Anxiolytic-like effects after vector-mediated overexpression of neuropeptide Y in the amygdala and hippocampus of mice

Christiansen, Søren H.; Olesen, Mikkel Vestergaard; Gøtzsche, Casper René

doi:10.1016/j.npep.2014.09.004

Cited by 23 publications

(10 citation statements)

References 76 publications

(98 reference statements)

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“…Studies have confirmed that NPY neurons are involved in the regulation of anxiety in mice ( 128 ). Moreover, direct injection or overexpression of NPY in the brain exerts anti-anxiety effects in rodents ( 129 ), and knockout of NPY exacerbates the anxiety phenotype in mice ( 130 ). In rodents, the alleviation of anxiety caused by overexpression of Y1R also corroborates the above findings ( 131 ).…”

Section: Npy Indirectly Regulates the Immune Responsementioning

confidence: 99%

Neuropeptide Y Is an Immunomodulatory Factor: Direct and Indirect

Chen

Liu

et al. 2020

Front. Immunol.

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Neuropeptide Y (NPY), which is widely distributed in the nervous system, is involved in regulating a variety of biological processes, including food intake, energy metabolism, and emotional expression. However, emerging evidence points to NPY also as a critical transmitter between the nervous system and immune system, as well as a mediator produced and released by immune cells. In vivo and in vitro studies based on gene-editing techniques and specific NPY receptor agonists and antagonists have demonstrated that NPY is responsible for multifarious direct modulations on immune cells by acting on NPY receptors. Moreover, via the central or peripheral nervous system, NPY is closely connected to body temperature regulation, obesity development, glucose metabolism, and emotional expression, which are all immunomodulatory factors for the immune system. In this review, we focus on the direct role of NPY in immune cells and particularly discuss its indirect impact on the immune response.

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Section: Npy Indirectly Regulates the Immune Responsementioning

confidence: 99%

Neuropeptide Y Is an Immunomodulatory Factor: Direct and Indirect

Chen

Liu

et al. 2020

Front. Immunol.

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“…Genetic studies in humans and rodents found that lower NPY levels are associated with more anxiety and higher reactivity to emotional and stressful challenges (Bannon et al 2000, Heilig 2004, Zhou et al 2008, Mickey et al 2011, Domschke et al 2010. Conversely, overexpression of NPY in hippocampus or amygdala in transgenic rats or with viral vectors produced anxiolytic-like effects (Thorsell et al 2000, Christiansen et al 2014.…”

Section: Neuropeptide Y and Resilience To Harmful Effects Of Stressmentioning

confidence: 99%

Potential of neuropeptide Y for preventing or treating post-traumatic stress disorder

2016

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There is extensive evidence that NPY in the brain can modulate the responses to stress and play a critical role in resistance to, or recovery from, harmful effects of stress. Development of PTSD and comorbid depression following exposure to traumatic stress are associated with low NPY. This review discusses putative mechanisms for NPY's anti-stress actions. Recent preclinical data indicating potential for intranasal delivery of NPY to brain as a promising non-invasive strategy to prevent a variety of neuroendocrine, molecular and behavioral impairments in PTSD model are summarized.

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“…Neuropeptide-receptor systems are thought to modulate these behaviors in the amygdala. For example, Neuropeptide Y (NPY), a peptide involved in regulation of feeding in the hypothalamus, has been shown to produce anxiolytic effects and lead to resilience after stress (Sajdyk et al, 2008;Desai et al, 2013;Christiansen et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

The BigLEN-GPR171 Peptide Receptor System Within the Basolateral Amygdala Regulates Anxiety-Like Behavior and Contextual Fear Conditioning

Bobeck

Gomes

Pena

et al. 2017

Neuropsychopharmacol.

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Studies show that neuropeptide-receptor systems in the basolateral amygdala (BLA) play an important role in the pathology of anxiety and other mood disorders. Since GPR171, a recently deorphanized receptor for the abundant neuropeptide BigLEN, is expressed in the BLA, we investigated its role in fear and anxiety-like behaviors. To carry out these studies we identified small molecule ligands using a homology model of GPR171 to virtually screen a library of compounds. One of the hits, MS0021570_1, was identified as a GPR171 antagonist based on its ability to block (i) BigLEN-mediated activation of GPR171 in heterologous cells, (ii) BigLEN-mediated hyperpolarization of BLA pyramidal neurons, and (iii) feeding induced by DREADD-mediated activation of BigLEN containing AgRP neurons in the arcuate nucleus. The role of GPR171 in anxiety-like behavior or fear conditioning was evaluated following systemic or intra-BLA administration of MS0021570_1, as well as following lentiviral-mediated knockdown of GPR171 in the BLA. We find that systemic administration of MS0021570_1 attenuates anxiety-like behavior while intra-BLA administration or knockdown of GPR171 in the BLA reduces anxiety-like behavior and fear conditioning. These results indicate that the BigLEN-GPR171 system plays an important role in these behaviors and could be a novel target to develop therapeutics to treat psychiatric disorders.

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Anxiolytic-like effects after vector-mediated overexpression of neuropeptide Y in the amygdala and hippocampus of mice

Cited by 23 publications

References 76 publications

Neuropeptide Y Is an Immunomodulatory Factor: Direct and Indirect

Neuropeptide Y Is an Immunomodulatory Factor: Direct and Indirect

Potential of neuropeptide Y for preventing or treating post-traumatic stress disorder

The BigLEN-GPR171 Peptide Receptor System Within the Basolateral Amygdala Regulates Anxiety-Like Behavior and Contextual Fear Conditioning

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