The effects of acute ethanol administration on ethanol withdrawal-induced anxiety-like syndrome in rats: A biochemical study

Kumar, Jaya; Hapidin, Hermizi; Yvonne-Tee, Get Bee; Ismail, Zawawi Bin

doi:10.1016/j.alcohol.2015.10.001

Cited by 19 publications

(24 citation statements)

References 39 publications

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“…Finally, mGlu5 scans have been performed within a rather large withdrawal time window (2-14 d). In view of the preclinical literature suggesting that mGlu5 expression varies depending on the time of abstinence and the brain regions being studied (6)(7)(8)(9), more studies are needed to investigate how mGlu5 expression regionally adapts over time in alcohol-dependent subjects.…”

Section: Discussionmentioning

confidence: 99%

“…To date, few preclinical studies have investigated the effect of chronic alcohol administration on mGlu5 density, revealing either a mGlu5 hypoexpression in the hippocampus (6), an overexpression in the amygdala (7), or no alterations (8) or overexpression (9) in the ventral striatum. In contrast, extensive research showed that blocking of mGlu5 signaling by genetic or pharmacologic interventions reduces alcohol-rewarding properties (10)(11)(12)(13)(14) and the severity of withdrawal and relapse behaviors after alcohol deprivation in rodents (13,(15)(16)(17)(18)(19).…”

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confidence: 99%

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Lower Limbic Metabotropic Glutamate Receptor 5 Availability in Alcohol Dependence

et al. 2018

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Animal studies suggest an important role for the metabotropic glutamate receptor subtype 5 (mGlu5) in the pathophysiology of alcohol dependence, but direct human evidence is lacking. The goal of this study was to investigate cerebral mGlu5 availability in alcohol-dependent subjects versus controls using F-3-fluoro-5-[(pyridin-3-yl)ethynyl]benzonitrile (F-FPEB) PET. Dynamic 90-minF-FPEB scans combined with arterial blood sampling were acquired for 16 recently abstinent alcohol-dependent subjects and 32 age-matched controls. Regional mGlu5 availability was quantified by the F-FPEB total distribution volume using both a voxel-by-voxel and a volume-of-interest analysis with partial-volume effect correction. Alcohol consumption within the last 3 mo was assessed by questionnaires and by hair ethyl glucuronide analysis. Craving was assessed using the Desire for Alcohol Questionnaire. mGlu5 availability was lower in mainly limbic regions of alcohol-dependent subjects than in controls ( < 0.05, familywise error-corrected), ranging from 14% in the posterior cingulate cortex to 36% in the caudate nucleus. Lower mGlu5 availability was associated with higher hair ethyl glucuronide levels for most regions and was related to a lower level of craving specifically in the middle frontal gyrus, cingulate cortex, and inferolateral temporal lobe. These findings provide human in vivo evidence that limbic mGlu5 has a role in the pathophysiology of alcohol dependence, possibly involved in a compensatory mechanism helping to reduce craving during abstinence.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Lower Limbic Metabotropic Glutamate Receptor 5 Availability in Alcohol Dependence

et al. 2018

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“…In addition, NMDARs are also modulated by metabotropic glutamate receptor subtype 5 (mGlu5) (Chen H. H. et al, 2011 ). Negative modulation of mGlu5 has been promising in attenuating hyperexcitability of central nervous system (Kumar et al, 2013 , 2016 , 2017 ) and even reducing the spike-wave discharges in numerous animal models of epilepsy (McCool et al, 1998 ; Chapman et al, 2000 ). More studies are needed to further elucidate the functional link between mGlu5, GABA, and NMDARs in epilepsy.…”

