Neuropeptide Y Produces Anxiety Via Y2-Type Receptors

Nakajima, Mitsutoshi; Inui, Akio; Asakawa, Akihiro; Momose, Kazuhiro; Ueno, Naohiko; Teranishi, A.; Baba, Shigeaki; Kasuga, Masato

doi:10.1016/s0196-9781(97)00298-2

Cited by 109 publications

(66 citation statements)

References 27 publications

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“…According to some earlier results obtained by our group and by other authors (Sajdyk et al, 1999;Wierońska et al, 2004Wierońska et al, , 2005, NPY shows anxiolytic activity in the amygdala, and this effect is mediated by Y1 receptors, as it is blocked by BIBO 3304. Moreover, Y2 receptors have been suggested to have an opposite, anxiogenic function (Nakajima et al, 1998;Sajdyk et al, 2002;Tschenett et al, 2003). Our present study indicates that in the hippocampus both Y1 and Y2 receptors seem to be implicated in the antianxiety effect of NPY, but differently in CA1 and DG.…”

Section: Anxiolytic Effect Of Intrahippocampal Mglur Ligands and Npy mentioning

confidence: 45%

The Effect of Intrahippocampal Injection of Group II and III Metobotropic Glutamate Receptor Agonists on Anxiety; the Role of Neuropeptide Y

Śmiałowska

Wierońska

Domin

et al. 2006

Neuropsychopharmacol

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Earlier studies conducted by our group and by other authors indicated that metabotropic glutamatergic receptor (mGluR) ligands might have anxiolytic activity and that amygdalar neuropeptide Y (NPY) neurons were engaged in that effect. Apart from the amygdala, the hippocampus, another limbic structure, also seems to be engaged in regulation of anxiety. It is rich in mGluRs and contains numerous NPY interneurons. In the present study, we investigated the anxiolytic activity of group II and III mGluR agonists after injection into the hippocampus, and attempted to establish whether hippocampal NPY neurons and receptors were engaged in the observed effects. Male Wistar rats were bilaterally microinjected with the group II mGluR agonist (2S,, NPY, the Y1 receptor antagonist BIBO 3304, and the Y2 receptor antagonist BIIE 0246 into the CA1 or dentate area (DG). The effect of those compounds on anxiety was tested in the elevated plus-maze. Moreover, the effects of L-CCG-I and L-SOP on the expression of NPYmRNA in the hippocampus were studied using in situ hybridization method. It was found that a significant anxiolytic effect was induced by L-SOP injection into the CA1 region or by L-CCG-I injection into the DG. The former effect was inhibited by BIBO 3304, the latter by BIIE 0246. NPY itself showed antianxiety action after injection into both structures. In the CA1 area, the effect of NPY was prevented by BIBO 3304, whereas in the DG by BIIE 0246. Both the mGluR agonists L-CCG-I and L-SOP induced a potent increase in NPYmRNA expression in the DG region of the hippocampal formation. The obtained results indicate that group II and III mGluR agonists, L-CCG-I and L-SOP, as well as NPY display anxiolytic activity in the hippocampus, but act differently in the CA1 and DG. It was observed that group III mGluRs and Y1 receptors were engaged in the response in the CA1 area, whereas group II mGluRs and Y2 receptors played a pivotal role in the DG region.

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Section: Anxiolytic Effect Of Intrahippocampal Mglur Ligands and Npy mentioning

confidence: 45%

The Effect of Intrahippocampal Injection of Group II and III Metobotropic Glutamate Receptor Agonists on Anxiety; the Role of Neuropeptide Y

Śmiałowska

Wierońska

Domin

et al. 2006

Neuropsychopharmacol

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“…For example, it has been shown that intracerebroventricular application of NPY elicits an anxiolytic effect (Heilig et al, 1989;Karlsson et al, 2005;Nakajima et al, 1998). Moreover, reduced anxiety-related behavior was found in the EPM in rats with upregulated NGUYEN et al…”

Section: Possible Mechanism(s) Underlying the Altered Challenge-indumentioning

confidence: 99%

“…Furthermore, NPY has a critical role in the regulation of anxiety-like responses as results from behavioral experiments indicate that central administration of NPY induces anxiolytic-like effects in various animal paradigms including the elevated plus maze (EPM), light/dark test, Montgomery's and Vogel's conflict tests (Heilig et al, 1989Karlsson et al, 2005;Kask et al, 1998;Nakajima et al, 1998;Pich et al, 1993). Accumulating evidence indicates that the anxiolytic-like response of NPY is mediated via Y1 receptors.…”

