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Brain research bulletin 16건

  1. [해외논문]   Editorial Board   SCI SCIE


    Brain research bulletin v.138 ,pp. ii - ii , 2018 , 0361-9230 ,

    초록

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  2. [해외논문]   Addiction: A multi-determined chronic disease   SCI SCIE

    Grigson, Patricia Sue
    Brain research bulletin v.138 ,pp. 1 - 4 , 2018 , 0361-9230 ,

    초록

    원문보기

    원문보기
    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  3. [해외논문]   Acute ethanol modulation of neurocircuit function in the nucleus of the tractus solitarius   SCI SCIE

    Aimino, Michael A. (Department of Neural and Behavioral Science, Penn State Hershey College of Medicine, United States ) , Coker, Caitlin R. (Graduate Program in Anatomy, Penn State Hershey College of Medicine, United States ) , Silberman, Yuval (Department of Neural and Behavioral Science, Penn State Hershey College of Medicine, United States)
    Brain research bulletin v.138 ,pp. 5 - 11 , 2018 , 0361-9230 ,

    초록

    Abstract The nucleus of the tractus solitarius (NTS) is a brain stem region critical to many physiologic processes and has been implicated in addiction to multiple classes of abused drugs, including alcohol (EtOH). That said, the mechanism by which EtOH modulates NTS neurocircuit activity is not well characterized and has yet to be examined utilizing electrophysiologic methods in mouse models of alcohol use disorders. To begin to address this gap in knowledge, we sought to use whole-cell and cell-attached recordings to determine the mechanism of acute EtOH action on GABAergic and glutamatergic neurotransmission, as well as on action potential firing in the NTS of adult male, EtOH naIve mice. Bath application of EtOH (50mM) significantly enhanced the frequency of spontaneous inhibitory postsynaptic current events, while increasing the amplitude of these events in half of the neurons tested. This finding suggests a presynaptic mechanism of EtOH action on GABAergic transmission in the NTS as well as a postsynaptic mechanism in subsets of NTS neurons. EtOH application was further associated with a significant decrease in action potential firing in most, but not all, NTS neurons tested. EtOH induced a small but significant decrease in spontaneous excitatory postsynaptic current frequency, indicating that EtOH may also inhibit NTS glutamatergic signaling to some degree. Intriguingly, in vivo EtOH exposure (4g/kg IP) enhanced c-FOS colocalization with tyrosine hydroxylase via immunohistochemical methods, indicating that NTS norepinephrine neurons may be activated by acute EtOH exposure. Although future work is needed, the current data indicate that acute EtOH may enhance GABAergic signaling in local NTS circuits resulting in disinhibition of NTS norepinephrine neurons. Such a finding has important implications in understanding the role of the NTS in the development of alcoholism. Highlights EtOH enhances pre- and post-synaptic GABAergic transmission in the NTS. EtOH has minimal effects on NTS glutamatergic transmission. EtOH decreases action potential firing in a majority of neurons. EtOH enhances c-FOS/tyrosine hydroxylase colocalization in the NTS. EtOH may disinhibit NTS TH neurons by increasing GABA signals between interneurons.

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    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

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  4. [해외논문]   Increased ethanol drinking in “humanized” mice expressing the mu opioid receptor A118G polymorphism are mediated through sex-specific mechanisms   SCI SCIE

    Henderson-Redmond, Angela N (Department of Anesthesiology & Perioperative Medicine, Penn State University College of Medicine, Hershey, PA 17033, United States ) , Lowe, Tammy E (Department of Anesthesiology & Perioperative Medicine, Penn State University College of Medicine, Hershey, PA 17033, United States ) , Tian, Xi B (Department of Anesthesiology & Perioperative Medicine, Penn State University College of Medicine, Hershey, PA 17033, United States ) , Morgan, Daniel J (Department of Anesthesiology & Perioperative Medicine, Penn State University College of Medicine, Hershey, PA 17033, United States)
    Brain research bulletin v.138 ,pp. 12 - 19 , 2018 , 0361-9230 ,

