Scientists from Stanford University found the malfunction of may be a reason for binge drinking turning into alcoholism. With further understanding and study, safer medication aiming to stop the desire for drinking may be designed according to the involved scientists.
Present medicines for alcoholism like disulfiram
only target to reduce the side effects of alcoholism, making people consuming alcohol while feel less uncomfortable, but not decreasing the urge for drinking from a fundamental base. Thus with these chemicals
alcohol bingers still carry a strong wish for drinking.
In a test, AlDH1a1 activities were blocked in mice
manually, which made the mice
present an increased urge for alcohol similar with the mice
that had experienced times of equivalent binge drinking. And making the AIDH1a1 perform normally, a reversed result was presented.
In new studies, scientists also found that AIDH1a1 enzyme
is involved in the formation of a neurotransmitter GABA
in a novel assemble line and it played an indispensable part in the process. GABA
is a type of important and main neurotransmitter
transmission. But the research team only found GABA
manufactured through the novel assemble line in nerve cells
which are related to addiction. This phenomenon may inspire new compounds to treat alcoholism by synthesizing GABA
in the novel way while keep its amount not increasing in other parts of a body to avoid side effects that may be caused by the raised amount of GABA
Furtherly, scientists put up more questions about how GABA
functions to counter addiction. Attention paid to the GABA
manufactured by the nerve cells
that at the same time producing dopamine
. Scientists wondered that what GABA
’s role in these cells
commonly exists in bodies.
By making the AIDH1a1 enzyme
malfunction in mice
, drop of GABA
amount in the dopamine
producing nerve cells
were detected, with which an increase desire for alcohol was presented in the mice
. And raising the level of AIDH1a1, a reverse result was showed.
Dr. Ding guessed that it might be right because of the GABA
co-released with dopamine
by nerve cells
that we didn’t get addicted to pleasurable feelings encountered in daily lives. At present, the study team is still working on to find more about the connection between such neurotransmitters
and other types of addiction.
The study was carried out by scientists from Stanford University of Medicine
School and founded by National institute and other two organizations. Related paper
has been published in Science
on 2nd October titled as Aldehyde dehydrogenase 1a1 mediates a GABA
in midbrain dopaminergic neurons with the doi number being 10.1126/science