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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Jeffrey F. DiBerto; orcid C. J. Malanga;
    C. J. Malanga
    ORCID
    Harvested from ORCID Public Data File

    C. J. Malanga in OpenAIRE
    Eric W. Fish; orcid J. Elliott Robinson;
    J. Elliott Robinson
    ORCID
    Harvested from ORCID Public Data File

    J. Elliott Robinson in OpenAIRE
    +1 Authors

    C57BL/6J (C57) and DBA/2J (DBA) mice respond differently to drugs that affect dopamine systems, including alcohol. The current study compared effects of D1 and D2 receptor agonists and antagonists, and the interaction between D1/D2 antagonists and alcohol, on intracranial self-stimulation in male C57 and DBA mice to determine the role of dopamine receptors in the effects of alcohol on brain stimulation reward (BSR). In the initial strain comparison, dose effects on BSR thresholds and maximum operant response rates were determined for the D1 receptor agonist SKF-82958 (±-6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine; 0.1–0.56 mg/kg) and antagonist SCH 23390 (+-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepinehydrochloride; 0.003–0.056 mg/kg), and the D2 receptor agonist quinpirole (0.1–3.0 mg/kg) and antagonist raclopride (0.01–0.56 mg/kg). For the alcohol interaction, SCH 23390 (0.003 mg/kg) or raclopride (0.03 mg/kg) was given before alcohol (0.6–2.4 g/kg p.o.). D1 antagonism dose-dependently elevated and SKF-82958 dose-dependently lowered BSR threshold in both strains; DBA mice were more sensitive to SKF-82958 effects. D2 antagonism dose-dependently elevated BSR threshold only in C57 mice. Low doses of quinpirole elevated BSR threshold equally in both strains, whereas higher doses of quinpirole lowered BSR threshold only in C57 mice. SCH 23390, but not raclopride, prevented lowering of BSR threshold by alcohol in DBA mice. Conversely, raclopride, but not SCH 23390, prevented alcohol potentiation of BSR in C57 mice. These results extend C57 and DBA strain differences to D1/D2 sensitivity of BSR, and suggest differential involvement of D1 and D2 receptors in the acute rewarding effects of alcohol in these two mouse strains.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Journal of Pharmacol...arrow_drop_down
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    Journal of Pharmacology and Experimental Therapeutics
    Article . 2014 . Peer-reviewed
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    Article . 2014
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Journal of Pharmacol...arrow_drop_down
      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      Journal of Pharmacology and Experimental Therapeutics
      Article . 2014 . Peer-reviewed
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      Article . 2014
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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: orcid Madalina Vlasceanu;
    Madalina Vlasceanu
    ORCID
    Harvested from ORCID Public Data File

    Madalina Vlasceanu in OpenAIRE
    orcid Kimberly C. Doell;
    Kimberly C. Doell
    ORCID
    Harvested from ORCID Public Data File

    Kimberly C. Doell in OpenAIRE
    orcid bw Joseph B. Bak-Coleman;
    Joseph B. Bak-Coleman
    ORCID
    Derived by OpenAIRE algorithms or harvested from 3rd party repositories

    Joseph B. Bak-Coleman in OpenAIRE
    orcid Boryana Todorova;
    Boryana Todorova
    ORCID
    Harvested from ORCID Public Data File

    Boryana Todorova in OpenAIRE
    +196 Authors

    Effectively reducing climate change requires marked, global behavior change. However, it is unclear which strategies are most likely to motivate people to change their climate beliefs and behaviors. Here, we tested 11 expert-crowdsourced interventions on four climate mitigation outcomes: beliefs, policy support, information sharing intention, and an effortful tree-planting behavioral task. Across 59,440 participants from 63 countries, the interventions’ effectiveness was small, largely limited to nonclimate skeptics, and differed across outcomes: Beliefs were strengthened mostly by decreasing psychological distance (by 2.3%), policy support by writing a letter to a future-generation member (2.6%), information sharing by negative emotion induction (12.1%), and no intervention increased the more effortful behavior—several interventions even reduced tree planting. Last, the effects of each intervention differed depending on people’s initial climate beliefs. These findings suggest that the impact of behavioral climate interventions varies across audiences and target behaviors.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Science Advancesarrow_drop_down
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    Science Advances
    Article . 2024 . Peer-reviewed
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    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    https://dx.doi.org/10.26181/27...
    Other literature type . 2024
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    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    https://dx.doi.org/10.26181/27...
    Other literature type . 2024
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    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Science Advances
    Article . 2024
    image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
    UNC Dataverse
    Article . 2024
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      Science Advances
      Article . 2024 . Peer-reviewed
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      https://dx.doi.org/10.26181/27...
      Other literature type . 2024
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      https://dx.doi.org/10.26181/27...
      Other literature type . 2024
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      Science Advances
      Article . 2024
      image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Jun He; orcid Fulton T. Crews;
    Fulton T. Crews
    ORCID
    Harvested from ORCID Public Data File