Section: Future Recommendationsmentioning

confidence: 99%

Sleep Related Epilepsy and Pharmacotherapy: An Insight

et al. 2018

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In the last several decades, sleep-related epilepsy has drawn considerable attention among epileptologists and neuroscientists in the interest of new paradigms of the disease etiology, pathogenesis and management. Sleep-related epilepsy is nocturnal seizures that manifest solely during the sleep state. Sleep comprises two distinct stages i.e., non-rapid eye movement (NREM) and rapid eye movement (REM) that alternate every 90 min with NREM preceding REM. Current findings indicate that the sleep-related epilepsy manifests predominantly during the synchronized stages of sleep; NREM over REM stage. Sleep related hypermotor epilepsy (SHE), benign partial epilepsy with centrotemporal spikes or benign rolandic epilepsy (BECTS), and Panayiotopoulos Syndrome (PS) are three of the most frequently implicated epilepsies occurring during the sleep state. Although some familial types are described, others are seemingly sporadic occurrences. In the present review, we aim to discuss the predominance of sleep-related epilepsy during NREM, established familial links to the pathogenesis of SHE, BECTS and PS, and highlight the present available pharmacotherapy options.

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“…One of the aforementioned transcription factors, Sp1 , has been shown to be downregulated following chronic ethanol exposure (Rulten et al, 2006 ). However, findings regarding PKCε gene expression have been rather inconclusive, with no definitive changes in PRKCE mRNA levels reported after long-term ethanol exposure (Kaiser et al, 2014 ; Kumar et al, 2016 ).…”

Section: Transcription Of Pkcεmentioning

confidence: 99%

“…PKCε is considered to mediate an ethanol-tolerant phenotype because of its interactions with receptors such as gamma aminobutyric acid (GABA A ) (Poisbeau et al, 1999 ) and metabotropic glutamate receptor subtype 5 (mGlu5) (Olive et al, 2005 ; Kumar et al, 2017 ) in CNS. Null mutations of PKCε have been found to attenuate ethanol drinking behavior in rodents (Lesscher et al, 2009 ; Maiya et al, 2016 ), and prolonged ethanol exposure significantly increases PKCε expression (Messing et al, 1991 ; Coe et al, 1996 ; Kumar et al, 2016 ). Thus, there is an incentive for developing potent, selective, and brain-penetrant PKCε inhibitors.…”

Section: Introductionmentioning

confidence: 99%

Ethanol-Induced Changes in PKCε: From Cell to Behavior

et al. 2018

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The long-term binge intake of ethanol causes neuroadaptive changes that lead to drinkers requiring higher amounts of ethanol to experience its effects. This neuroadaptation can be partly attributed to the modulation of numerous neurotransmitter receptors by the various protein kinases C (PKCs). PKCs are enzymes that control cellular activities by regulating other proteins via phosphorylation. Among the various isoforms of PKC, PKCε is the most implicated in ethanol-induced biochemical and behavioral changes. Ethanol exposure causes changes to PKCε expression and localization in various brain regions that mediate addiction-favoring plasticity. Ethanol works in conjunction with numerous upstream kinases and second messenger activators to affect cellular PKCε expression. Chauffeur proteins, such as receptors for activated C kinase (RACKs), cause the translocation of PKCε to aberrant sites and mediate ethanol-induced changes. In this article, we aim to review the following: the general structure and function of PKCε, ethanol-induced changes in PKCε expression, the regulation of ethanol-induced PKCε activities in DAG-dependent and DAG-independent environments, the mechanisms underlying PKCε-RACKε translocation in the presence of ethanol, and the existing literature on the role of PKCε in ethanol-induced neurobehavioral changes, with the goal of creating a working model upon which further research can build.

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The effects of acute ethanol administration on ethanol withdrawal-induced anxiety-like syndrome in rats: A biochemical study

Cited by 19 publications

References 39 publications

Lower Limbic Metabotropic Glutamate Receptor 5 Availability in Alcohol Dependence

Lower Limbic Metabotropic Glutamate Receptor 5 Availability in Alcohol Dependence

Sleep Related Epilepsy and Pharmacotherapy: An Insight

Ethanol-Induced Changes in PKCε: From Cell to Behavior

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