    초록

    Abstract The A118G single nucleotide polymorphism (SNP) of the mu-opioid receptor gene (Oprm1) has been implicated in mediating the rewarding effects of alcohol. Clinical and preclinical studies suggest that the G allele may confer a genetic vulnerability to alcohol dependence, though it remains unknown whether these effects are sex-specific. We used male and female mice homozygous for the “humanized” 118AA or 118GG alleles to determine whether the A118G SNP potentiates ethanol consumption in a sex-specific manner in both the two-bottle choice and drinking-in-the-dark (DID) paradigms. Mice were also assessed for differences in naltrexone sensitivity, ethanol reward assessed via conditioned place preference (CPP), and sensitivity to the sedative/ataxic effects of ethanol using the rota-rod and loss of righting reflex (LORR) assays. We found that male and female 118GG mice drank significantly more ethanol than 118AA littermates using a continuous access, two-bottle choice paradigm. In the limited-access DID drinking model, (i) female (but not male) 118GG mice consumed more ethanol than 118AA mice and (ii) naltrexone pretreatment was equally efficacious at attenuating ethanol intake in both 118AA and 118GG female mice while having no effect in males. Male and female 118GG and female 118AA mice developed a robust conditioned place preference (CPP) for ethanol. Female 118GG mice displayed less sensitivity to the sedative/ataxic effects of ethanol compared to female 118AA mice on both the rota-rod and the LORR assays while male mice did not differ in their responses on either assay. Our findings suggest that increased ethanol consumption in male 118GG mice may be due to increased ethanol reward, while increased drinking in female 118GG mice might be due to decreased sensitivity to the sedative/ataxic effects of ethanol. Collectively, these data might be used to help identify sex-specific pharmacotherapies to combat alcohol use disorders. Highlights 118GG Male and female mice drink more EtOH than 118AA mice. Male A118G mice differed in their response to the rewarding effects of EtOH via CPP. Female A118G mice differed in sensitivity to the sedative/ataxic effects of EtOH. Increased EtOH intake in 118GG mice is likely mediated by sex-specific mechanisms.

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    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  5. [해외논문]   Varenicline modulates ethanol and saccharin consumption in adolescent male and female C57BL/6J mice   SCI SCIE

    Kamens, Helen M. (Corresponding author at: 219 Biobehavioral Health Building, University Park, PA 16802, United States.) , Silva, Constanza , Peck, Colette , Miller, Carley N.
    Brain research bulletin v.138 ,pp. 20 - 25 , 2018 , 0361-9230 ,

    초록

    Abstract Adolescence is a critical period in brain development that coincides with the initiation of alcohol use. Nicotinic acetylcholine receptors (nAChR) have been shown to modulate ethanol behaviors in adult humans and in animal models; however, the role of these receptors in adolescent ethanol behaviors has not been explored. Throughout adolescence, nAChR expression undergoes large-scale developmental changes which may alter behavioral responses to ethanol. Here we examined the effect of varenicline, a nAChR partial agonist, on ethanol consumption, ataxia, sedation, and metabolism in adolescent male and female C57BL/6J mice. The effect of varenicline on ethanol consumption was tested through the Drinking-in-the-Dark (DID) paradigm that models binge-like ethanol consumption. To ensure that results were specific for ethanol, we also tested the effect of varenicline on saccharin consumption. Additionally, varenicline was administered 30min prior to an acute injection of ethanol before being tested for ataxia on the balance beam, sedation using the loss of righting reflex, or ethanol metabolism. Varenicline dose dependently decreased ethanol consumption, but also influenced saccharin intake. Varenicline showed no significant effect on ethanol metabolism, ataxia, or sedation. Unlike its effects in adult animals, varenicline is able to reduce ethanol consumption without increasing the ataxic and sedative effects of ethanol. This work suggests that the neurobiological mechanisms of ethanol behaviors may change across the lifespan and highlights the need for more research on the role of nAChRs in ethanol behaviors throughout development. Highlights Varenicline decreases ethanol consumption in adolescent mice. Varenicline decreases saccharin consumption in adolescent mice. Varenicline does not influence ethanol ataxia, sedation, or metabolism in adolescent mice. Effects of varenicline on ethanol behaviors appear to be age specific.

