Common effects of fat, ethanol, and nicotine on enkephalin in discrete areas of the brain

Chang, Guo‐Qing; Karatayev, Olga; Barson, Jessica R.; Liang, Sherry; Leibowitz, Sarah F.

doi:10.1016/j.neuroscience.2014.07.050

Cited by 15 publications

(7 citation statements)

References 125 publications

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“…In a recent report, high-fat diet itself protected against stress-induced general anxiety- and depression-like behaviors (Finger et al, 2011). Fat, ethanol, and nicotine intake have been shown to increase the single- and double-labeling of the endogenous opioid peptide, enkephalin (ENK)- and c-Fos-immunoreactivity in precisely the same brain areas, the medial area of the paraventricular nucleus of the hypothalamus, central nucleus of the amygdala, and the core of the nucleus accumbens (Chang et al, 2014). These findings suggest that food rich in fat has effects in common with addictive drugs which are known to activate the same populations of ENK-expressing neurons in these nuclei of the hypothalamus and limbic system, thereby affecting behaviors such as social interaction, rewording seeking, and preference decision making.…”

Section: Discussionmentioning

confidence: 99%

Alcohol and high fat induced chronic pancreatitis: TRPV4 antagonist reduces hypersensitivity

et al. 2015

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The pathogenesis of pain in chronic pancreatitis is poorly understood, and its treatment can be a major clinical challenge. Surgical and other invasive methods have variable outcomes that can be unsatisfactory. Therefore, there is a great need for further discovery of the pathogenesis of pancreatitis pain and new therapeutic targets. Human and animal studies indicate a critical role for oxidative stress and activation of transient receptor potential (TRP) cation channel subfamily members TRPV1 and TRPA1 on pancreatic nociceptors in sensitization mechanisms that result in pain. However, the in vivo role of TRPV4 in chronic pancreatitis needs further evaluation. The present study characterized a rat alcohol/high fat diet (AHF) induced chronic pancreatitis model with hypersensitivity, fibrotic pathology, and fat vacuolization consistent with the clinical syndrome. The rats with AHF induced pancreatitis develop referred visceral pain-like behaviors, i.e. decreased hindpaw mechanical thresholds and shortened abdominal and hindpaw withdrawal latency to heat. In this study, oxidative stress was characterized as well as the role of TRPV4 in chronic visceral hypersensitivity. Lipid peroxidase and oxidative stress were indicated by increased plasma thiobarbituric acid reactive substances (TBARS) and diminished pancreatic manganese superoxide dismutase (MnSOD). The secondary sensitization associated with AHF induced pancreatitis was effectively alleviated by the TRPV4 antagonist, HC 067047. Similarity of the results to those with the peripherally restricted µ-opiate receptor agonist, loperamide, suggested TRPV4 channel activated peripheral sensitization. This study using a reliable model that provides pre-clinical correlates of human chronic pancreatitis provides further evidence that TRPV4 channel is a potential therapeutic target for treatment of pancreatitis pain.

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Section: Discussionmentioning

confidence: 99%

Alcohol and high fat induced chronic pancreatitis: TRPV4 antagonist reduces hypersensitivity

et al. 2015

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“…Both gene expression and peptide levels of ENK are increased in the PVN in response to moderate and excessive alcohol drinking (Chang et al, 2007; Oliva and Manzanares, 2007), and this effect occurs with as little as a single alcohol injection (Chang et al, 2007; de Gortari et al, 2000). Anatomical analysis has shown that the alcohol-induced transcriptional activation of ENK neurons specifically occurs in the medial parvocellular area of the PVN at all anterior-posterior levels (Chang et al, 2014). Therefore, just as with GAL, hypothalamic ENK not only endogenously promotes alcohol drinking, but the drinking of alcohol in turn increases the activity and levels of hypothalamic ENK, completing the positive feedback circuit.…”