    Fulton T. Crews in OpenAIRE
    orcid Martin Styner;
    Martin Styner
    ORCID
    Harvested from ORCID Public Data File

    Martin Styner in OpenAIRE
    Joohwi Lee; +1 Authors

    Binge-drinking is common in human adolescents. The adolescent brain is undergoing structural maturation and has a unique sensitivity to alcohol neurotoxicity. Therefore, adolescent binge ethanol may have long-term effects on the adult brain that alter brain structure and behaviors that are relevant to alcohol use disorders.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Alcoholism Clinical ...arrow_drop_down
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    image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
    Alcoholism Clinical and Experimental Research
    Article . 2011 . Peer-reviewed
    License: Wiley TDM
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    Article . 2011
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Alcoholism Clinical ...arrow_drop_down
      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
      Alcoholism Clinical and Experimental Research
      Article . 2011 . Peer-reviewed
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      Article . 2011
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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: orcid Clyde W. Hodge;
    Clyde W. Hodge
    ORCID
    Harvested from ORCID Public Data File

    Clyde W. Hodge in OpenAIRE
    Joyce Besheer; Veronique Lepoutre;

    Background:  Many of the neurobehavioral effects of ethanol are mediated by inhibition of excitatory N‐methyl‐d‐aspartate (NMDA) and enhancement of inhibitory γ‐amino‐butyric‐acid (GABA) receptor systems. There is growing interest in drugs that alter these systems as potential medications for problems associated with alcoholism. The drug riluzole, approved for treatment of amyotrophic lateral sclerosis (ALS), inhibits NMDA and enhances GABAA receptor system activity. This study was designed to determine the preclinical efficacy of riluzole to modulate ethanol self‐administration and withdrawal.Methods:  Male C57BL/6J mice were trained to lever press on a concurrent fixed‐ratio 1 schedule of ethanol (10% v/v) versus water reinforcement during daily 16‐hour sessions. Riluzole (1 to 40 mg/kg, IP) was evaluated on ethanol self‐administration after acute and chronic (2 week) treatment. To determine if riluzole influences ethanol withdrawal‐associated seizures, mice were fed an ethanol‐containing or control liquid diet for 18 days. The effects of a single injection of riluzole (30 mg/kg) were examined on handling‐induced convulsions after ethanol withdrawal.Results:  Acute riluzole (30 and 40 mg/kg) reduced ethanol self‐administration during the first 4 hours of the session, which corresponds to the known pharmacokinetics of this drug. Ethanol self‐administration was also reduced by riluzole after chronic treatment. Riluzole (30 mg/kg) significantly decreased the severity of ethanol‐induced convulsions 2 hours after ethanol withdrawal.Conclusions:  These results demonstrate that riluzole decreases ethanol self‐administration and may reduce ethanol withdrawal severity in mice. Thus, riluzole may have utility in the treatment of problems associated with alcoholism.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Alcoholism Clinical ...arrow_drop_down
    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
    Alcoholism Clinical and Experimental Research
    Article . 2009 . Peer-reviewed
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    Article . 2009
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      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Alcoholism Clinical ...arrow_drop_down
      image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
      image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
      Alcoholism Clinical and Experimental Research
      Article . 2009 . Peer-reviewed
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      Article . 2009
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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Chris E. Comerford; Sandeep Kumar; A. Leslie Morrow; orcid David F. Werner;
    David F. Werner
    ORCID
    Harvested from ORCID Public Data File

