Other symptoms of cocaine overdose include difficulty breathing, high blood pressure, high body temperature, hallucinations, and extreme agitation or anxiety. (Main panel) Cocaine causes the neurotransmitter dopamine to build up at the interface between VTA cells and NAc cells, triggering pleasurable feelings and NAc cellular activities that sensitize the brain to future exposures to the drug. Among the activities are increased production of genetic transcription factors, including ΔFosB; altered gene activity; altered production of potentially many proteins; and sprouting of new dendrites and dendritic spines. If a drug test result is positive during substance use disorder treatment, health care providers may prescribe additional or alternative treatments. However, actual consequences of a positive drug test during substance use treatment may depend on state laws and the individual program.
Each neuron acts as a switch controlling the flow of information. If a neuron receives enough signals from other neurons that it is connected to, it fires, sending its own signal on to other neurons in the circuit. This three-pound mass of gray and white matter sits at the center of all human activity—you need it to drive a car, to enjoy a meal, to breathe, to create an artistic masterpiece, and to enjoy everyday activities. The brain regulates your body’s basic functions, enables you to interpret and respond to everything you experience, and shapes your behavior.
- When stimulated by dopamine, cells in the NAc produce feelings of pleasure and satisfaction.
- Although cocaine also inhibits the transporters for other neurotransmitter chemicals (norepinephrine and serotonin), its actions on the dopamine system are generally thought to be most important.
- Cocaine is typically used orally, intranasally, intravenously, or by inhalation.
- Although health care providers can use it for valid medical purposes, such as local anesthesia for some surgeries, recreational cocaine use is illegal.
- As a result, people take stronger and more frequent doses to feel the same high they did initially and to obtain relief from withdrawal.
Can NIDA assist me with interpreting or disputing the results of a drug screen?
Injecting or smoking cocaine produces a quicker and stronger but shorter-lasting high than snorting. Effective medications for treating cocaine addiction will eventually be developed, and the best strategy for progress in this area is to target neurobio-logical mechanisms, such as those described above. Although the process takes a very long time—it can take 10 to 20 how does cocaine produce its effects national institute on drug abuse nida years to advance from identification of a disease mechanism to development of a new treatment—this work is in progress and represents the best hope for those who are addicted. (Graph inset) The time courses of cocaine-induced buildup of ΔFosB and cocaine-related structural changes (dendrite sprouting) suggest that these neurobiological effects may underlie some of the drug’s short-term, medium-term, and long-term behavioral effects. Every individual is born with a unique combination of roughly 30,000 genes.
There was a substantial increase in the number ofthese students who reported having used cocaine both during the yearand the month preceding the survey, i.e., from 5.6% to 12.4% and from1.9% to 5.8%, respectively. The brain is often likened to an incredibly complex and intricate computer. Instead of electrical circuits on the silicon chips that control our electronic devices, the brain consists of billions of cells, called neurons, which are organized into circuits and networks.
- Now, the person needs to keep taking drugs to experience even a normal level of reward—which only makes the problem worse, like a vicious cycle.
- Cocaine affects the expression of numerous genes within the NAc, including some that influence the important neurotransmitter chemical glutamate and the brain’s natural opioid-like compounds produced by the body (Kalivas and McFarland, 2003; Nestler, 2001).
- If left untreated, they can last a lifetime and may lead to death.
- This finding has shed new light on mechanisms underlying cocaine’s very long-lasting effects on the brain (Nestler, 2001).
- Risk and protective factors may be either environmental or biological.
Although cocaine also inhibits the transporters for other neurotransmitter chemicals (norepinephrine and serotonin), its actions on the dopamine system are generally thought to be most important. To understand the powerful nature of cocaine’s actions, it is helpful to realize that dopamine pathways in the brain are very old in evolutionary terms. Early rudiments are found in worms and flies, which take us back 2 billion years in evolution. Thus, cocaine alters a neural circuit in the brain that is of fundamental importance to survival. Such alterations affect the individual in profound ways that scientists are still trying to understand.
While NIDA-supported research may inform the development and validation of drug-screening technologies, NIDA does not manufacture, regulate, or distribute laboratory or at-home drug screening products. The U.S. Food and Drug Administration (FDA) regulates most of these products in the United States. Those with concerns about drug screening results may consider reaching out to the drug-screening program or a qualified health care professional.
