Researchers from the Universities of Cologne, Mannheim, and Heidelberg have
shown that even a single alcohol dose permanently changes the architecture
of neurons. Alcohol specifically affects the synapses' shape as well as the
kinetics of the mitochondria. Professor Dr. Henrike Scholz and her research
members Michèle Tegtmeier and Michael Berger demonstrated that alterations
in the migration of mitochondria in the synapses lessen the rewarding effect
of alcohol using the genetic model system of the fruit fly Drosophila
melanogaster. These findings imply that even a single drinking incident
might set the stage for alcohol addiction. The research was published in
PNAS (Proceedings of the National Academy of Sciences).
What brain changes occur as random drinking develops into chronic alcohol
abuse? That was the topic of a collaborative research study between working
groups at the Universities of Cologne and Mannheim-Heidelberg. The
hippocampus, which is the brain's control center, has been the subject of
the majority of scientific study. Henrike Scholz noted that as a result,
little is understood about the acute neural interactions of important risk
factors, such as a first alcohol intoxication at a young age.
"We sought to identify ethanol-dependent molecular alterations. Following a
single episode of acute ethanol intoxication, they in turn serve as the
foundation for long-lasting cellular alterations. At the molecular,
cellular, and behavioral levels, the consequences of a single alcohol dosage
were investigated "Scholz stated. The working premise was that a single
injection of ethanol would create a favorable connection with alcohol, much
to how memories are created after a single instruction.
The researchers used fruit flies and mouse models to test their theory and
discovered ethanol-induced alterations in two areas: mitochondrial dynamics
and the harmony of synapses in neurons. Energy is provided to cells by
mitochondria, especially nerve cells. The mitochondria shift to best supply
the energy to the cells. In the ethanol-treated cells, the mitochondria's
mobility was erratic. A few synapses' chemical equilibrium was also out of
whack. Animal behavior alterations, such as increased alcohol intake and
alcohol relapse later in life in mice and fruit flies, demonstrated that
these effects remained permanent.
It is generally known that learning and memory are based on the
morphological remodeling of neurons. Associative memories for drug-related
rewards are believed to be formed by means of the same cellular plasticity
mechanisms that are crucial to learning and memory. Consequently, some of
the reported morphological alterations could have an impact on how ethanol
affects memory formation. The researchers hypothesize that these
ethanol-dependent cellular alterations are essential for the emergence of
addictive behaviors, along with the migration of mitochondria in neurons,
which is also crucial for synaptic transmission and plasticity.
The amazing conservation of the molecular mechanisms behind such intricate
reward behavior across animals, according to Scholz, points to a comparable
function in humans. It could be a common cellular function necessary for
memory and learning.
A single intoxicated experience can increase alcohol intake and alcohol
relapse later in life, according to research done on mice. Both of the
reported processes may be able to explain these findings. According to
Professor Scholz, "These processes may even be pertinent to the discovery in
humans that the first alcohol intoxication at a young age is a key risk
factor for subsequent alcohol intoxication and the emergence of alcohol
addiction." This means that the first step in understanding how acute
drinking might develop into chronic alcohol consumption is to detect
long-lasting ethanol-dependent alterations.