    David F. Werner in OpenAIRE
    +1 Authors

    Ethanol exposure produces alterations in GABAergic signaling that are associated with dependence and withdrawal. Previously, we demonstrated that ethanol-induced protein kinase C (PKC) γ signaling selectively contributes to changes in GABAAα1 synaptic receptor activity and surface expression. Here, we demonstrate that protein kinase A (PKA) exerts opposing effects on GABAA receptor adaptations during brief ethanol exposure. Cerebral cortical neurons from day 0–1 rat pups were tested after 18 days in culture. Receptor trafficking was assessed by Western blot analysis, and functional changes were measured using whole-cell patch-clamp recordings of evoked and miniature inhibitory postsynaptic current (mIPSC) responses. One-hour ethanol exposure increased membrane-associated PKC and PKA, but steady-state GABAAα1 subunit levels were maintained. Activation of PKA by Sp-adenosine 3′,5′-cyclic monophosphothioate triethylamine alone increased GABAAα1 subunit surface expression and zolpidem potentiation of GABA responses, whereas coexposure of ethanol with the PKA inhibitor Rp-adenosine 3′,5′-cyclic monophosphothioate triethylamine decreased α1 subunit expression and zolpidem responses. Exposure to the PKC inhibitor calphostin-C with ethanol mimicked the effect of direct PKA activation. The effects of PKA modulation on mIPSC decay τ were consistent with its effects on GABA currents evoked in the presence of zolpidem. Overall, the results suggest that PKA acts in opposition to PKC on α1-containing GABAA receptors, mediating the GABAergic effects of ethanol exposure, and may provide an important target for the treatment of alcohol dependence/withdrawal.

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    Journal of Pharmacology and Experimental Therapeutics
    Article . 2013 . Peer-reviewed
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    Article . 2013
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      Journal of Pharmacology and Experimental Therapeutics
      Article . 2013 . Peer-reviewed
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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: David H. Overstreet; George R. Breese; Darin J. Knapp;

    Background: Repeated exposures to forced ethanol diets (EDs) or restraint stress sensitize anxiety‐like behavior during a future ethanol withdrawal. The present investigation assessed whether pretreatment of rats with agents targeting receptor systems thought to be important in treating relapse in alcoholic patients would prevent sensitization of anxiety‐like behavior.Methods: Groups of rats were exposed to either (1) three 5‐day cycles of ED with 2 days of withdrawal between cycles, (2) continuous ED, or (3) 5 days of ED in a single cycle preceded by 2 episodes of restraint stress 6 days apart. Drugs [baclofen, acamprosate, naloxone, lamotrigine, ifenprodil, dizocilpine (MK‐801), CGS19755, diazepam, flumazenil, or 6‐methyl‐2‐(phenylethynyl)pyridine] were given prophylactically during the first and second withdrawal periods only or, in separate baclofen experiments, acutely during the third withdrawal or during withdrawal from continuous ED. Baclofen administration preceded each stress session in the stress‐withdrawal protocols. Anxiety‐like behavior was assessed in the social interaction (SI) test 5 hours after the ethanol was removed or after 3 days of abstinence.Results: Baclofen (1.25, 2.5, and 5 mg/kg), flumazenil (5 mg/kg), and diazepam (1 mg/kg) blocked the reduction in SI induced by ethanol withdrawal. Among the drugs that alter glutamate function, only acamprosate (300 mg/kg) was effective. In the stress protocols, baclofen (5 mg/kg) given before each of the 2 restraint stress sessions before ethanol exposure or before stress during abstinence also attenuated SI deficits.Conclusions: These findings suggest that GABAB and GABAA, but not glutamate or opioid mechanisms, are involved in adaptive changes associated with anxiety‐like behavior induced by these repeated ethanol‐withdrawal and stress‐withdrawal paradigms. The lack of action of agents attenuating different aspects of glutamate function suggests that acamprosate's action is related to some other, as yet undetermined, mechanism.

