Differential effects of methamphetamine on expression of neuropeptide Y mRNA in hypothalamus and on serum leptin and ghrelin concentrations in ad libitum-fed and schedule-fed rats

Crowley, William R.; Ramoz, Gina; Keefe, Kristen A.; Torto, Rita; Kalra, Satya P.; Hanson, Glen R.

doi:10.1016/j.neuroscience.2004.11.037

Cited by 33 publications

(20 citation statements)

References 40 publications

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“…This result confirmed that NPY gene was involved in regulating both the anorectic response of PPA, which was related to a decrease of NPY, and the tolerant response of PPA, which was relevant to the restoration of NPY gene expression (Hsieh et al 2007b). Together with previous reports indicating that NPY gene participates in the anorectic effect of AMPH (Hsieh et al 2006), methAMPH (Crowley et al 2005), and ephedrine (Kim et al 2004), it is suggested that NPY gene may be a critical mediator for appetite-suppressing effect of AMPH-like anorectic drugs which release monoamine from nerve cells by acting as substrates for biogenic amine transporters (Alexander et al 2005).…”

Section: Discussionsupporting

confidence: 89%

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Roles of protein kinase Cα isozyme in the regulation of oxidative stress and neuropeptide Y gene expression in phenylpropanolamine‐mediated appetite suppression

Kuo

Yang

Chu

et al. 2009

Journal of Neurochemistry

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Hypothalamic neuropeptide Y (NPY) is an appetite stimulant in the brain. Although regulation of NPY expression has been reported to contribute to the appetite‐suppressing effect of phenylpropanolamine (PPA), it is still unknown if protein kinase C (PKC) is involved in this effect. Rats were daily treated with PPA for 4 days. Changes in food intake, hypothalamic NPY, PKC, and proopiomelanocortin (POMC) mRNA levels were assessed and compared. Results showed that the NPY gene was down‐regulated following PPA treatment, which was parallel with the decrease of feeding. Moreover, several isotypes of PKC mRNA level (α, βI, βII, γ, δ, η, λ, ε, and ζ) were changed. Among these, α, δ, and λ PKC were up‐regulated along with POMC gene expression which coincided with down‐regulation of the NPY gene. To further determine if PKCα was involved, infusions of antisense oligonucleotide into the cerebroventricle were performed at 1 h before daily PPA treatment in free‐moving rats. Results showed that PKCα knock‐down could modify both anorexia induced by PPA and the NPY mRNA levels. Moreover, PKCα knock‐down could also modify superoxide dismutase (SOD) gene expression. It is suggested that PKCα participates in the regulation of PPA‐mediated appetite suppression via the modulation of NPY and SOD gene expression.

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Section: Discussionsupporting

confidence: 89%

“…Together with previous reports indicating that NPY gene participates in the anorectic effect of AMPH (Hsieh et al. 2006), methAMPH (Crowley et al. 2005), and ephedrine (Kim et al.…”

Section: Discussionsupporting

confidence: 86%

Roles of protein kinase Cα isozyme in the regulation of oxidative stress and neuropeptide Y gene expression in phenylpropanolamine‐mediated appetite suppression

Kuo

Yang

Chu

et al. 2009

Journal of Neurochemistry

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“…Similarly, an acute single dose of METH increased NPY mRNA expression in both rat hypothalamic arcuate and dorsomedial nuclei, but in food‐deprived mice NPY mRNA expression was no longer upregulated (Crowley et al . ). These observations suggest that METH‐induced alterations in NPY in the hypothalamus may depend on feeding conditions.…”

Section: Psychostimulant Drugsmentioning

confidence: 97%

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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“…Therefore, NPY might be essential for the appetite‐suppressing effect of AMPH‐like anorectic drugs as it participated in the anorectic effect of AMPH (Hsieh et al. 2006), methAMPH (Crowley et al. 2005) and ephedrine (Kim et al.…”

Section: Discussionmentioning

confidence: 99%

The effect of protein kinase C‐delta knockdown on anti‐free radical enzyme and neuropeptide Y gene expression in phenylpropanolamine‐treated rats

Kuo

Yang

Chu

et al. 2010

Journal of Neurochemistry

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J. Neurochem. (2010) 114, 1217–1230. Abstract Hypothalamic neuropeptide Y (NPY) has been reported to involve in regulating behavioral response of phenylpropanolamine (PPA), a sympathomimetic agent. This study explored if protein kinase C (PKC)‐δ signaling participated in this regulation. Moreover, possible roles of anti‐free radical enzyme catalase (CAT) and nitrogen oxide synthase (NOS) were also examined. Rats were treated daily with PPA for 4 days. Changes in food intake and hypothalamic NPY, PKCδ, CAT, and NOS contents were assessed and compared. Results showed that PKCδ and CAT increased during PPA treatment, which were concomitant with decreases in NPY content and food intake, while the change of NOS was expressed differently. Moreover, PKCδ knockdown could modify PPA anorexia as well as NPY and CAT expression, while NOS expression remained unchanged. Furthermore, pre‐treatment with NOS inhibitor could modify both PPA anorexia and NPY content. It is suggested that PKCδ participates in the anorectic response of PPA via the modulation of NPY and CAT, while NOS contribute to this modulation via a different mechanism during PPA treatment. Results provide molecular mechanism of NPY‐mediated PPA anorexia and may aid the therapeutic research of PPA and other anti‐obesity drugs.

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Differential effects of methamphetamine on expression of neuropeptide Y mRNA in hypothalamus and on serum leptin and ghrelin concentrations in ad libitum-fed and schedule-fed rats

Cited by 33 publications

References 40 publications

Roles of protein kinase Cα isozyme in the regulation of oxidative stress and neuropeptide Y gene expression in phenylpropanolamine‐mediated appetite suppression

Roles of protein kinase Cα isozyme in the regulation of oxidative stress and neuropeptide Y gene expression in phenylpropanolamine‐mediated appetite suppression

Effects of drugs of abuse on the central neuropeptide Y system

The effect of protein kinase C‐delta knockdown on anti‐free radical enzyme and neuropeptide Y gene expression in phenylpropanolamine‐treated rats

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