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    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  6. [해외논문]   Effect of vertical sleeve gastrectomy on alcohol consumption and preferences in dietary obese rats and mice: A plausible role for altered ghrelin signaling   SCI SCIE

    Orellana, Elise R. (Corresponding author at: Penn State University, College of Medicine, 500 University Drive, H109, Hershey, PA 17033, USA.) , Jamis, Catherine , Horvath, Nelli , Hajnal, Andras
    Brain research bulletin v.138 ,pp. 26 - 36 , 2018 , 0361-9230 ,

    초록

    Abstract Vertical sleeve gastrectomy (VSG) and Roux-en-Y gastric bypass (RYGB) are the most common surgical options for the treatment of obesity and metabolic disorder. Whereas RYGB may result in greater and more durable weight loss, recent clinical and pre-clinical studies in rats have raised concerns that RYGB surgery may increase risk for alcohol use disorder (AUD). In contrast, recent clinical reports suggest a lesser risk for AUD following VSG, although no preclinical studies have been done to confirm that. Therefore, the present study sought to determine the effects of VSG on ethanol intake and preferences in rodent models using protocols similar to those previously used in animal studies for RYGB. Male Sprague Dawley rats and male C57B6 mice were made obese on a high fat diet (60%kcal from fat) and received VSG or no surgery (controls). All animals then were given access to increasing concentrations of ethanol (2%, 4%, 6%, and 8%), presented for few days each. Compared to controls, VSG rats consumed significantly less of 2, 6 and 8% ethanol and showed significantly reduced preferences to 6 and 8% ethanol over water. VSG mice also displayed reduced intake and preference for 6 and 8% ethanol solutions. After a two-week period of forced abstinence, 8% ethanol was reintroduced and the VSG rats and mice continued to exhibit reduced consumption and less preference for ethanol. Regarding the underlying mechanism, we hypothesized that the removal of the ghrelin producing part of the stomach in the VSG surgery is a possible contributor to the observed reduced ethanol preference. To test for functional changes at the ghrelin receptors, the VSG and control rats were given IP injections of acyl-ghrelin (2.5nmol and 5nmol) prior to ethanol access. Neither concentration of ghrelin resulted in a significant increase in 8% ethanol consumption of VSG or control subjects. Next, the rats were given IP injections of the ghrelin receptor antagonist, JMV (2.5mg/kg body weight). This dose induced a significant reduction in 8% ethanol consumption in the VSG group, but no effect on ethanol intake in the controls. While ghrelin injection was uninformative, increased sensitivity to subthreshold doses of the ghrelin receptor antagonist may indicate reduced ghrelin signaling following VSG. Overall, these findings suggest that bariatric patients with increased susceptibility to AUD may benefit from receiving VSG instead of RYGB surgery, and that changes in ghrelin signaling, at least in part, may play a role in the differential AUD risks between the two most commonly performed bariatric surgical procedures. Highlights As opposed to RYGB, VSG does not result in increased alcohol intake in mice or rats. VSG in rats increases sensitivity to GHS-R1a antagonism in decreasing alcohol intake. VSG could be an alternative to RYGB for bariatric patients with increased risk of AUD.

