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Illicit drugs are defined as those that are illegal to use, make and sell. Drugs that fall under this category include cocaine, heroin, amphetamines (METH), and various hallucinogens. Unfortunately, these same drugs are some of the most used and abused drugs in the world, and often become addictive very quickly.

Psychostimulants and opioids affect the central nervous system (CNS), which controls most functions of the brain and body. These drugs not only affect memory and decision making, but can cause oxidative stress, DNA damage, and epigenetic modifications on a cellular level.

Scientists from Texas A&M University wanted to determine the effect that certain psychostimulants and opioids have on epigenetic modifications in specialized glial cells called astrocytes. Dr. Samikkannu Thangavel and his team focused on changes made to histone acetyltransferases (HAT) and histone deacetylases (HDAC)—the enzymes involved in histone acetylation.

Histone acetylation/deacetylation involves the addition (by HATs) or removal (by HDACs) of an acetyl group on a lysine residue in core histone proteins. This mechanism is directly involved in many processes, including chromatin transcription, gene expression, cell differentiation, DNA replication, and DNA repair.

In addition to these illicit drugs, the team wanted to measure the effects of another drug not like the others. Piracetam is a neuroprotective drug that is used by some to treat anxiety, dementia Alzheimer’s, and alcoholism—though it is not overly successful.

To begin, the team tested each drug to see its impact on class I HDAC protein levels, which are made up of HDACs 1-3. These proteins play a large role in histone deacetylation and are found throughout brain tissues.

They exposed astrocytes to cocaine, METH, and morphine for 24 hrs. They also exposed the cells to those same drugs, but paired with piracetam, and compared all combinations with a control group. Histones were extracted from the astrocytes using the EpiQuik Total Histone Extraction Kit, and HDAC levels were measured.

Cocaine significantly increased HDAC1 levels, but had no notable impact on HDAC2 or 3 levels, either by itself or when paired with piracetam. METH also increased HDAC 1 levels, and substantially increased HDAC3 levels when paired with piracetam. Morphine exposure led to a decrease in HDAC2, but had little to no effect on HDACs 1 and 3.

When the three drugs were paired with piracetam, upregulation of HDAC1 returned to levels similar to the control samples. Overexpression of HDAC1 has been linked to different neurodegenerative diseases, indicating that Piracetam may have some neuroprotective qualities.