Disease relevance of NPY

• RESULTS: NPY-like immunoreactive (LI) nerve terminals surrounded 80% of ciliary ganglion cells, but ciliary ganglion cell somata were unstained [1].

Psychiatry related information on NPY

• Severalfold regional and individual differences in the density of NPY-positive somata were found in supra- and infragranular layers [2].

High impact information on NPY

• Specifically, the dynamics in the postnatal ontogeny of hypothalamic GnRH gene expression and release are described, and the roles of neuropeptide Y and gamma-aminobutyric acid in imposing the restraint on pulsatile GnRH release during juvenile development are examined [3].
• Cell imaging indicated that the developmentally regulated NPY neurons may be located in regions dorsal to the arcuate nucleus [4].
• Here, we show that, in the male rhesus monkey, the postnatal pattern in GnRH pulse generator activity is inversely related to that in neuropeptide Y (NPY) gene and protein expression in the mediobasal hypothalamus and that central administration of an NPY Y(1) receptor antagonist to juvenile animals elicits precocious GnRH release [4].
• The Y2 subtype of neuropeptide tyrosine (NPY) receptors (Y2R) and some neuropeptides have been studied with in situ hybridization in sensory and autonomic neurons of rat and monkey [5].
• GALP neurons were found to express both neuropeptide Y Y1 receptor and serotonin 2C receptor by double-label in situ hybridization [6].

Biological context of NPY

• Thus, endogenous NPY is likely to be involved in the regulation of food intake in the nonhuman primate, and this effect is at least partially mediated via Y1-like receptors [7].
• Since sex differences in LHRH response to NPY were not present, data from males and females were combined for analysis [8].
• Comparison of our results for NPY binding sites with the distribution of alpha 1-adrenergic receptors, as recently described by Rakic et al [9].
• NPY+ cell density was fairly constant prenatally and then rose 300% by adulthood [10].
• We conclude that: (1) adrenal medulla transplantation into the third ventricle accelerates the age of first ovulation; (2) this is likely due to neuroactive substances (e.g., catecholamines and NPY) from the graft tissue; and (3) grafted adrenal medulla tissue can survive for at least 30-40 months [11].

Anatomical context of NPY

• Numerous nerve fibers near the meibomian gland acini were immunoreactive for NPY and VIP, but nerve fibers containing TH, CGRP, and SP were more sparse in the meibomian glands [12].
• METHODS: Cryostat tissue sections of fixed rhesus monkey ciliary, pterygopalatine, superior cervical, and trigeminal ganglia were incubated with antisera to neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptide (VIP), tyrosine hydroxylase (TH), and dopamine-beta-hydroxylase (DBH) [1].
• No NPY-containing neurons were found in layer IV of any area, except layers IVA and B of the visual cortex [13].
• The regional differences in the distribution of NPY-like immunoreactivity in the neocortex may reflect innate characteristics of local neuronal circuits serving specialized functions [2].
• The possibility of additional neuronal types containing NPY is suggested by labeled densely spinous dendrites in area 6 and recurving axons and axonal loops in the supragranular layers in areas 7 and 9 [13].

Associations of NPY with chemical compounds

• Blood glucose levels were unaffected by intracerebroventricular administration of NPY, but animals receiving either 20 or 50 microg displayed increased plasma levels of insulin and cortisol at few time points [7].
• The ability of estrogen feedback to alter the response to NPY treatment supports a physiological role for NPY in controlling reproduction in the primate [14].
• NPY pulse frequency also increased significantly (P < 0.05) 4-8 h after progesterone treatment, whereas mean release and pulse amplitude did not change in response to progesterone [15].
• NPY and LHRH concentrations in aliquots of the same perfusate sample from the S-ME and circulating LH levels were concurrently measured in 8 monkeys sedated with Saffan [16].
• The presence of catecholamines and NPY in graft tissue was confirmed by tyrosine-hydroxylase-positive, dopamine beta-hydroxylase-positive, and NPY-positive cells [11].

Regulatory relationships of NPY

• NPY infusion into the S-ME stimulated LHRH release in a dose-dependent manner (P less than 0.001) [8].
• In the hypothalamus, UCP2 was coexpressed with neuropeptide Y, CRH, oxytocin, and vasopressin [17].

Other interactions of NPY

• 2) How does NPY release relate to LHRH release [16]?

Analytical, diagnostic and therapeutic context of NPY

• In the present experiment the effects of NPY on LHRH release were examined in conscious monkeys using a push-pull perfusion method [8].
• Cryostat tissue sections of the lids were stained by immunohistochemistry using rabbit antisera to neuron-specific enolase (NSE), tyrosine hydroxylase (TH), neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP), and substance P (SP), followed by a fluorescence visualization system [12].
• NPY dissolved in a modified Krebs-Ringer phosphate buffer solution at concentrations of 10(-8), 10(-7), 10(-6), and 10(-5) M was directly infused into the S-ME through the push cannula for 10 min at 90-min intervals [8].
• By means of in vitro receptor autoradiography, NPY binding sites in primate and feline visual cortex were specifically labeled with 3H-NPY [9].
• The distribution of neuropeptide Y (NPY) in microdissected brain regions of male macaques was quantified with a specific radioimmunoassay (RIA) [18].

References