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    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  7. [해외논문]   Adolescent chronic variable social stress influences exploratory behavior and nicotine responses in male, but not female, BALB/cJ mice   SCI SCIE

    Caruso, M.J. (Department of Biobehavioral Health, Pennsylvania State University, University Park, PA 16802, USA ) , Reiss, D.E. (Department of Biobehavioral Health, Pennsylvania State University, University Park, PA 16802, USA ) , Caulfield, J.I. (Department of Biobehavioral Health, Pennsylvania State University, University Park, PA 16802, USA ) , Thomas, J.L. (Department of Biobehavioral Health, Pennsylvania State University, University Park, PA 16802, USA ) , Baker, A.N. (The Huck Institutes for the Life Sciences, Pennsylvania State University, University Park, PA 16802, USA ) , Cavigelli, S.A. (Department of Biobehavioral Health, Pennsylvania State University, University Park, PA 16802, USA ) , Kamens, H.M. (Department of Biobehavioral Health, Pennsylvania State University, University Park, PA 16802, USA)
    Brain research bulletin v.138 ,pp. 37 - 49 , 2018 , 0361-9230 ,

    초록

    Abstract Anxiety disorders and nicotine use are significant contributors to global morbidity and mortality as independent and comorbid diseases. Early-life stress, potentially via stress-induced hypothalamic-pituitary-adrenal axis (HPA) dysregulation, can exacerbate both. However, little is known about the factors that predispose individuals to the development of both anxiety disorders and nicotine use. Here, we examined the relationship between anxiety-like behaviors and nicotine responses following adolescent stress. Adolescent male and female BALB/cJ mice were exposed to either chronic variable social stress (CVSS) or control conditions. CVSS consisted of repeated cycles of social isolation and social reorganization. In adulthood, anxiety-like behavior and social avoidance were measured using the elevated plus-maze (EPM) and social approach-avoidance test, respectively. Nicotine responses were assessed with acute effects on body temperature, corticosterone production, locomotor activity, and voluntary oral nicotine consumption. Adolescent stress had sex-dependent effects on nicotine responses and exploratory behavior, but did not affect anxiety-like behavior or social avoidance in males or females. Adult CVSS males exhibited less exploratory behavior, as indicated by reduced exploratory locomotion in the EPM and social approach-avoidance test, compared to controls. Adolescent stress did not affect nicotine-induced hypothermia in either sex, but CVSS males exhibited augmented nicotine-induced locomotion during late adolescence and voluntarily consumed less nicotine during adulthood. Stress effects on male nicotine-induced locomotion were associated with individual differences in exploratory locomotion in the EPM and social approach-avoidance test. Relative to controls, adult CVSS males and females also exhibited reduced corticosterone levels at baseline and adult male CVSS mice exhibited increased corticosterone levels following an acute nicotine injection. Results suggest that the altered nicotine responses observed in CVSS males may be associated with HPA dysregulation. Taken together, adolescent social stress influences later-life nicotine responses and exploratory behavior. However, there is little evidence of an association between nicotine responses and prototypical anxiety-like behavior or social avoidance in BALB/cJ mice. Highlights Adolescent social stress altered nicotine responses in male but not female mice. Adolescent social stress altered exploratory behavior in male mice. Stress-effects on nicotine responses were associated with exploratory behavior. Adolescent stress may have sex-specific effects on development of nicotine responses.

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    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

    이미지

    Fig. 1 이미지
  8. [해외논문]   Pre-adolescent and adolescent mice are less sensitive to the effects of acute nicotine on extinction and spontaneous recovery   SCI SCIE

    Kutlu, Munir Gunes (Department of Biobehavioral Health, Penn State University, University Park, PA, USA ) , Zeid, Dana (Department of Biobehavioral Health, Penn State University, University Park, PA, USA ) , Tumolo, Jessica M. (Department of Psychology, Neuroscience Program, Weiss Hall, Temple University, Philadelphia, PA, USA ) , Gould, Thomas J. (Department of Biobehavioral Health, Penn State University, University Park, PA, USA)
    Brain research bulletin v.138 ,pp. 50 - 55 , 2018 , 0361-9230 ,

