Addiction and Dopamine

Addiction is where someone has little or zero control over doing, taking or using something to a potentially harmful point. The most common addictions are that of drugs, alcohol, and nicotine.

Brain Neurons

Image Credit: Naeblys/Shutterstock.com

However, addiction can also be related to gambling, work, internet/gadgets, solvents, shopping, and sex amongst other things.  Addictions can have devastating effects on a person’s health, finances, and relationships. Here, only drug addiction will be discussed.

Usually, addictions begin due to neurochemical changes that occur within the brain after using a substance that affects the way you feel both physically and psychologically – often leading to feelings of reward and pleasure.

As such, users often want to use such substances again to achieve the same feelings. When the substance is removed or not taken for a while, withdrawal symptoms can occur which are often unpleasant.

The user thus engages with the addictive activity repeatedly creating a vicious cycle that can get out of control, as you need more and more to satisfy your cravings and urges.

Dopamine, Reward & Addictive Potential

Dopamine is involved with positive reinforcement pathways in the brain and many studies have shown that intoxication is involved with the stimulation of ventral striatal dopaminergic (dopamine-producing) regions and limbic regions.

Withdrawal has been shown to be associated with a reduced function of the dopaminergic system leading to negative emotional symptoms as well as hyperactivity of the stress pathways in the brain which lead to negative reinforcements upon withdrawal.

At this stage, the addictive substance is no longer needed for the positive effects, rather the avoidance of the negative effects.

Controlled administration of cocaine and methamphetamine (intravenously in PET imaging studies) has shown increased dopamine levels in the brain due to the inhibition of dopamine transporters.

The enhanced dopaminergic levels in the striatum are related to self-reporting of ‘highs’ and ‘euphoria’, adding support to the notion that dopamine pathways in the striatum are involved in reward and reinforcement.

Drugs that get to the brain quicker (e.g. intravenously, snorting and smoking) produce significantly quicker increases to the levels of dopamine in the striatum and correlate with feelings of a ‘high’ more than orally administered drugs, thus reflecting the higher addictive potential of drugs that enter the brain quickly compared with those that are ingested, for example.

Indeed, cocaine and nicotine; typically smoked or snorted, along with heroin/morphine (injected) are more addictive than MDMA, caffeine and LSD, which are typically ingested, irrespective of the overall self-reported effects (which are mediated by serotonin, in the case of MDMA). Alcohol is an anomaly in this respect, having a high addictive potential despite being ingested.

Why do substances that cause a sudden increase in dopamine levels (intravenously, snorted or inhaled) lead to a higher addictive potential? Typically, dopaminergic neurons fire tonically around 5Hz to maintain baseline steady-states that also maintain a dopamine-response threshold.

Drugs such as cocaine and heroin lead to a high level of phasic dopaminergic neuronal firing involving fast bursts (> 30Hz) that lead to abrupt oscillatory fluctuations in total extracellular dopamine levels that relate to the saliency of the stimulus.

Ingested drugs, including those used to treat addiction, lead to a moderate phasic dopaminergic release in the brain (between 5Hz-30Hz).

Long-Term Changes to the Brain

Recreational drug users; who are not addicted to drugs, also display the same dopaminergic changes discussed above. Only a small proportion of drug users ever become addicted.

As such, the short-term (acute) effects of drug usage do not explain addiction. Only long-term chronic usage of drugs leads to neuro-adaptation in reward, motivation, inhibition and executive function circuitry – all of which are dopaminergic.

Stimulants, nicotine and other chemical substances used for recreational usage produce persistent changes to the structure of the neurons and glia, their dendrites and dendritic spines within particular dopaminergic brain regions.

This is known as synaptic plasticity, or neuroplasticity, and refers to the structural and functional adaptations of brain cells to recurrent stimuli, in this case, drugs. Synaptic plasticity includes the strengthening, novel formation and elimination of synapses.

Persons who are addicted to various drugs such as cocaine, heroin, and methamphetamine exhibit reductions in dopaminergic receptors (D2DA) within the striatum, which can even persist for some time after total rehabilitation and detoxification.

This also occurs with nicotine and alcohol. The total dopamine being released in addicted individuals is substantially lower for cocaine abusers and alcoholics compared to controls. Consequentially, there is a decreased sensitivity in addicts to both natural endogenous reinforcement as well as the more potent drugs, though they are able to excite the system more.

Over time, regular daily rewards in life may no longer feel rewarding and only drugs will be able to activate these reward systems in the brain, just to ‘feel normal’.  

Other studies have shown reduced regional brain glucose metabolism, as determined by FGD-PET imaging, in particular to the orbitofrontal cortex, cingulate gyrus and dorsolateral prefrontal cortex in persons with addiction.

The decreased energy metabolism in these areas in cocaine addicts is associated with a reduction (and decreased availability) of D2DA receptors in the striatum. These areas are involved in inhibition control and emotional processing; therefore, the reduced function in these areas (all dopaminergic) may underlie the loss of control of intake and emotional self-regulation.

Addiction is not simply related to repeated usage of a drug, but also heavily influenced by other cues in the environment – most notably related to the higher incidences of relapse. Dopamine is involved with the prediction of reward in addition to rewarding itself.

As such, dopamine is therefore involved in conditioned responses that trigger a craving. Animals that are presented neutral stimuli with repeated drug administration will over time be able to increase dopamine in the brain when only exposed to the previously neutral stimuli and the basis of drug-seeking behavior.

When addicts were shown rolled up bank notes, dopamine was released in the striatum and served the basis for drug craving in a cue-dependent manner. This is because habits are associated with the striatum and addiction is a neurobiological adaptation to cortico-striatal pathways that regulate dopamine release.

In summary, dopamine seems to be a key player in the onset and maintenance of drug addiction, though there are other notable neurochemicals at play too which have not been discussed in this article. Dopaminergic pathways in the brain are involved in reward, motivation and executive control with key regions of the brain, all of which are implicated in addiction.

Given that dopamine dysfunction is critical in addiction, dopamine-targeted therapies may be beneficial for neurochemical rehabilitation and recovery. By targeting reward and motivation pathways in the brain, the value of a drug and motivation to use it by strengthening executive control would be beneficial for patients.

Sources:

Volkow et al, 2009. Imaging dopamine's role in drug abuse and addiction. Neuropharmacology. 56 Suppl 1:3-8. https://www.ncbi.nlm.nih.gov/pubmed/18617195

Solinas et al, 2019. Dopamine and addiction: what have we learned from 40 years of research. J Neural Transm (Vienna). 126(4):481-516. https://www.ncbi.nlm.nih.gov/pubmed/30569209

Last Updated: Jan 24, 2020

Osman Shabir

Written by

Osman Shabir

Osman is a Neuroscience PhD Research Student at the University of Sheffield studying the impact of cardiovascular disease and Alzheimer's disease on neurovascular coupling using pre-clinical models and neuroimaging techniques.

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