Translation from nonautonomous type IAP retrotransposon is a critical determinant of transposition activity: implication for retrotransposon-mediated genome evolution.

Retrotransposons constitute a major component of the genome and their proliferation significantly impacts genome evolution. Retrotransposons can propagate autonomously or nonautonomously. Nonautonomous type transposition occurs through trans-complementation by autonomous type retrotransposons.

Retrotransposons influence the mouse transcriptome: implication for the divergence of genetic traits.

Massive accumulation of retrotransposons, comprising >40% of human and mouse genomes, is one of the major events in the evolution of the genome. However, most retrotransposons have lost retrotransposition competency, which makes studying their role in genome evolution elusive. Intracisternal A-particle (IAP) elements are long terminal repeat (LTR)-type mouse retrotransposons consisting of full-length and internally deleted types.

Changes in ghrelin levels of plasma and proventriculus and ghrelin mRNA of proventriculus in fasted and refed layer chicks.

This is a test-report of ghrelin levels in plasma and proventriculus, the glandular portion of the avian stomach, by using a specific radioimmunoassay for acylated ghrelin, as well as the expression of the ghrelin gene in the proventriculus after a 12-h fasting period followed by a 6-h feeding period with 6-day-old layer chicks. After fasting, the plasma ghrelin levels increased from 21.3+/-4.

Inhibitory effect of ghrelin on food intake is mediated by the corticotropin-releasing factor system in neonatal chicks.

It is known that, in rats, central and peripheral ghrelin increases food intake mainly through activation of neuropeptide Y (NPY) neurons. In contrast, intracerebroventricular (ICV) injection of ghrelin inhibits food intake in neonatal chicks. We examined the mechanism governing this inhibitory effect in chicks.

Anorexigenic effects of pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal peptide in the chick brain are mediated by corticotrophin-releasing factor.

Intracerebroventricular (ICV) injection of pituitary adenylate cyclase-activating polypeptide-38 (PACAP) or vasoactive intestinal peptide (VIP) inhibits feeding in chicks. However, the underlying anorexigenic mechanism(s) has not yet been investigated. The present study investigated whether these peptides influence the activity of corticotrophin-releasing factor (CRF) neural pathways in the brain of chicks.

Effect of central administration of carnosine and its constituents on behaviors in chicks.

Even though their contents in the brain are high, the function of brain carnosine and its constituents has not been clarified. Both carnosine and anserine inhibited food intake in a dose dependent fashion when injected intracerebroventricularly. The constituents of carnosine, beta-alanine (beta-Ala) and l-histidine (His), also inhibited food intake, but their effects were weaker than carnosine itself.

Comparison of brain arginine-vasotocin and corticotrophin-releasing factor for physiological responses in chicks.

Arginine-vasotocin (AVT), a non-mammalian homologue of mammalian arginine-vasopressin, is a stress-related peptide in the brain of birds. The aim of the present study was to determine the effects of intracerebroventricular (ICV) injection of AVT on feeding behavior, body temperature, corticosterone release and several behavioral parameters in chicks. These effects were compared with those of corticotrophin-releasing factor (CRF), another stress-related peptide.

Effect of central administration of prolactin-releasing peptide on feeding in chicks.

Prolactin-releasing peptide (PrRP) is one of the inhibitory factors in feeding regulation of mammals. However, no information is available for avian species. The present study was done to clarify the effect of intracerebroventricular (ICV) injection of PrRP on feeding in chicks.

Pituitary adenylate cyclase activating polypeptide and vasoactive intestinal peptide inhibit feeding in the chick brain by different mechanisms.

Intracerebroventricular (ICV) injections of pituitary adenylate cyclase-activating polypeptide-38 (PACAP) and vasoactive intestinal peptide (VIP) inhibit feeding in chicks. However, the precise anorexigenic mechanisms have not been investigated, since both peptides activate the VPAC receptor in mammals. We investigated which receptor mediates the anorexigenic effects of these peptides in chicks.

Central pipecolic acid increases food intake under ad libitum feeding conditions in the neonatal chick.

It has been demonstrated that L-pipecolic acid (L-PA) is a major metabolic intermediate of L-lysine in the mammalian and chicken brain. A previous study showed that intracerebroventricular (i.c.

Beta 3-adrenergic receptor is involved in feeding regulation in chicks.

We examined whether the brain beta 3-adrenergic receptor (B3-AR) is involved in the feeding regulation of chicks. Intracerebroventricular (ICV) injection of BRL37344, a B3-AR agonist, reduced food intake of chicks under ad libitum, but not fasting, feeding conditions. The ICV injection of BRL37344 did not affect chick posture or locomotion activity suggesting that BRL37344 inhibited feeding without induction of sleep-like behavior as caused by norepinephrine.

Intracerebroventricular injection of vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide inhibits feeding in chicks.

Previous research has indicated an involvement of glucagon superfamily peptides in the regulation of feeding in the domestic chick brain. However the possible roles of vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide-38 (PACAP) have not yet been investigated. We therefore examined the effect of intracerebroventricular (ICV) injections of VIP or PACAP on food intake in chicks.

Chicken ghrelin and growth hormone-releasing peptide-2 inhibit food intake of neonatal chicks.

Ghrelin is an endogenous ligand for the growth hormone secretagogue (GHS) receptor. Ghrelin stimulates feeding in rats, however, intracerebroventricular (i.c.