    초록

    Abstract Adolescence is a period of high risk for the initiation of nicotine product usage and exposure to traumatic events. In parallel, nicotine exposure has been found to age-dependently modulate acquisition of contextual fear memories; however, it is unknown if adolescent nicotine exposure alters extinction of fear related memories. Age-related differences in sensitivity to the effects of nicotine on fear extinction could increase or decrease susceptibility to anxiety disorders. In this study, we examined the effects of acute nicotine administration on extinction and spontaneous recovery of contextual fear memories in pre-adolescent (PND 23), late adolescent (PND 38), and adult (PND 53) C57B6/J mice. Mice were first trained in a background contextual fear conditioning paradigm and given an intraperitoneal injection of one of four doses of nicotine (0.045, 0.09, 0.18, or 0.36mg/kg, freebase) prior to subsequent extinction or spontaneous recovery sessions. Results indicated that all acute nicotine doses impaired extinction of contextual fear in adult mice. Late adolescent mice exhibited impaired extinction of contextual fear only following higher doses of acute nicotine, and extinction of contextual fear was unaffected by acute nicotine exposure in pre-adolescent mice. Finally, acute nicotine exposure enhanced spontaneous recovery of fear memory, but only in adult mice. Overall, our results suggest that younger mice were less sensitive to nicotine’s impairing effects on extinction of contextual fear and to nicotine’s enhancing effects on spontaneous recovery of contextual fear memory. Highlights Acute nicotine impaired extinction and increased recovery of fear in adult mice. Acute nicotine impaired fear extinction but not recovery during late adolescence. Pre-adolescent fear extinction and recovery were not affected by acute nicotine.

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    무료다운로드 유료다운로드

    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  9. [해외논문]   Changes in resting state functional brain connectivity and withdrawal symptoms are associated with acute electronic cigarette use   SCI SCIE

    Hobkirk, André (Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, 2812 Erwin Rd, Durham, NC 27708, USA ) , a L. (VA North Texas Health Care System, 4500 S. Lancaster Rd, Dallas, TX 75216, USA ) , Nichols, Travis T. (Department of Public Health Sciences, Pennsylvania State University, College of Medicine, Cancer Institute, 500 University Drive, PO Box 850, Hershey, PA 17033, USA ) , Foulds, Jonathan (Department of Public Health Sciences, Pennsylvania State University, College of Medicine, Cancer Institute, 500 University Drive, PO Box 850, Hershey, PA 17033, USA ) , Yingst, Jessica M. (Department of Public Health Sciences, Pennsylvania State University, College of Medicine, Cancer Institute, 500 University Drive, PO Box 850, Hershey, PA 17033, USA ) , Veldheer, Susan (Department of Public Health Sciences, Pennsylvania State University, College of Medicine, Cancer Institute, 500 University Drive, PO Box 850, Hershey, PA 17033, USA ) , Hrabovsky, Shari (Department of Public Health Sciences, Pennsylvania State University, College of Medicine, Cancer Institute, 500 University Dri) , Richie, John , Eissenberg, Thomas , Wilson, Stephen J.
    Brain research bulletin v.138 ,pp. 56 - 63 , 2018 , 0361-9230 ,

    초록

    Abstract Resting state functional brain connectivity (rsFC) may be an important neuromarker of smoking behavior. Prior research has shown, among cigarette smokers, that nicotine administration alters rsFC within frontal and parietal cortices involved in executive control, as well as striatal regions that drive reward processing. These changes in rsFC have been associated with reductions in withdrawal symptom severity. We currently have a limited understanding of how rsFC is affected by the use of electronic cigarettes (ecigs), an increasingly popular class of products, the members of which deliver nicotine with varying effectiveness. The current study used fMRI to determine the effects of ecig use on rsFC and withdrawal symptoms. Independent component, dual regression, and permutation analyses were conducted on rsFC collected from ecig users before and after an ecig use episode (n=9) that occurred after 14h of nicotine abstinence. Similar to the known effects of nicotine administration, ecig use decreased rsFC of two clusters in the right frontal pole and frontal medial cortex with an attentional control salience network, and decreased rsFC of five clusters in the left thalamus, insula, and brain stem with a reward network encompassing the striatum. Ecig use increased inverse coupling between the prefrontal reward network and the right frontoparietal executive control network. Reductions in craving and difficulty with concentration were correlated with decreases in coupling strength between reward and executive control networks. These preliminary results suggest that the effects of ecig use on rsFC are similar to those seen with nicotine administration in other forms. In order to gain insight into the addictive potential of ecigs, further research is needed to understand the neural influence of ecigs across the range of nicotine delivery within this class of products.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  10. [해외논문]   Alterations in nociception and morphine antinociception in mice fed a high-fat diet   SCI SCIE

