The neuroprotective and neurogenic effects of neuropeptide Y administration in an animal model of hippocampal neurodegeneration and temporal lobe epilepsy induced by trimethyltin

Corvino, Valentina; Marchese, Elisa; Giannetti, Stefano; Lattanzi, Wanda; Bonvissuto, Davide; Biamonte, Filippo; Mongiovì, Adriana Maria; Michetti, Fabrizio; Geloso, Maria Concetta

doi:10.1111/j.1471-4159.2012.07770.x

Cited by 47 publications

(53 citation statements)

References 71 publications

(106 reference statements)

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“…Furthermore, modulation of the NPY system could be involved in regulation of alcohol-induced reactive neurogenesis. For example, neurotoxin-induced reactive neurogenesis can be enhanced with exogenous NPY treatment (Corvino et al, 2012), while seizure-induced neurogenesis is attenuated in NPY knockout mice (Howell et al, 2007). Importantly, alcohols effects on NPY mirror its effects on adult neurogenesis observed following alcohol dependence.…”

Section: Potential Mechanisms Of Alcohol's Effects On Adult Neurogmentioning

confidence: 99%

Alcohol and adult hippocampal neurogenesis: Promiscuous drug, wanton effects

Geil

Hayes

McClain

et al. 2014

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Adult neurogenesis is now widely accepted as an important contributor to hippocampal integrity and function but also dysfunction when adult neurogenesis is affected in neuropsychiatric diseases such as alcohol use disorders. Excessive alcohol consumption, the defining characteristic of alcohol use disorders, results in a variety of cognitive and behavioral impairments related wholly or in part to hippocampal structure and function. Recent preclinical work has shown that adult neurogenesis may be one route by which alcohol produces hippocampal neuropathology. Alcohol is a pharmacologically promiscuous drug capable of interfering with adult neurogenesis through multiple mechanisms. This review will discuss the primary mechanisms underlying alcohol-induced changes in adult hippocampal neurogenesis including alcohol's effects on neurotransmitters, CREB and its downstream effectors, and the neurogenic niche.

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Section: Potential Mechanisms Of Alcohol's Effects On Adult Neurogmentioning

confidence: 99%

Alcohol and adult hippocampal neurogenesis: Promiscuous drug, wanton effects

Geil

Hayes

McClain

et al. 2014

Progress in Neuro-Psychopharmacology and Biological Psychiatry

View full text Add to dashboard Cite

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“…BDNF modulates hippocampal plasticity and hippocampal-dependent memory (Egan et al, 2003), dopaminergic reward processing (Pecina et al, 2014), as well as cocaine and alcohol responses (Horger et al, 1999; Lu et al, 2004; Jeanblanc et al, 2009). Multiple studies have demonstrated that BDNF induces Npy expression (Scharfman and MacLusky, 2008; Yoshimura et al, 2009), and likewise, NPY administration up-regulates Bdnf expression (Corvino et al, 2012; Croce et al, 2013). In agreement with those findings, the expression of Bdnf was observed to be significantly lower in both Npy −/− and Npy +/− rats compared to WT controls (Fig.…”

Section: Resultsmentioning

confidence: 99%

Npy deletion in an alcohol non-preferring rat model elicits differential effects on alcohol consumption and body weight

Qiu

Bell

Cao

et al. 2016

Journal of Genetics and Genomics

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Neuropeptide Y (NPY) is widely expressed in the central nervous system and influences many physiological processes. It is located within the rat quantitative trait locus (QTL) for alcohol preference on chromosome 4. Alcohol-nonpreferring (NP) rats consume very little alcohol, but have significantly higher NPY expression in the brain than alcohol-preferring (P) rats. We capitalized on this phenotypic difference by creating an Npy knockout (KO) rat using the inbred NP background to evaluate NPY effects on alcohol consumption. Zinc finger nuclease (ZNF) technology was applied, resulting in a 26-bp deletion in the Npy gene. RT-PCR, Western blotting and immunohistochemistry confirmed the absence of Npy mRNA and protein in KO rats. Alcohol consumption was increased in Npy+/− but not Npy−/− rats, while Npy−/− rats displayed significantly lower body weight when compared to Npy+/+ rats. In whole brain tissue, expression levels of Npy-related and other alcohol-associated genes, Npy1r, Npy2r, Npy5r, Agrp, Mc3r, Mc4r, Crh and Crh1r, were significantly greater in Npy−/− rats, whereas Pomc and Crhr2 expressions were highest in Npy+/− rats. These findings suggest that the NPY-system works in close coordination with the melanocortin (MC) and corticotropin-releasing hormone (CRH) systems to modulate alcohol intake and body weight.

