In the cerebral cortex and caudate-putamen (CP) nuclei, neuropeptide Y (NPY) immunoreactivity is detectable within 1-2% of all neurons. The NPY-immunoreactive neurons are interneuronal and are believed to be mostly GABAergic in the cerebral cortex but not in the CP nuclei. Thus NPY and GABA may play different roles in the circuitry within these 2 regions. We tested this possibility by comparing...

Neuropeptide Y (NPY) was first identified from porcine brain in 1982, and plays its biological functions in humans through NPY receptors (Y1, Y2, Y4 and Y5). NPY receptors are known to mediate various physiological functions and involve in a majority of human diseases, such as obesity, hypertension, epilepsy and metabolic disorders. Recently, NPY receptors have been found to be overexpressed in...

Microinjections of neuropeptide Y (NPY) (1-36) and of the NPY Y1 agonist [Leu31,Pro34]NPY into the caudal dorsomedial part of the nucleus tractus solitarius (Sol) in the anaesthetized rat led to the development of dose-related vasodepressor and bradycardic responses. The threshold dose of the NPY Y2 agonist NPY(13-36) (50 fmol) significantly counteracted the vasodepressor actions of a close to ...

Neuropeptide Y (NPY) conjugated to saporin (NPY-SAP), a ribosomal inactivating toxin, is a newly developed compound designed to selectively target and lesion NPY receptor-expressing cells. We injected NPY-SAP into the basomedial hypothalamus (BMH), just dorsal to the arcuate nucleus (ARC), to investigate its neurotoxicity and to determine whether ARC NPY neurons are required for glucoprivic fee...

No information exists on the role of neuropeptide Y (NPY) in cholangiocarcinoma growth. Therefore, we evaluated the expression and secretion of NPY and its subsequent effects on cholangiocarcinoma growth and invasion. Cholangiocarcinoma cell lines and nonmalignant cholangiocytes were used to assess NPY mRNA expression and protein secretion. NPY expression was assessed by immunohistochemistry in...

Fasting increases neuropeptide Y (NPY) expression, peptide levels, and the excitability of NPY-expressing neurons in the hypothalamic arcuate (ARC) nucleus. A subpopulation of ARC-NPY neurons ( approximately 40%) are glucose-inhibited (GI)-type glucose-sensing neurons. Hence, they depolarize in response to decreased glucose. Because fasting enhances NPY neurotransmission, we propose that during...

Fasting increases neuropeptide Y (NPY) expression, peptide levels and the excitability of NPY-expressing neurons in the hypothalamic arcuate (ARC) nucleus. A subpopulation of ARC-NPY neurons (~ 40%) are glucose-inhibited (GI)-type glucose sensing neurons. Hence, they depolarize in response to decreased glucose. Because fasting enhances NPY neurotransmission, we propose that during fasting GI ne...

To investigate how compensatory responses develop after the onset of inhibition of NPY signaling, we examined the effect of continuous intracerebroventricular (ICV) injection of neutralizing NPY antibodies (NPY-ab) on daily and fast-induced food intake in mice. A single ICV injection of NPY-ab reduced food intake in fasted mice. In contrast to a single injection, continuous ICV injection of NPY...

Despite numerous experiments showing that administration of neuropeptide Y (NPY) to rodents stimulates feeding and obesity, whereas acute interference with NPY signaling disrupts feeding and promotes weight loss, NPY-null mice have essentially normal body weight regulation. These conflicting observations suggest that chronic lack of NPY during development may lead to compensatory changes that n...

Delivery of neuropeptide Y (NPY) to the brain by intranasal infusion soon after traumatic stress has shown therapeutic potential, and prevented development of many behavioral and neuroendocrine impairments in the single prolonged stress (SPS) animal model of PTSD. Therefore, we examined whether the Y1R preferring agonist [Leu31Pro34]NPY is sufficient to prevent development of SPS induced depres...