The Epigenetics of Drug Abuse

At the Society for Neuroscience conference, researchers present results linking the epigenome to heroin and cocaine addiction.

By | November 11, 2013

WIKIMEDIA, LSDBStudying post-mortem human brains of heroin abusers, Yasmin Hurd of the Icahn School of Medicine at Mount Sinai and her colleagues found significant changes in gene networks related to glutamate pathways in the striatum, an area commonly linked to drug use. Moreover, the researchers found that these differences in gene expression resulted from epigenetic alterations in this brain region, and that these changes were more pronounced among long-term users. “In heroin users, there are clear disturbances of epigenetic mechanisms that directly correlate with their years of drug use,” Hurd said today (November 11) during a press conference at the annual conference of the Society for Neuroscience (SfN). The researchers also found evidence of chromatin restructuring that could underlie habit formation, she added.

In other new research presented at SfN, Eric Nestler, also of the Icahn School of Medicine, discussed the possibility that cocaine addiction may result from epigenetic changes in the brain. He and his colleagues examined the effects of cocaine use on the mouse nucleus accumbens, a brain region involved in reward and goal-directed behavior.

Once again, the researchers found evidence of alterations to DNA’s structure, including its chromatin, to produce repeatable, predictable changes in gene expression. “It’s well established that cocaine addiction has lasting effects on the brain,” Nestler said in a press release. “But studies in our lab begin to reveal just how extensive these changes are and how they might change brain function. This level of understanding could lead to better treatments for addiction.”

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Avatar of: ironjustice

ironjustice

Posts: 28

November 12, 2013

Why does the same mouse not acquire an addiction when acetylcholine is enhanced?

"Acetylcholine enhancement in the nucleus accumbens

prevents addictive behaviors of cocaine and morphine"

They've shown consumption of lecithin raises acetylcholine.

“Lecithin consumption raises serum-free-choline levels”

“Lecithin may therefore be the method of choice for accelerating acetylcholine synthesis”

Lecithin was used back in the fifties in India as a treatment for opoid addiction.

“Results of treatment with lecithin and glucose: Mass scale trials”

Does acetylcholine figure in preventing epigenic changes?

Avatar of: ironjustice

ironjustice

Posts: 28

November 12, 2013

Nicotine and acetylcholine affect the same receptors and nicotine is shown to possibly prevent chromatin remodeling?

"nicotine"

"it did modulate expression of 129 genes that could be relevant to the neuroprotective effects of smoking, including genes involved in (1) the ubiquitin-proteasome pathway, (2) cell cycle regulation, (3) chromatin modification, and (4) DNA binding and RNA regulation. We also report preliminary transcriptome data for single-cell dopaminergic and GABAergic neurons isolated from midbrain cultures. These novel techniques will facilitate advances in understanding the mechanisms taking place at the cellular level and may have applications elsewhere in the fields of neuroscience and molecular biology. The results give an emerging picture of the role of nicotine on the SNc and on dopaminergic neurons."

Avatar of: James V. Kohl

James V. Kohl

Posts: 156

November 16, 2013

I included a section on addiction in "Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors."

Excerpt: The Public Policy Statement: Definition of Addiction (ASAM, 2011) represents a paradigm shift that may move the current practice of clinical psychology forward. It dictates the adoption and integration of neuroscientific principles that are required in order to understand differences between genetically predisposed brain disease, naturally occurring variations of behavioral development, and choice. These neuroscientific principles include focus on how sensory input influences behavior. The statement specifically mentions food and sex along with drugs and alcohol; each seems to chemically condition changes in hormones and in behavioral responses. Although no link between cause and effect is mentioned by ASAM, these principles could incorporate the GnRH neurophysiological mechanism and levels of LH, which link food odors and pheromones to chemically conditioned behaviors.

The molecular mechanisms of epigenetically-effected addiction are clearly conserved across species, and I have since published a model detailing that fact. Nutrient-dependent/pheromone-controlled adaptive evolution: a model. I don't think anyone disagrees that the need to understand how the epigenetic landscape becomes the physical landscape of DNA in the organized genomes of species from microbes to man is important, and several people are aware that olfactory/pheromonal input is the key to epigenetic effects on alternative splicings associated with addiction.

 What's next from neuroscientists? Should we expect them to understand the singularity of monoallelic olfactory receptor gene expression in the context of all addictions that involve receptor-mediated behavior? Or must more research be done to avoid the most obvious direct link between epigenetics and receptor-mediated cause and effect. It's olfactory/pheromonal input, the key to survival in species from microbes to man. The molecular mechanisms of addiction involve the same pathway essential to species survival, and that's the problem.

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