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    Alcoholism Clinical and Experimental Research
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      Alcoholism Clinical and Experimental Research
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    Authors: orcid Shabbir H. Gheewala;
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    Shabbir H. Gheewala; Richard M. Kamens; Richard M. Kamens; +8 Authors

    The Thai government’s implementation of its 10 year renewable energy plan was done to help increase energy independence and reduce emissions resulting from energy production. Due to Thailand’s wind regime, wind turbines which can operate in low wind speeds will be needed to meet this goal. Small wind turbines typically operate at higher efficiency in lower winds, and thus they might prove to be a good option for wind power production in Thailand. Incorporating small wind turbines into power production can be difficult because of the perception of high investment costs and because their net benefit has not been adequately studied. Using a functional unit of producing 50 kWh per month for 10 years we conducted a Life Cycle Assessment comparing the global warming potential (GWP), embodied energy (EE), and levelized cost of electricity (LCOE) of four small wind turbines (≤20 kW), a diesel generator, and the Thai Grid. When analyzing GWP of the turbines it was found that they had a lower overall GWP than the diesel generator when in areas with reasonable wind resources. The same is true for embodied energy. Interestingly, in most available wind speed categories in Thailand the LCOE for wind turbines was lower than for the diesel generator. However, neither could compare to the LCOE of the Thai Grid, except in the areas with the highest average wind speeds (7.0 -­‐9.4 m/s). With this in mind, it is clear that the most important factor when considering wind power generation is the wind regime available in an area. Because of the increased cost relative to the Thai grid, implementation of wind turbines in Thailand was not found to be economically viable. This could be changed given lower costs for turbines and/or government incentives.

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    Energy for Sustainable Development
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    Authors: orcid David F. Werner;
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    orcid Patrizia Porcu;
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    Sandeep Kumar; A. Leslie Morrow; +3 Authors

    The past decade has brought many advances in our understanding of GABAA receptor-mediated ethanol action in the central nervous system. We now know that specific GABAA receptor subtypes are sensitive to ethanol at doses attained during social drinking while other subtypes respond to ethanol at doses attained by severe intoxication. Furthermore, ethanol increases GABAergic neurotransmission through indirect effects, including the elevation of endogenous GABAergic neuroactive steroids, presynaptic release of GABA, and dephosphorylation of GABAA receptors promoting increases in GABA sensitivity. Ethanol’s effects on intracellular signaling also influence GABAergic transmission in multiple ways that vary across brain regions and cell types. The effects of chronic ethanol administration are influenced by adaptations in GABAA receptor function, expression, trafficking, and subcellular localization that contribute to ethanol tolerance, dependence, and withdrawal hyperexcitability. Adolescents exhibit altered sensitivity to ethanol actions, the tendency for higher drinking and longer lasting GABAergic adaptations to chronic ethanol administration. The elucidation of the mechanisms that underlie adaptations to ethanol exposure are leading to a better understanding of the regulation of inhibitory transmission and new targets for therapies to support recovery from ethanol withdrawal and alcoholism.

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    Psychopharmacology
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    Authors: Kristen E. Pleil; Thomas L. Kash; Sophie Masneuf; Andrew Holmes; +11 Authors

    Alcoholism is frequently co-morbid with posttraumatic stress disorder (PTSD) but it is unclear how alcohol impacts neural circuits mediating recovery from trauma. We found that chronic intermittent ethanol (CIE) impaired fear extinction and remodeled the dendritic arbor of medial prefrontal cortical (mPFC) neurons in mice. CIE impaired extinction encoding by infralimbic (IL) mPFC neurons in vivo, and functionally downregulated burst-mediating NMDA GluN1 receptors. These findings suggest alcohol may increase risk for trauma-related anxiety disorders by disrupting mPFC-mediated extinction of fear.

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    Authors: Hugh E. Criswell; M. Katherine Kelm; George R. Breese;

    While research on the actions of ethanol at the GABAergic synapse has focused on postsynaptic mechanisms, recent data have demonstrated that ethanol also facilitates GABA release from presynaptic terminals in many, but not all, brain regions. The ability of ethanol to increase GABA release can be regulated by different G protein-coupled receptors (GPCRs), such as the cannabinoid-1 receptor, corticotropin-releasing factor 1 receptor, GABAB receptor, and the 5-hydroxytryptamine 2C receptor. The intracellular messengers linked to these GPCRs, including the calcium that is released from internal stores, also play a role in ethanol-enhanced GABA release. Hypotheses are proposed to explain how ethanol interacts with the GPCR pathways to increase GABA release and how this interaction contributes to the brain region specificity of ethanol-enhanced GABA release. Defining the mechanism of ethanol-facilitated GABA release will further our understanding of the GABAergic profile of ethanol and increase our knowledge of how GABAergic neurotransmission may contribute to the intoxicating effects of alcohol and to alcohol dependence.

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    Brain Research Reviews
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