-
High Npy2r expression is associated with chronic social defeat stress.
-
These results indicate that endogenous PYY has a hypoalgesic effect on somatic thermal and visceral chemical pain. The effect on visceral pain seems to be mediated by peripheral Y2 receptors.
-
NPY and agonists of Y2R and Y5R may be neuroprotective against oxygen-glucose deprivation-induced neuronal cell death in primary cortical cell cultures after delayed treatment. A Y2R agonist not only diminished transient cerebral ischemia-induced neuronal injury, but also improved functional outcome after delayed treatment. Y5 and especially Y2 receptors may be promising targets for neuroprotection against ischemic damage
-
Findings suggest that neuropeptide Y is expressed by distinct populations of neurons can modulate afferent and efferent projections of the central amygdala via presynaptic Y2 receptors located at inhibitory and excitatory synapses.
-
confirms the critical role of Y2 signalling to control neuropeptide Y and associated pro-opiomelanocortin expression in the arcuate nuclei
-
Study shows that NPY inhibits fear learning and promotes cued extinction by reducing fear expression also via activation of presynaptic Y2 receptors on central amygdala neurons
-
Study shows pronounced adaptive changes in the mouse hippocampus both with regard to NPY synthesis and NPY receptor synthesis and binding, which may contribute to regulating neuronal seizure susceptibility after kainate
-
an integrated neural circuit modulates growth hormone release relative to food intake; data provide essential information to address the differential roles of Y1 and Y2 receptors in regulating the release of GH under fed and fasting states
-
Our results showed the altered expression of NPY, Y1R and Y2R but not Y5R in hippocampus and temporal lobe cortex of tremor rat brain.
-
Data from knockout (KO) mice suggest roles for neuropeptide Y (NPY) and NPY2 receptors in fear acquisition/fear stimulus discrimination. Npy1r/Npy2r double KO mice display excessive recall of conditioned fear/impaired fear extinction.
-
NPY Y2 receptors control the level of hyperactive behavior under conditions of limited food access.
-
Peripheral Y2 receptor signaling is critical in the regulation of oxidative fuel selection and physical activity and protects against high-fat diet-induced obesity.
-
Data show that Y2R is mostly presynaptic, coexists with NPY and NPY Y1R, and suggest that Y2Rs thus have a modulatory role in mediating presynaptic neurotransmitter release.
-
NPY-Y2 receptor exerts a direct control over both the tonic and phasic release of dopamine
-
Data describe the complex interaction between Y2/Y4 receptors in control of bone mass, and suggest that the reduction in cortical bone observed in the absence of leptin is due to the anti-osteogenic effect of elevated hypothalamic NPY levels.
-
Data from studies in knockout mice suggest that signaling through Y2 receptor prevents development of long-term anxiety-/depression-like behaviour caused by acute immune challenge. Study includes comparison with Y4 receptor knockout mice.
-
Taken together, this work demonstrates the critical roles of Y2 and Y4 receptors in the regulation of body composition and energy metabolism, highlighting dual antagonism of Y2 and Y4 receptors as a potentially effective anti-obesity treatment.
-
PYY/PYY(3-36) potently inhibits basal and stress/serotonin/cholinergic-stimulated propulsive colonic motor function in conscious mice, likely via Y(2) receptors
-
data reveal an anti-osteogenic effect of Y2 receptors on hypothalamic NPY-expressing neurons on trabecular but not on cortical bone
-
In Y2 knockout mice motor activity in the antrum was more affected than that in the duodenum, and both fed and fasted motor activities were affected in the antrum.