Section: Neuropeptides With a Positive Feedback Relationship To Almentioning

confidence: 99%

Hypothalamic neuropeptide signaling in alcohol addiction

Barson

Leibowitz

2016

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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The hypothalamus is now known to regulate alcohol intake in addition to its established role in food intake, in part through neuromodulatory neurochemicals termed neuropeptides. Certain orexigenic neuropeptides act in the hypothalamus to promote alcohol drinking, although they affect different aspects of the drinking response. These neuropeptides, which include galanin, the endogenous opioid enkephalin, and orexin/hypocretin, appear to stimulate alcohol intake not only through mechanisms that promote food intake but also by enhancing reward and reinforcement from alcohol. Moreover, these neuropeptides participate in a positive feedback relationship with alcohol, whereby they are upregulated by alcohol intake to promote even further consumption. They contrast with other orexigenic neuropeptides, such as melanin-concentrating hormone and neuropeptide Y, which promote alcohol intake under limited circumstances, are not consistently stimulated by alcohol, and do not enhance reward. They also contrast with neuropeptides that can be anorexigenic, including the endogenous opioid dynorphin, corticotropin-releasing factor, and melanocortins, which act in the hypothalamus to inhibit alcohol drinking as well as reward and therefore counter the ingestive drive promoted by orexigenic neuropeptides. Thus, while multiple hypothalamic neuropeptides may work together to regulate different aspects of the alcohol drinking response, excessive signaling from orexigenic neuropeptides or inadequate signaling from anorexigenic neuropeptides can therefore allow alcohol drinking to become dysregulated.

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“…The subcellular localization of DOPR within the BLA and CeA suggests that DOPR may function to inhibit the excitation of BLA and CeA neurons in the presence of a stressor (Herringa et al, 2004; Tye et al, 2011). The postsynaptic localization of DOPR is also supported by in situ hybridization and immunohistochemical data of enkephalin mRNA and immunoreactivity in the amygdalar complex including the BLA and CeA (Berube et al, 2013; Chang et al, 2014; Chieng et al, 2006; Zhang and McDonald, 2016). …”

Section: Discussionmentioning

confidence: 70%

Localization of the delta opioid receptor and corticotropin-releasing factor in the amygdalar complex: role in anxiety

et al. 2016

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It is well established that central nervous system norepinephrine (NE) and corticotropin releasing factor (CRF) systems are important mediators of behavioral responses to stressors. More recent studies have defined a role for delta opioid receptors (DOPR) in maintaining emotional valence including anxiety. The amygdala plays an important role in processing emotional stimuli, and has been implicated in the development of anxiety disorders. Activation of DOPR or inhibition of CRF in the amygdala reduces baseline and stress-induced anxiety-like responses. It is not known whether CRF- and DOPR-containing amygdalar neurons interact or whether they are regulated by NE afferents. Therefore, the present study sought to better define interactions between the CRF, DOPR and NE systems in the basolateral (BLA) and central nucleus of the amygdala (CeA) of the male rat using anatomical and functional approaches. Irrespective of the amygdalar subregion, dual immunofluorescence microscopy showed that DOPR was present in CRF-containing neurons. Immunoelectron microscopy confirmed that DOPR was localized to both dendritic processes and axon terminals in the BLA and CeA. Semi-quantitative dual immunoelectron microscopy analysis of gold-silver labeling for DOPR and immunoperoxidase labeling for CRF revealed that 55% of the CRF neurons analyzed contained DOPR in the BLA while 67% of the CRF neurons analyzed contained DOPR in the CeA. Furthermore, approximately 41% of DOPR-labeled axon terminals targeted BLA neurons that expressed CRF while 29% of DOPR-labeled axon terminals targeted CeA neurons that expressed CRF. Triple label immunofluorescence microscopy revealed that DOPR and CRF were co-localized in common cellular profiles that were in close proximity to NE-containing fibers in both subregions. These anatomical results indicate significant interactions between DOPR and CRF in this critical limbic region and reveal that NE is poised to regulate these peptidergic systems in the amygdala. Functional studies were performed to determine if activation of DOPR could inhibit the anxiety produced by elevation of NE in the amygdala using the pharmacological stressor yohimbine. Administration of the DOPR agonist, SNC80, significantly attenuated elevated anxiogenic behaviors produced by yohimbine as measured in the rat on the elevated zero maze. Taken together, results from this study demonstrate the convergence of three important systems, NE, CRF, and DOPR, in the amygdala and provide insight into their functional role in modulating stress and anxiety responses.

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Common effects of fat, ethanol, and nicotine on enkephalin in discrete areas of the brain

Cited by 15 publications

References 125 publications

Alcohol and high fat induced chronic pancreatitis: TRPV4 antagonist reduces hypersensitivity

Alcohol and high fat induced chronic pancreatitis: TRPV4 antagonist reduces hypersensitivity

Hypothalamic neuropeptide signaling in alcohol addiction

Localization of the delta opioid receptor and corticotropin-releasing factor in the amygdalar complex: role in anxiety

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