Gen terkait Ketergantungan alkohol dengan neurotransmiter--T-REC--komunitas reptil-semarang--KSE--komunitas satwa eksotik

SILAHKAN MENGGUNAKAN " MESIN TRANSLATE "..GOOGLE TRANSLATE 
DISAMPING KANAN INI.............

PLEASE USE ........ "TRANSLATE MACHINE" .. GOOGLE TRANSLATE BESIDE RIGHT THIS

.................

T-REC -TUGUMUDA REPTILES COMMUNITY-INDONESIA

More info :

www.trecsemarang2011.blogspot.com

minat gabung : ( menerima keanggotaan seluruh kota dan daerah di Indonesia )

08995557626

..................................

KSE – KOMUNITAS SATWA EKSOTIK – EXOTIC PETS COMMUNITY-- INDONESIA

Visit Our Community and Joint W/ Us....Welcome All Over The World

www.facebook.com/groups/komunitassatwaeksotik/

 KSE = KOMUNITAS SATWA EKSOTIK

MENGATASI KENDALA MINAT DAN JARAK

KAMI ADA DI TIAP KOTA DI INDONESIA 

DETAIL TENTANG KSE-----KLIK : www.komunitassatwaeksotik-pendaftaran.blogspot.com 

GABUNG......... ( menerima keanggotaan seluruh kota dan daerah di Indonesia )

HUBUNGI   :  089617123865

.........................

 

Gen terkait Ketergantungan alkohol  dengan neurotransmiter

Para ilmuwan telah memecahkan misteri mengapa jalur signaling tertentu dapat dikaitkan dengan ketergantungan alkohol. Penelitian baru menunjukkan gen, Nf1, mengatur asam gamma - aminobutirat (GABA), neurotransmitter yang menurunkan kecemasan dan meningkatkan perasaan relaksasi..........

Alcohol-dependence gene linked to neurotransmitter

Date:

August 27, 2014

Source:

Scripps Research Institute

Summary:

Scientists have solved the mystery of why a specific signaling pathway can be associated with alcohol dependence. The new research shows the gene, Nf1, regulates gamma-aminobutyric acid (GABA), a neurotransmitter that lowers anxiety and increases relaxation feelings

..................

Scientists at The Scripps Research Institute (TSRI) have solved the mystery of why a specific signaling pathway can be associated with alcohol dependence.

This signaling pathway is regulated by a gene, called neurofibromatosis type 1 (Nf1), which TSRI scientists found is linked with excessive drinking in mice. The new research shows Nf1 regulates gamma-aminobutyric acid (GABA), a neurotransmitter that lowers anxiety and increases feelings of relaxation.

"This novel and seminal study provides insights into the cellular mechanisms of alcohol dependence," said TSRI Associate Professor Marisa Roberto, a co-author of the paper. "Importantly, the study also offers a correlation between rodent and human data."

In addition to showing that Nf1 is key to the regulation of the GABA, the research, which was published recently in the journal Biological Psychiatry, shows that variations in the human version of the Nf1 gene are linked to alcohol-dependence risk and severity in patients.

Pietro Paolo Sanna, associate professor at TSRI and the study's corresponding author, was optimistic about the long-term clinical implications of the work. "A better understanding of the molecular processes involved in the transition to alcohol dependence will foster novel strategies for prevention and therapy," he said.

A Genetic Culprit

Researchers have long sought a gene or genes that might be responsible for risk and severity of alcohol dependence. "Despite a significant genetic contribution to alcohol dependence, few risk genes have been identified to date, and their mechanisms of action are generally poorly understood," said TSRI Staff Scientist Vez Repunte-Canonigo, co-first author of the paper with TSRI Research Associate Melissa Herman.

This research showed that Nf1 is one of those rare risk genes, but the TSRI researchers weren't sure exactly how Nf1 affected the brain. The TSRI research team suspected that Nf1 might be relevant to alcohol-related GABA activity in an area of the brain called the central amygdala, which is important in decision-making and stress- and addiction-related processes.

"As GABA release in the central amygdala has been shown to be critical in the transition from recreational drinking to alcohol dependence, we thought that Nf1 regulation of GABA release might be relevant to alcohol consumption," said Herman.

The team tested several behavioral models, including a model in which mice escalate alcohol drinking after repeated withdrawal periods, to study the effects of partially deleting Nf1. In this experiment, which simulated the transition to excessive drinking that is associated with alcohol dependence in humans, they found that mice with functional Nf1 genes steadily increased their ethanol intake starting after just one episode of withdrawal. Conversely, mice with a partially deleted Nf1 gene showed no increase in alcohol consumption.

Investigating further, the researchers found that in mice with partially deleted Nf1 genes, alcohol consumption did not further increase GABA release in the central amygdala. In contrast, in mice with functional Nf1 genes, alcohol consumption resulted in an increase in central amygdala GABA.

In the second part of the study, a collaboration with a distinguished group of geneticists at various U.S. institutions, the team analyzed data on human variations of the Nf1 gene from about 9,000 people. The results showed an association between the gene and alcohol-dependence risk and severity.

The team sees the new findings as "pieces to the puzzle." Sanna believes future research should focus on exactly how Nf1 regulates the GABA system and how gene expression may be altered during early development.

---

Story Source:

The above story is based on materials provided by Scripps Research Institute. Note: Materials may be edited for content and length.

---

Journal Reference:

1. Vez Repunte-Canonigo, Melissa Herman, Tomoya Kawamura, Henry R. Kranzler, Richard Sherva, Joel Gelernter, Lindsay A. Farrer, Marisa Roberto, Pietro Paolo Sanna. Nf1 regulates alcohol dependence-associated excessive drinking and GABA release in the central amygdala in mice, and is associated with alcohol dependence in humans.. Biological Psychiatry, 2014; DOI: 10.1016/j.biopsych.2014.07.031

http://www.sciencedaily.com/releases/2014/08/140827141408.htm

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Share this: