Modulation of methamphetamine-induced nitric oxide production by neuropeptide Y in the murine striatum

Yarosh, Haley L.; Angulo, Jesús A.

doi:10.1016/j.brainres.2012.09.013

Cited by 8 publications

(6 citation statements)

References 48 publications

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“…). More recently, it was also demonstrated that the administration of both Y 1 R and Y 2 R agonists attenuate METH‐induced striatal upregulation of 3‐nitrotyrosine, oxide nitric and caspase‐3, events that usually precede apoptosis (Yarosh & Angulo ). Additionally, it is important to highlight that METH by itself can interfere with NPY system.…”

Section: Psychostimulant Drugsmentioning

confidence: 99%

Effects of drugs of abuse on the central neuropeptide Y system

et al. 2015

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Neuropeptide Y (NPY), which is widely expressed in the central nervous system is involved in several neuropathologies including addiction. Here we comprehensively and systematically review alterations on the central NPY system induced by several drugs. We report on the effects of psychostimulants [cocaine, amphetamine, methamphetamine, 3,4-methylenedioxymethamphetamine (MDMA) and nicotine], ethanol, and opioids on NPY protein levels and expression of different NPY receptors. Overall, expression and function of NPY and its receptors are changed under conditions of drug exposure, thus affecting several physiologic behaviors, such as feeding, stress and anxiety. Drugs of abuse differentially affect the components of the NPY system. For example methamphetamine and nicotine lead to a consistent increase in NPY mRNA and protein levels in different brain sites whereas ethanol and opioids decrease NPY mRNA and protein expression. Drug-induced alterations on the different NPY receptors show more complex regulation pattern. Manipulation of the NPY system can have opposing effects on reinforcing and addictive properties of drugs of abuse. NPY can produce pro-addictive effects (nicotine and heroin), but can also exert inhibitory effects on addictive behavior (AMPH, ethanol). Furthermore, NPY can act as a neuroprotective agent in chronically methamphetamine and MDMA-treated rodents. In conclusion, manipulation of the NPY system seems to be a potential target to counteract neural alterations, addiction-related behaviors and cognitive deficits induced by these drugs.

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Section: Psychostimulant Drugsmentioning

confidence: 99%

Effects of drugs of abuse on the central neuropeptide Y system

et al. 2015

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“…Therefore, over-expression of NPY could potentially be utilized to increase autophagic breakdown of toxic ubiquinated aggregates in ALS Suppression of intracellular lipid peroxides is one of the main mechanisms by which the ALS therapeutic Edaravone is thought to supress the death of motor neurons in ALS patients, alongside reducing the production of reactive oxygen species (Homma, Kobayashi, Sato, & Fujii, 2019). NPY has also been implicated in the attenuation of oxidative stress through inhibition of reactive oxidative species via Y1 and Y2 receptor modulation (Yarosh & Angulo, 2012).…”

Section: F I G U R Ementioning

confidence: 99%

Pathogenic or protective? Neuropeptide Y in amyotrophic lateral sclerosis

Clark

Hoyle

et al. 2020

Journal of Neurochemistry

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Neuropeptide Y (NPY) is an endogenous peptide of the central and enteric nervous systems which has gained significant interest as a potential neuroprotective agent for treatment of neurodegenerative disease. Amyotrophic lateral sclerosis (ALS) is an aggressive and fatal neurodegenerative disease characterized by motor deficits and motor neuron loss. In ALS, recent evidence from ALS patients and animal models has indicated that NPY may have a role in the disease pathogenesis. Increased NPY levels were found to correlate with disease progression in ALS patients. Similarly, NPY expression is increased in the motor cortex of ALS mice by end stages of the disease. Although the functional consequence of increased NPY levels in ALS is currently unknown, NPY has been shown to exert a diverse range of neuroprotective roles in other neurodegenerative diseases; through modulation of potassium channel activity, increased production of neurotrophins, inhibition of endoplasmic reticulum stress and autophagy, reduction of excitotoxicity, oxidative stress, neuroinflammation and hyperexcitability. Several of these mechanisms and signalling pathways are heavily implicated in the pathogenesis of ALS. Therefore, in this review, we discuss possible effects of NPY and NPY‐receptor signalling in the ALS disease context, as determining NPY’s contribution to, or impact on, ALS disease mechanisms will be essential for future studies investigating the NPY system as a therapeutic strategy in this devastating disease.

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“…Exposure to METH increases the levels of preproNPY mRNA suggesting increased utilization of this neuropeptide [34]. In addition, genetic and pharmacological studies demonstrate that NPY counters the damaging effects of METH, protecting striatal neurons from this psychostimulant [61,69]. The same population of striatal interneurons making NPY also makes the neuropeptide somatostatin [41].…”

Section: Discussionmentioning

confidence: 99%

“…We have found that the striatal neuropeptide substance P synergizes with METH in elevating the production of nitric oxide [64] and consequently striatal injury [73]. Interestingly, two other striatal neuropeptides, somatostatin and neuropeptide Y, attenuate the METH-induced striatal production of nitric oxide [1,69]. In addition to endogenous agents such as neuropeptides, it is advantageous to identify exogenous substances that ameliorate oxidative stress and thus could be neuroprotective in the presence of METH.…”

Section: Introductionmentioning

confidence: 99%

Protection against Methamphetamine-Induced Striatal Apoptosis by Epigallocatechin Gallate (EGCG) in the Mouse Brain

Liu¹,

Hazan²,

Eaton³

et al. 2014

J Drug Alcohol Res

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Methamphetamine (METH) is a psychostimulant abused worldwide and shown to be neurotoxic to both dopamine terminals and striatal neurons. Thus it would be advantageous to discover natural compounds that protect the brain from the METH-induced neural injury. In the present study, we tested the ability of epigallocatechin gallate (EGCG), the most abundant antioxidant in green tea, to attenuate the METH-induced striatal injury. A dose of 2 mg/kg of EGCG (IP) given 30 min prior to METH (30 mg/kg, IP) significantly reduced the METH-induced depletion of striatal tyrosine hydroxylase (a marker of the dopamine terminals) and the apoptosis of some striatal neurons. Moreover, the neuroprotective effects exerted by EGCG in the striatum were independent of the METH-induced hyperthermia. Our data are consistent with the hypothesis that active ingredients in green tea are neuroprotective in the presence of METH and may prove useful in halting the progress of some neurodegenerative diseases of the nervous system and for the treatment of drug abuse.

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Modulation of methamphetamine-induced nitric oxide production by neuropeptide Y in the murine striatum

Cited by 8 publications

References 48 publications

Effects of drugs of abuse on the central neuropeptide Y system

Effects of drugs of abuse on the central neuropeptide Y system

Pathogenic or protective? Neuropeptide Y in amyotrophic lateral sclerosis

Protection against Methamphetamine-Induced Striatal Apoptosis by Epigallocatechin Gallate (EGCG) in the Mouse Brain

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