Pubdate: Mon, 04 Dec 2017
Source: Blade, The (Toledo, OH)
Copyright: 2017 The Blade
Author: Stuart Collins


For someone caught up in the heat of the moment at a local dance club
or rave scene, taking ecstasy may not seem like a life-changing event.
But as studies have shown, this decision may indeed be

A frequent consequence of taking ecstasy is a trip to the hospital.
This is because the short-term effects of ecstasy can produce
life-threatening increases in temperature and heart rate, and

Stuart Collins is a PhD student in the neurosciences and neurological
disorders at the University of Toledo college of medicine.

According to the Substance Abuse and Mental Health Services
Administration, more than 17,000 hospital visitations resulted from
individuals who had taken ecstasy in 2008 alone. Ecstasy has been
known as a drug of abuse since the 1970s, but it only exploded into
popular abuse in the mid-1990s. A recent survey from the National
Institute of Drug Abuse has found that 11 million people have taken
ecstasy at least once.

The long-term effects of ecstasy have also been documented in many
studies. These studies show that ecstasy damages neurons, which are
our core brain cells. This damage can last for months and even longer.

The goal of our research is to understand the mechanisms by which
ecstasy damages the brain. Specifically, the focus of our project is
to determine how a subset of neurons is decreased by ecstasy and how
this affects brain function. These particular neurons (parvalbumin
interneurons) provide inhibitory signaling to the brain to filter out
nonimportant information.

This is similar to noise cancelling headphones that can filter out
extra noise, allowing the listener to hear the music more clearly.
Ecstasy causes a loss of these cells in an area of the brain
associated with learning and memory. Therefore, such a loss is
believed to reduce the ability of the brain to form new memories. This
is correlated with numerous studies that have shown learning
deficiencies in people that have taken Ecstasy.

Using techniques that can measure brain activity, we have shown that
inhibitory signaling is reduced in the brains of rats that had been
given Ecstasy. This supports our idea that losing these cells after
Ecstasy exposure results in a loss of this inhibitory effect,
therefore causing less filtering out of extra noise.

Further studies will determine whether this is a direct result of
losing parvalbumin interneurons that, in turn, could lead to learning
deficiencies observed after using Ecstasy.

To aide our understanding of how Ecstasy may be causing these learning
deficiencies, we sought to determine how Ecstasy may promote a loss in
the parvalbumin interneurons. To accomplish this goal, we have focused
our studies on the mechanisms by which Ecstasy creates its appeal.

One major effect of Ecstasy is to increase release of
neurotransmitters, which are used by neurons for cell-to-cell
communication. Serotonin is one of the neurotransmitters that undergo
increased release after exposure to Ecstasy. Increased serotonin
causes the reduced anxiety and increased feelings of intimacy that
occur after taking Ecstasy. Importantly, our experiments have shown
that increased serotonin release also increases cell damage because of
increased inflammation in the brain.

Notably, we have also shown that the loss of parvalbumin brain cells
caused by Ecstasy can be prevented by inhibiting the effects of
serotonin, including inflammation.

We are planning future experiments to build upon this information.
This research will help scientists understand how Ecstasy causes a
loss of neurons to produce learning deficiencies. This information, in
turn, will form the building blocks of strategies to prevent loss of
these important cells.

Stuart Collins is a PhD graduate student in the neurosciences and
neurological disorders track at the University of Toledo college of
medicine and life sciences biomedical science program, formerly the
Medical College of Ohio. Mr. Collins is doing his research in the
laboratory of Bryan Yamamoto. For information,  ---
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