Comparative distribution of neuropeptide Y Y1 and Y5 receptors in the rat brain by using immunohistochemistry

Abstract

Neuropeptide Y (NPY) Y1 and Y5 receptor subtypes mediate many of NPY's diverse actions in the central nervous system. The present studies use polyclonal antibodies directed against the Y1 and Y5 receptors to map and compare the relative distribution of these NPY receptor subtypes within the rat brain. Antibody specificity was assessed by using Western analysis, preadsorption of the antibody with peptide, and preimmune serum controls. Immunostaining for the Y1 and Y5 receptor subtypes was present throughout the rostral-caudal aspect of the brain with many regions expressing both subtypes: cerebral cortex, hippocampus, hypothalamus, thalamus, amygdala, and brainstem. Further studies using double-label immunocytochemistry indicate that Y1R immunoreactivity (-ir) and Y5R-ir are colocalized in the cerebral cortex and caudate putamen. Y1 receptor ir was evident in the central amygdala, whereas both Y1- and Y5-immunoreactive cells and fibers were present in the basolateral amygdala. Corresponding with the physiology of NPY in the hypothalamus, both Y1R- and Y5R-ir was present within the paraventricular (PVN), supraoptic, arcuate nuclei, and lateral hypothalamus. In the PVN, Y5R-ir and Y1R-ir were detected in cells and fibers of the parvo- and magnocellular divisions. Intense immunostaining for these receptors was observed within the locus coeruleus, A1-5 and C1-3 nuclei, subnuclei of the trigeminal nerve and nucleus tractus solitarius. These data provide a detailed and comparative mapping of Y1 and Y5 receptor subtypes within cell bodies and nerve fibers in the brain which, together with physiological and electrophysiological studies, provide a better understanding of NPY neural circuitries.

Glutamate Microinjected in the Posterodorsal Medial Amygdala Induces Subtle Increase in the Consumption of a Three‐Choice Macronutrient Self‐Selection Diet in Male Rats

“…The MePD is an interesting forebrain area where to look for the central control of feeding behavior due to its relevant neural connections and the presence of neurotransmitters or neuropeptides that modulate this activity, such as neuropeptide Y (Wolak et al, 2003), cholecystokinin (De Vries and Simerly, 2002), and urocortin 3 (Cavalcante et al, 2006). Comparatively, it was reported that glutamate microinjected in the lateral hypothalamus induced a dose-dependent eating response in satiated male rats of up to 5 g of food within 1 hr (Stanley et al, 1993).…”

Central neuropeptide Y infusion and melanocortin 4 receptor antagonism inhibit thyrotropic function by divergent pathways

“…Moreover, TRH-expressing neurons in the PVN of the mouse are known to express Y1 receptor-like immunoreactivity (Broberger et al, 1999). Unlike the MC3 receptor, MC4 receptor mRNA (Mountjoy et al, 1994) as well as Y1 and Y5 receptor immunoreactivity (Wolak et al, 2003) are found in both parvicellular and magnocellular neurons of the PVN as recently reviewed , suggesting direct effects of NPY and melanocortins on the thyrotropic axis at the level of the hypothalamus. Indeed, central administration of NPY, Y1 or Y5 receptor agonists, AgRP or MC4 receptor antagonists to normal rodents significantly reduces function of the thyrotropic axis, indicated by reductions in expression of TRH in the PVN, and a decrease in circulating concentrations of TSH and T3 or T4 (Fekete et al, 2001, Fekete et al, 2002a, Fekete et al, 2002b, Small et al, 2001and Kim et al, 2000.…”

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

“…Neuropeptide Y (NPY) is a 36-amino acid neuroactive peptide found in the cerebral cortex, hippocampus, hypothalamus, thalamus, amygdala, striatum, brainstem, and cerebellum (Allen et al, 1983;Dumont et al, 1993;Parker and Herzog, 1999;Wolak et al, 2003). NPY colocalizes with somatostatin, gamma-aminobutric acid (GABA), and nitric oxide synthase (Bidmon et al, 2001a;Kowianski et al, 2004;Kubota et al, 1994), and can modulate neuronal excitability by multiple pre-and postsynaptic mechanisms under both physiological and pathophysiological conditions.…”