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Cocaine and the brain

Cut – N – Paste Notes for my education group, except for the first one the web page is on the top. Emphasis is mine.

Cocaine in the Brain

Melissa Hoegler

“Cocaine delivers an intensity of pleasure – and despair – beyond the bounds of normal human experience.”

When a person takes cocaine, it causes a rush. There is between one or two minutes of intense pleasure. This is followed by five to 8 minutes of euphoria, then as the high comes down, an overwhelming urge for more, which may last for a day. When a user is between cocaine doses or halts usage, the opposite effects occur. The user is depressed and tired.

Cocaine is attractive to users because it triggers dopamine. Dopamine is a neurotransmitter that is present in many regions of the brain. In normal mice, the introduction of cocaine increases dopamine by 150 percent. Dopamine regulates movement, emotion, motivation, and the feeling of pleasure. In a normal brain, dopamine is released by a neuron into a synapse and then it moves to dopamine receptors on other neurons. It is then moved back to the neuron that transmitted the dopamine initially.

When cocaine enters the area of the brain where the dopamine is located, it blocks the reuptake pumps that remove the dopamine from the synapse of the nerve cell. Thus, more dopamine gathers at the synapse and feelings of intense pleasure result. This feeling continues until cocaine is naturally removed from the system. Research findings by the National Institute of Drug Addiction (NIDA) demonstrate that cocaine not only effects the level of dopamine in the brain, but also the level of seratonin. In a study using mice without dopamine transporters, the mice were given cocaine and they still experienced rewarding effects. This was obvious because the animals kept on attempting to get or self-administer more. These researchers speculate that more than one neurotransmitter is responsible for the pleasurable feeling cocaine yields. Although main hypothesis as to why cocaine is so pleasurable, is that it alters levels of dopamine, norepinephrine, and seratonin, some scientists report that cocaine effects approximately 90 different parts of the brain, not just the two main regions of the amygdala and the nucleus accumbens. However, it is interesting that it is these two regions of the brain that remain active after the cocaine has left the system, and the powerful, uncontrollable desire for the drug has set in.

It was recently discovered through newer imaging techniques that cocaine hinders blood flow. This is why is it can cause brain damage or defects. Recent research demonstrates that if a cocaine user even thinks about cocaine, the blood flow is altered . This suggests that the addictive nature of the drug is stronger than we think, because simply thinking about it produces similar results in addicts’ brains’. This is likely to be a result of the way in which cocaine changes the structure of an abuser’s brain. For example n experiments done with lab rats, scientists reported that after repeated exposure to cocaine, the rats’ dendrites changed by becoming bigger and denser. This means that an increase in synaptic connectivity results from cocaine use which triggers people and animals to work harder to attain the drug.

www.cocaine.org

When Is It Best To Take Crack Cocaine?

As a rule of thumb, it is profoundly unwise to take crack-cocaine. The brain has evolved a truly vicious set of negative feedback mechanisms. Their functional effect is to stop us from being truly happy for long. Nature is cruelly parsimonious with pleasure. The initial short-lived euphoria of a reinforcer as uniquely powerful as crack will be followed by a “crash”. This involves anxiety, anhedonia, depression, irritability, extreme fatigue and possibly paranoia. Physical health may deteriorate. An intense craving for more cocaine develops. In heavy users, stereotyped compulsive and repetitive patterns of behaviour may occur. So may tactile hallucinations of insects crawling underneath the skin (“formication”). Severe depressive conditions may follow; agitated delirium; and also a syndrome sometimes known as toxic paranoid psychosis. The neural after-effects of chronic cocaine use include changes in monoamine metabolites and uptake transporters. There is down-regulation of dopamine D2 receptors to compensate for their drug-induced overstimulation. Thus the brain’s capacity to experience pleasure is diminished.

/www.drugabuse.gov/infofacts/cocaine.html

Researchers have found that the human liver combines cocaine and alcohol to produce a third substance, cocaethylene, which intensifies cocaine’s euphoric effects. Cocaethylene is associated with a greater risk of sudden death than cocaine alone.

Behavioral interventions—particularly, cognitive-behavioral therapy—have been shown to be effective for decreasing cocaine use and preventing relapse. Treatment must be tailored to the individual patient’s needs in order to optimize outcomes—this often involves a combination of treatment, social supports, and other services.

Currently, there are no FDA-approved medications for treating cocaine addiction

www.drugabuse.gov/NIDA_notes/NNvol22N2/LongTerm.html

Chronic exposure to cocaine depresses neural activity. Initially, the effect shows up mostly in the brain’s reward areas. With longer exposure, however, neural depression spreads to circuits that form cognitive and emotional memories and associations.

