Mayo Clinic Bağımlılık Laboratuvarı ekibiyle yaptığımız, Alkol YoksunluÄŸu Sendromunda (Alcohol Withdrawal Syndrome) tamamen yeni bir model öneren ve sakıncaları olan benzodiyazepin tedavisinine alternatif sunabilecek nörobiyolojik bir tedavi modalitesini kanıtlayan, yaklaşık 1 yılllık yıpratıcı bir laboratuvar sürecininin ürünü olan çalışmamız Nature-Neuropsychopharmacology Dergisi’ne yayınlanmak üzere kabul edildi. Çalışmanın literatüre iki önemli katkısı var:
- Alkol YoksunluÄŸu deÄŸerlendirmesinde insan ve hayvan literatürü de dahil olmak üzere, ilk kez kesintisiz bir objektif deÄŸerlendirme yaparak yoksunluk sendromunu deÄŸerlendirmesi ve bu konudaki mevcut “altın standardı”  belirleme gayretini taşıması
- Alkol YoksunluÄŸu’nda halen yaygın bir ÅŸekilde kullanılan ve sakıncaları bilinen benzodiyazepin tedavisine alternatif bir nörobiyolojik devrenin çalıştığını göstermesi ve insanlarda potansiyel ilaç üretimi için yeni bir yol açması
Esas olarak Yoksunluk Sendromu Davranışsal Kodlamasını üstlendiÄŸim, bu çok yorucu, ve sayısız engellerin aşılmasıyla sonuçlanan çalışmadaki çalışma arkadaÅŸlarım baÅŸta Dr Abulseoud ve Dr Choi olmak üzere Mayo Clinic Bağımlılık Psikiyatrisi öğretim üyelerine teÅŸekkür ederim. Çalışmanın özetini ilginize sunuyorum.  Dr UlaÅŸ Çamsarı, Jacksonville, Florida – 24 Ocak 2014
http://www.ncbi.nlm.nih.gov/pubmed/24452391
http://www.nature.com/npp/index.html
Attenuation of Ethanol Withdrawal by Ceftriaxone-Induced Upregulation of Glutamate Transporter EAAT2.
Abstract
Alcohol Withdrawal Syndrome (AWS) is a potentially fatal outcome of severe alcohol dependence that presents a significant challenge to treatment. Although AWS is thought to be driven by a hyperglutamatergic brain state, benzodiazepines, which target the GABAergic system, comprise the first-line of treatment for AWS. Using a rat model of ethanol withdrawal, we tested whether ceftriaxone, a β-lactam antibiotic known to increase the expression and activity of glutamate uptake transporter EAAT2, reduces the occurrence or severity of ethanol withdrawal manifestations. After a two-week period of habituation to ethanol in two-bottle choice, alcohol-preferring (P) and Wistar rats received ethanol (4.0 g/kg) every 6 hours for 3-5 consecutive days via gavage. Rats were then deprived of ethanol for 48 h during which time they received ceftriaxone (50 mg or 100 mg/kg, I.P.) or saline twice a day starting 12 h after the last ethanol administration. Withdrawal manifestations were captured by continuous video recording and coded. The evolution of ethanol withdrawal was markedly different for P rats versus Wistar rats, with withdrawal manifestations occurring >12 h later in P rats than in Wistar rats. Ceftriaxone 100 mg/kg/injection twice per day (200 mg/kg/day) reduced or abolished all manifestations of ethanol withdrawal in both rat variants and prevented withdrawal-induced escalation of alcohol intake. Finally, ceftriaxone treatment was associated with lasting upregulation of ethanol withdrawal-induced downregulation of EAAT2 in the striatum. Our data support the role of ceftriaxone in alleviating alcohol withdrawal and open a novel pharmacologic avenue that requires clinical evaluation in patients with AWS.Neuropsychopharmacology accepted article preview online, 23 January 2014. doi:10.1038/npp.2014.14.
- PMID:
 24452391
[PubMed – as supplied by publisher]
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