Neuropeptide Y gene expression in male sheep: influence of photoperiod and testosterone.

The frequency of pulsatile release of gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) is high in the breeding season and low in the nonbreeding season. These alterations in the patterns of GnRH and LH release are due to an interaction of daylength and gonadal steroid negative feedback. A vast amount of data indicates that steroid-responsive neural systems may play a role in regulating seasonal changes in GnRH release. One candidate system is neuropeptide Y (NPY). To determine the independent and interactive influences of photoperiod and steroid exposure on NPY mRNA levels, we used hypothalamic tissue from four groups (n = 4 per group) of castrated male sheep that were simultaneously housed in photochambers and exposed to: (1) a 16L:8D photoperiod (LD); (2) LD and implanted with testosterone (LD + T); (3) a 10L:14D photoperiod (SD), and (4) SD + T. Circulating levels of T averaged 2.8 +/- 0.2 ng/ml in implanted animals, but were undetectable in nonimplanted males. Mean LH levels were significantly reduced (p < 0.01) in the LD + T group as compared with the other groups which did not differ from each other. The silver grain area per NPY neuron in the arcuate nucleus, as assessed by in situ hybridization, was inversely related to mean LH values, with the grain area per cell being significantly greater (p < 0.05) for LD + T males than for all other groups which did not differ from each other. NPY cell numbers were not significantly different (p > 0.10) among the treatment groups. These results show that NPY mRNA expression is increased in male sheep during a LD photoperiod in a T-dependent manner. Our data are consistent with the idea that NPY is involved in the seasonal regulation of GnRH and LH release in the male sheep.

Quantitative autoradiography of adrenergic, neuropeptide Y and angiotensin II receptors in the nucleus tractus solitarii and hypothalamus of rats with experimental hypertension.

Catecholamines, neuropeptide Y (NPY) and angiotensin II (Ang II) are known to participate in the central control of blood pressure. However, the modulation of these neurotransmitter receptors in response to a hypertensive stimulus is not appropriately established. The purpose of the present study was to examine binding parameters of alpha(2)-adrenergic, NPY and Ang II receptors in the nucleus tractus solitarii (NTS) and paraventricular hypothalamic nucleus (PVN) following a hypertensive stimulus in the aortic-coarcted rat by means of quantitative receptor autoradiography. No changes were seen in binding parameters of alpha(2)-adrenergic and NPY receptors in the NTS of the hypertensive rat compared to control. However, an increased affinity (54%) of noradrenaline competing for 3H-PAC was seen in the PVN. Moreover, an increased binding (49%) of 125I-PYY was also observed in the PVN. The affinity of Ang II for 125I-Sar(1)Ile(8)-Ang II binding sites was also increased (57%) in the NTS of the hypertensive rat. No changes in the binding parameters of radioactive Ang II were observed in the PVN. The results suggest that systems involved with hypertension like Ang II in the NTS and catecholamines in the PVN might collaborate in the development/maintenance of high blood pressure in the aortic-coarcted rat.

Microwave irradiation increases recovery of neuropeptides from brain tissues.

The effect of focused high energy microwave treatment (MW) on brain concentrations and molecular forms of substance P, neurokinin A, neuropeptide Y, neurotensin, galanin and calcitonin gene-related peptide was investigated. Groups of rats were treated as follows: 1) MW, storage for 60 min at 22 degrees C, 2) Decapitation, storage for 60 min at 22 degrees C. 3) Decapitation, storage for 60 min at 22 degrees C, MW treatment, 4) MW, decapitation, storage for 2 min at 22 degrees C and 5) Decapitation, storage for 2 min at 22 degrees C. Peptide concentrations were in all instances highest in the MW sacrificed groups. MW increased the concentration of intact peptides by rapid inhibition of peptidase activity and increase in peptide solubility/extractability.