Section: Introductionmentioning

confidence: 99%

Effect of neuropeptide Y Y2 receptor deletion on emotional stress‐induced neuronal activation in mice

Nguyen

Sartori

Herzog

et al. 2008

Synapse

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In different behavioral paradigms including the elevated plus maze (EPM), it was observed previously that deletion of the neuropeptide Y Y2 receptor subtype results in potent suppression of anxiety-related and stress-related behaviors. To identify neurobiological correlates underlying this behavioral reactivtiy, expression of c-Fos, an established early marker of neuronal activation, was examined in Y2 receptor knockout (Y2 −/− ) vs. wildtype (WT) mice. Mice were placed on the open arm (OA) or closed arm (CA) of the EPM for 10 min and the effect on regional c-Fos expression in the brain was investigated. The number of c-Fos positive neurons was significantly increased in both WT and Y2 −/− lines after OA and CA exposure in 51 of 54 regions quantified. These regions included various cortical, limbic, thalamic, hypothalamic, and hindbrain regions. Genotype influenced c-Fos responses to arm exposures in 6 of the 51 activated regions: the cingulate cortex, barrel field of the primary somatosensory cortex, nucleus accumbens, dorsal lateral septum, amygdala and lateral periaqueductal gray. These differences in neuronal activity responses to the novel environments were more pronounced after OA than after CA exposure. Mice lacking Y2 receptors exhibited reduced neuronal activation when compared to WT animals in response to the emotional stressors. Reduced neuronal excitability in the identified brain areas relevant to the processing of motivated, explorative as well as anxiety-related behaviors is suggested to contribute to the reduced anxiety-related behavior observed in Y2 −/− mice.

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“…(Britton et al, 1997(Britton et al, , 2000Broqua et al, 1995;Heilig et al, 1989;Nakajima et al, 1998). In contrast, NPY Y2 receptor agonists decrease the percent time spent in the open arms of the plus maze, which is indicative of increased levels of anxiety (Nakajima et al, 1998). I.c.v.…”

Section: Introductionmentioning

confidence: 99%

Effects of Altered Amygdalar Neuropeptide Y Expression on Anxiety-Related Behaviors

Primeaux

Wilson

Cusick

et al. 2005

Neuropsychopharmacol

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Neuropeptide Y (NPY) decreases anxiety-related behaviors in various animal models of anxiety. The purpose of the present study was to examine the role of the amygdalar NPY system in anxiety-related responses in the elevated plus maze. The first experiment determined if herpes virus-mediated alterations in amygdalar NPY levels would alter anxiety-related behaviors in the elevated plus maze. Viral vectors encoding NPY, NPY antisense, or LacZ (control virus) were bilaterally injected into the amygdala, and 4 days postinjection, rats were tested in the elevated plus maze test. NPY-like immunoreactivity (NPY-ir) was measured in the amygdala of these rats. In rats injected with the viral vector encoding NPY, reduced anxiety-related behaviors in the elevated plus maze accompanied by moderate increases in NPY-ir were detected compared to NPY-antisense viral vector-treated subjects. Elevated plus maze behavior did not differ compared to LacZ-treated controls. NPY overexpression at this time point was also suggested by enhanced NPY mRNA expression seen in the amygdala 4 days postinjection using real-time polymerase chain reaction analysis. Experiment 2 was conducted to provide further evidence for a role of amygdalar NPY in regulating anxiety-related behaviors in the elevated plus maze test. The nonpeptide NPY Y1 receptor antagonist, BIBP 3226 (1.5 mg/ml), was bilaterally injected into the amygdala and rats were tested in the elevated plus maze test. Rats receiving BIBP 3226 exhibited increased anxiety-related behaviors in this test. The results of these experiments provide further support for the role of amygdalar NPY in anxiety-related behaviors. Neuropsychopharmacology (2005) 30, 1589-1597.

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Neuropeptide Y Produces Anxiety Via Y2-Type Receptors

Cited by 109 publications

References 27 publications

The Effect of Intrahippocampal Injection of Group II and III Metobotropic Glutamate Receptor Agonists on Anxiety; the Role of Neuropeptide Y

The Effect of Intrahippocampal Injection of Group II and III Metobotropic Glutamate Receptor Agonists on Anxiety; the Role of Neuropeptide Y

Effect of neuropeptide Y Y2 receptor deletion on emotional stress‐induced neuronal activation in mice

Effects of Altered Amygdalar Neuropeptide Y Expression on Anxiety-Related Behaviors

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