All the monkeys that had self-administered cocaine showed some localized depression of glucose metabolism. In the monkeys that self-administered cocaine daily for just 5 days, neural depression was largely restricted to pleasure and motivation areas, especially the reward circuit and areas that process expectations of rewards.

In the 100-day test, animals that had received the high dose of the drug revealed less neural activity in 40 of the 77 brain regions analyzed as compared with animals that had received only food morsels (see table). The high-dose monkeys incurred a 16 percent drop, on average, in overall cerebral glucose metabolism. The low dose of cocaine depressed metabolism in 14 of the regions, but not overall.

The tests suggest that with longer exposure to cocaine, reductions in neural activity expand within and beyond the pleasure and motivation centers, says Dr. Porrino. “Within the structure called the striatum, the blunting of activity spreads from the nucleus accumbens, a reward area, to the caudate-putamen, which controls behavior based on repetitive action,” she says. Long-term cocaine use also depressed memory and information-processing areas.

The findings accord well with those of human imaging studies, which have found general depression in cerebral blood flow among chronic cocaine abusers compared with nonabusers. By using animals, however, Dr. Porrino eliminated two sources of uncertainty in those clinical studies: differences in metabolic rates that may have predated cocaine abuse and abuse of drugs other than cocaine. “My team can directly attribute to cocaine the depressed brain metabolism observed in the study,” says Dr. Porrino.

“Our 100-day experimental protocol for rhesus monkeys gives a good picture of what might happen in the brains of cocaine abusers,” she says. “Some addiction researchers believe that the shift in activity within the striatum may, in part, underlie the progression from voluntary drug taking to addiction. Moreover, human imaging research has linked drug craving with the amygdala and insula, temporal lobe areas depressed by cocaine in our study.”

COCAINE SELF-ADMINISTERED BY MONKEYS FOR 100 DAYS DEPRESSES NEURAL ACTIVITY IN SPECIFIC BRAIN AREAS. Name of area Selected roles in behavior Depression of metabolic activity* (percentage) Nucleus accumbens (ventral striatum) Processes reward and motivation 16-31 Caudate-putamen (dorsal striatum) Controls behaviors based on repetitive action 10-23 Hypothalamus Controls eating, fighting, mating, and sleep 18-22 Insula Translates body signals into subjective feelings 17-19 Hippocampus Consolidates memories and influences mood 15-23 Amygdala Forms emotional and motivational memories, e.g., linking a cue and a drug to produce craving 13-19 Temporal cortex areas Processes emotional and cognitive information, e.g., recognition and short-term memory 17-22

alcoholism.about.com/cs/coke/a/blyale030835.htm

A diuretic commonly used to treat hypertension and congestive heart failure may improve brain blood flow in cocaine addicts, according to a study in the August 2003 issue of Drug and Alcohol Dependence.

Chronic cocaine use is associated with decreases in blood flow to the brain, but the mechanism for this decrease is not fully understood. Researchers theorize cocaine-induced constriction of the arteries in the brain and/or increased blood clotting may be involved.

The problems associated with decreased brain blood flow in some cocaine abusers are the results of major stokes such as paralysis, loss of ability to speak, severe cognitive impairment and in the worst cases death. The patients in these studies with reduced blood flow to their brain had significant impairment in thinking, concentrating, reading and remembering things. They also had significant depressive symptoms that may be related to these deficiencies in brain functioning due to lack of sufficient blood flow to the neurons.

Thus, increasing blood flow back to normal can reverse these cognitive impairments and make these patients more responsive to our behavioral treatments which require learning of new skills to refuse drugs. These improvements in cognition can also enable these patients to return to productive employment and be active members of society.

To gauge the effects of the diuretic amiloride on cocaine dependent subjects, Thomas Kosten, M.D., professor of psychiatry at Yale School of Medicine, and colleagues administered amiloride, aspirin or placebo to 49 patients for one month while they resided on a research unit. Blood flow in the brain was measured on admission to the unit and at the end of treatment.

At the time they were enrolled in the study, cocaine-dependent subjects showed decreased cerebral blood flow compared to 18 control subjects. After four weeks of treatment the researchers found that the amiloride, but not aspirin or placebo, improved blood flow in the brain. None of the treatments affected blood clotting.

The authors speculate that the improvement by amiloride may be due to the medication’s ability to dilate the arteries in the brain. The authors also pointed out that amiloride may be used in combination with other medications that also increase cerebral blood flow to treat cocaine dependent patients.

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