    Nealon, Caitlin M. (Department of Anesthesiology and Perioperative Medicine, Penn State College of Medicine, Hershey, PA, 17033, USA ) , Patel, Chandni (Department of Anesthesiology and Perioperative Medicine, Penn State College of Medicine, Hershey, PA, 17033, USA ) , Worley, Beth L. (Department of Anesthesiology and Perioperative Medicine, Penn State College of Medicine, Hershey, PA, 17033, USA ) , Henderson-Redmond, Angela N. (Department of Anesthesiology and Perioperative Medicine, Penn State College of Medicine, Hershey, PA, 17033, USA ) , Morgan, Daniel J. (Department of Anesthesiology and Perioperative Medicine, Penn State College of Medicine, Hershey, PA, 17033, USA ) , Czyzyk, Traci A. (Department of Anesthesiology and Perioperative Medicine, Penn State College of Medicine, Hershey, PA, 17033, USA)
    Brain research bulletin v.138 ,pp. 64 - 72 , 2018 , 0361-9230 ,

    초록

    Abstract Currently, more than 78.6 million adults in the United States are obese. A majority of the patient population receiving treatment for pain symptoms is derived from this subpopulation. Environmental factors, including the increased availability of food high in fat and sugar, contribute to the continued rise in the rates of obesity. The focus of this study was to investigate whether long-term exposure to a high-fat, energy-dense diet enhances baseline thermal and inflammatory nociception while reducing sensitivity to morphine-induced antinociception. Antinociceptive and hypothermic responses to morphine were determined in male and female C57BL/6N mice fed either a “western-style” diet high in fat and sucrose (HED) or a standard low-fat chow diet for 15 weeks. Antinociception was assessed using both the hot plate and tail flick tests of acute thermal pain and the formalin test of inflammatory pain. Acute administration of morphine dose-dependently increased antinociception in the hot plate and tail flick assays for mice of both sexes fed chow and HED. However, female mice displayed lower antinociceptive response to morphine compared to males in the tail-flick test. Hypothermic responses to acute morphine were also assessed in mice fed chow or HED. Male and female mice fed chow, and female mice fed HED displayed similar hypothermic responses to morphine. However, males fed HED did not exhibit morphine-induced hypothermia. Tolerance to the antinociceptive and hypothermic effects of morphine was assessed after ten days of repeated daily administration (10mg/kg morphine). Male mice fed chow or HED developed tolerance to morphine in the hot plate test. However, females fed HED did not. In the tail flick assay, only mice fed HED developed tolerance to morphine. All groups showed tolerance to morphine-induced hypothermia. In the formalin test, we found that both male and female mice fed HED had reduced sensitivity to the antinociceptive effects of morphine (6mg/kg). Collectively, these data suggest that sensitivity and tolerance to the antinociceptive effects of morphine may be dependent on diet and sex in the hot plate and tail flick thermal pain models, and that the acute antinociceptive effects of morphine in the formalin inflammatory pain model may also be dependent on these two factors. In addition, diet and sex can influence morphine-induced hypothermia. Exposure to an HED may lead to changes in neuronal signaling pathways that alter nociceptive responses to noxious stimuli in a sex-specific manner. Thus, dietary modifications might be a useful way to impact pain therapy. Highlights Females are less responsive to the antinociceptive effects of morphine than male littermates. HED increases tolerance to the antinociceptive effects of morphine on acute thermal pain. HED exposure reduces morphine antinociception in an inflammatory pain model. Male mice fed HED are resistant to the hypothermic effects of acute morphine. Dietary modifications may be relevant for pain therapy.

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