For more information on workplace drug screening, please visit the Substance Abuse and Mental Health Services Administration (SAMSHA) Division of Workplace Programs website. The specific genes that confer risk for cocaine addiction remain unknown. One possibility is that at least some of them are the same genes that are affected by cocaine exposure. For example, variations in the genes encoding ΔFosB or any of hundreds of other genes affected by cocaine could conceivably contribute to the genetic risk for addiction. It is also possible that other genes—genes not affected by cocaine exposure—are responsible. However, instead of leaving the cell that produces it and stimulating neighboring cells as dopamine does, ΔFosB remains in its original cell and stimulates certain genes.
The Neurobiology of Cocaine Addiction
Drug testing can sometimes also detect passive exposure to drugs, such as secondhand smoke or prenatal exposure. The length of time following exposure that a drug can be detected during testing can vary. Drug testing is different than “drug checking,” which helps people who use drugs determine which chemicals are found in the substance they intend to take. Snorted, smoked, or injected, cocaine rapidly enters the bloodstream and penetrates the brain. The drug achieves its main immediate psychological effect—the high—by causing a buildup of the neurochemical dopamine.
FROM THE RUSH TO THE ADDICTION, COCAINE’S EFFECTS IN THE BRAIN.
This too amplifies or disrupts the normal communication between neurons. One of the brain areas still maturing during adolescence is the prefrontal cortex—the part of the brain that allows people to assess situations, make sound decisions, and keep emotions and desires under control. The fact that this critical part of a teen’s brain is still a work in progress puts them at increased risk for trying drugs or continuing to take them. Introducing drugs during this period of development may cause brain changes that have profound and long-lasting consequences. When they first use a drug, people may perceive what seem to be positive effects.
Drug Misuse and Addiction
To keep the receiving cells in each brain region functioning at appropriate intensities for current demands—neither too high nor too low—the dopaminergic cells continually increase and decrease the number of dopamine molecules they launch. They further regulate the amount of dopamine available to stimulate the receptors by pulling some previously released dopamine molecules back into themselves. An initial report from the early 1970s stated that little cost tosociety attributed to cocaine use had been verified in the UnitedStates (1).
To date, most efforts to develop new medications for treatment of cocaine addiction have focused on preventing or suppressing the drug’s acute effects. Cocaine “vaccines,” for example, are designed to bind cocaine molecules in the blood with antibodies and so keep them from getting into the brain. A related approach seeks to develop a medication that keeps cocaine from tying up the dopamine transporter without itself interfering with the transporter’s normal function of dopamine retrieval.
Among the most intriguing of these mechanisms is elevation of the genetic transcription factor ΔFosB, a molecule that lasts for approximately 2 months and theoretically can promote neuron structural changes that have potentially lifelong persistence. The most important goal for the next decade is to translate the knowledge we have already gained, along with any future advances we make, into better treatments for addiction. Scientists currently are working to identify which specific genes ΔFosB stimulates to produce its effects. Comparisons of genes expressed in NAc nerve cells in mice that make ΔFosB versus mice that lack the transcription factor have revealed more than a hundred ΔFosB-mediated changes in gene expression (McClung and Nestler, 2003).
Explore Topics in Substance Use and Addiction Science
One particular part of the limbic system, the nucleus accumbens (NAc), seems to be the most important site of the cocaine high. When stimulated by dopamine, cells in the NAc produce feelings of pleasure and satisfaction. The natural function of this response is to help keep us focused on activities that promote the basic biological goals of survival and reproduction. When a thirsty person drinks or someone has an orgasm, for example, dopaminergic cells flood the NAc with dopamine molecules.
Cocaine increases levels of the natural chemical messenger dopamine in brain circuits related to the control of movement and reward. Normally, dopamine recycles back into the cell that released it, shutting off the signal between nerve cells. However, cocaine prevents dopamine from being recycled, causing large amounts to build up in the space between two nerve cells, stopping their normal communication. This flood of dopamine in the brain’s reward circuit strongly reinforces drug-taking behaviors. With continued drug use, the reward circuit may adapt, becoming less sensitive to the drug. As a result, people take stronger and more frequent doses in an attempt to feel the same high, and to obtain relief from withdrawal.
Why do some people become addicted to drugs, while others do not?
To send a message, a neuron releases a neurotransmitter into the gap (or synapse) between it and the next cell. The neurotransmitter crosses the synapse and attaches to receptors on the receiving neuron, like a key into a lock. Other molecules called transporters recycle neurotransmitters (that is, bring them back into the neuron that released them), thereby limiting or shutting off the signal between neurons.
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