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“…Treatment with NPY has been shown to have therapeutic effects for both kainate-and trimethyltin-induced seizure models of temporal lobe epilepsy (43,44). The major protective effect of NPY in these models is thought to be through direct stimulation of neurons.…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide Y Negatively Influences Monocyte Recruitment to the Central Nervous System during Retrovirus Infection

Woods

Carmody

et al. 2016

J Virol

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Monocyte infiltration into the CNS is a hallmark of several viral infections of the central nervous system (CNS), including retrovirus infection.Understanding the factors that mediate monocyte migration in the CNS is essential for the development of therapeutics that can alter the disease process. In the current study, we found that neuropeptide Y (NPY) suppressed monocyte recruitment to the CNS in a mouse model of polytropic retrovirus infection. NPY ؊/؊ mice had increased incidence and kinetics of retrovirus-induced neurological disease, which correlated with a significant increase in monocytes in the CNS compared to wildtype mice. Both Ly6C hi inflammatory and Ly6C lo alternatively activated monocytes were increased in the CNS of NPY ؊/؊ mice following virus infection, suggesting that NPY suppresses the infiltration of both cell types. Ex vivo analysis of myeloid cells from brain tissue demonstrated that infiltrating monocytes expressed high levels of the NPY receptor Y2R. Correlating with the expression of Y2R on monocytes, treatment of NPY ؊/؊ mice with a truncated, Y2R-specific NPY peptide suppressed the incidence of retrovirus-induced neurological disease. These data demonstrate a clear role for NPY as a negative regulator of monocyte recruitment into the CNS and provide a new mechanism for suppression of retrovirus-induced neurological disease. IMPORTANCEMonocyte recruitment to the brain is associated with multiple neurological diseases. However, the factors that influence the recruitment of these cells to the brain are still not well understood. In the current study, we found that neuropeptide Y, a protein produced by neurons, affected monocyte recruitment to the brain during retrovirus infection. We show that mice deficient in NPY have increased influx of monocytes into the brain and that this increase in monocytes correlates with neurological-disease development. These studies provide a mechanism by which the nervous system, through the production of NPY, can suppress monocyte trafficking to the brain and reduce retrovirus-induced neurological disease. The recruitment of monocytes into the central nervous system (CNS) is associated with a number of neurological diseases. Monocyte recruitment to the CNS has been reported for traumatic brain injury (TBI), misfolded-protein diseases, and multiple sclerosis (MS), as well as many different viral infections, including West Nile virus (WNV), herpes simplex virus (HSV), and retroviruses, such as HIV (1-4). Monocyte trafficking is particularly important for retrovirus-induced neurological diseases, as monocytes are susceptible to retrovirus infection (5, 6).Monocytes recruited to the CNS may contribute to pathogenesis in these neurological diseases. Decreased cognitive performance correlated with increased monocyte infiltration in HIVassociated neurocognitive disorders (HAND) (1). Additionally, infiltration of monocytes was found to be important for seizure development in a mouse model of Theiler's murine encephalitis (7). Recent studies in a mouse mo...

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The neuroprotective and neurogenic effects of neuropeptide Y administration in an animal model of hippocampal neurodegeneration and temporal lobe epilepsy induced by trimethyltin

Cited by 47 publications

References 71 publications

Alcohol and adult hippocampal neurogenesis: Promiscuous drug, wanton effects

Alcohol and adult hippocampal neurogenesis: Promiscuous drug, wanton effects

Npy deletion in an alcohol non-preferring rat model elicits differential effects on alcohol consumption and body weight

Neuropeptide Y Negatively Influences Monocyte Recruitment to the Central Nervous System during Retrovirus Infection

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