How Drugs Get You High

Some drugs, like heroin and marijuana, have molecular structures so similar to the brain’s natural neurotransmitters that they mimic the neurotransmitters themselves, dock directly with receptors on neurons and overstimulate them.

Heroin is an opiate. It’s molecular structure is similar to neurotransmitters made by the brain called opioids, which are responsible for alleviating pain and promoting a sense of well-being. Heroin’s molecular structure correlates to opioids so closely it can dock directly with the brain’s opioid receptors, ultimately stimulating the reward system in much greater concentrations than the brain is used to. Similarly, an ingredient of marijuana mimics another class of neurotransmitters, cannabinoids. Delta-9 tetrahydrocannabinol (THC), the psychoactive component in marijuana, mirrors the brain’s naturally-occurring cannabinoids. The result of heroin mimicking opioids and marijuana mimicking cannabinoids is the same: overstimulating the reward center, resulting in a euphoric high.

Other drugs use different mechanisms. Rather than impersonating neurotransmitters, they cause an increase in the production of neurotransmitters which stimulate reward. Amphetamines, for example, induce increased production of dopamine, the primary reward-center neurotransmitter. Cocaine uses a third mechanism: it prevents the brain from mopping-up excess dopamine. Either way, neurons experience dopamine spikes, resulting in a drug-induced high.

The dopamine neurotransmitter-receptor system manipulated by psychoactive drugs has been used in nature for eons and isn’t exclusive to human brains. As Science Magazine put it, “Most drugs of abuse act on ancient and remarkably conserved neural mechanisms, associated with positive emotions, that evolved to mediate incentive behavior. Heroin, cocaine, alcohol, marijuana, amphetamine, and their synthetic analogs activate …. a system that may be a ‘common neural currency’ for reward…. Some of the transmitter molecules used by these systems evolved as much as 1000 million years ago, and mammalian dopamine, [and] serotonin… neurotransmitters are also used by invertebrate phyla, such as mollusks and arthropods, that diverged from prevertebrate lines roughly 600 million years ago.”

Because these neural systems are so old, they predate the development of consciousness and rational thought. That is, they’re pre-rational.

From an evolutionary perspective, the human brain is innately vulnerable to addiction to psychoactive drugs. Having evolved over millennia, the brain is “not designed to cope with ready access to” modern drugs of relatively high purity available today. “Pure psychoactive drugs and direct routes of administration are evolutionarily novel features of our environment. They are inherently pathogenic [ie., disease causing] because they bypass adaptive information processing systems and act directly on ancient brain mechanisms that control emotion and behavior.”

Bypassing the brain’s normal mechanisms for adaptation leaves it inherently susceptible to substance abuse: “Any organism with a chemically mediated incentive system and technological capabilities is intrinsically vulnerable to addiction, but these special design features of vertebrate reward systems magnify the risks and may explain the otherwise bizarre phenomenon of addicts who sacrifice everything else in life to get drugs that do not reliably bring pleasure, and who return to drug use even after extended periods of abstinence.”

Ominously, some scientists predict that because drug abuse is “rooted in the fundamental design of the human nervous system,” the problem is likely to get worse: “[T]he mismatch between novel pharmacological hyper-incentives and ancient brain mechanisms is likely to worsen with the discovery of new drugs and new routes of administration.”1

For the next article in the Why Drugs Can Be Addicting series click here.

To go back to the Addiction Science Menu click here.

 1. All references in this article are to Psychoactive Drug Use in Evolutionary Perspective, Science Magazine, October 3, 1997


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