com
JT CLARK, PS KALRA, SP KALRA
Endocrinology, 1985academic.oup.com
The effects of neuropeptide Y (NPY), a tyrosinerich peptide found in the rat brain, on feeding
and sexual behavior were studied in male and female rats. Intraventricular (ivt) injections of
NPY during the final hours of the light period induced feeding in a dose-related manner.
While the lowest dose tested (0.02 nm) was without effect, higher doses (0.12, 0.47, 2.3 nm)
uniformly elicited feeding with a latency of about 15 min in male rats. With the most effective
dose, 0.47 nm, the increased food intake was due to an increased local eating fate. In …
Abstract
The effects of neuropeptide Y (NPY), a tyrosinerich peptide found in the rat brain, on feeding and sexual behavior were studied in male and female rats. Intraventricular (ivt) injections of NPY during the final hours of the light period induced feeding in a dose-related manner. While the lowest dose tested (0.02 nm) was without effect, higher doses (0.12, 0.47, 2.3 nm) uniformly elicited feeding with a latency of about 15 min in male rats. With the most effective dose, 0.47 nm, the increased food intake was due to an increased local eating fate. In contrast, the pattern of feeding behavior after a related peptide, rat pancreatic polypeptide (rPP), was quite different and less impressive. During the first hour, only one ivt dose of rPP (0.45 nm) evoked an increase in food intake, due to an increased time spent eating. Further, the effects of NPY on food intake were greater during the nocturnal period. Interestingly, increased food intake in nocturnal tests (4 h) was due solely to augmented intake during the first 60 min after ivt administration.
In mating tests, initiated 2 h after the onset of darkness and 10 min after ivt administration of peptide, all but the lowest dose of NPY (0.01 nm) drastically suppressed ejaculatory behavior. Most rats treated with higher doses of NPY (0.02, 0.12, or 0.47 nm) mounted and intromitted only a few times before the cessation of sexual activity, and elongated latencies to the initial mount and intromission were observed. In contrast to the dramatic NPY-induced suppression of ejaculatory behavior, rPP (0.11 and 0.45 nm) was without effect on copulatory behavior. To substantiate further that the impairment of sexual behavior seen in NPY-treated rats was not due to an attenuated sexual ability, an additional experiment was performed. Penile reflexes, including erection, were monitored 10 min after ivt injection of NPY (0.12 nm), rPP (0.11 nm), or saline. No effect of NPY or rPP was observed on the proportion of rats showing erection or latency to initial erection, or in the number of erections per test. In fact, a slight facilitation of penile dorsiflexion responses was seen after NPY. These findings suggest that NPY selectively depresses sexual motivation in the male rat.
In ovariectomized female rats responding to estrogen plus progesterone with a good level of sexual receptivity (lordosis quotient > 70), ivt saline and 0.01 nm NPY were without effect on sexual behavior. However, higher doses of NPY (0.12 and 0.47 nm) promptly suppressed sexual behavior in tests initiated 10 min after treatment: A significant 50% decrement in receptivity and a virtual elimination of proceptive behavior were observed. Further, although a low level of mounting (one to five mounts in 15 min) was seen in both the saline (33% mounting) and the 0.01 nm NPY (38% mounting) treated groups, none was observed in animals treated with the higher NPY doses. These observations indicate that NPY may also suppress female sexual behavior.
These studies demonstrate that NPY, a novel hypothalamic peptide, stimulates feeding in male rats in both diurnal and nocturnal tests and suppresses sexual behavior in male and female rats. We suggest that NPY may be an endogenous neurochemical signal that decreases sexual motivation and subsequently increases the appetite for food in the rat. (Endocrinology117: 2435–2442, 1985)
Oxford University Press