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Probing cocaine in the heart and the brain.

Probing cocaine in the heart and the brain

Two recent drug studies add new details to the picture of how cocaine damages the body and point to a way of easing withdrawal pangs in addicts.

At Brookhaven National Laboratory in Upton, N.Y., researchers injected healthy volunteers with radioactively labeled cocaine at doses far too small to induce addiction or a "high." They discovered that the drug binds strongly to human heart cells, particularly in the left ventricle. Study leader Nora D. Volkow says the research, undertaken with permission from the Food and Drug Administration, suggests that cocaine overdose may pose a triple threat to the heart.

Scientiests already knew that cocaine abuse can cause heart failure through its indirect effects -- constricting blood vessels and manipulating the brain to disrupt normal heart rhythm. But in binding directly to cardiac tissue, cocaine may add a third lethal punch by slowing the passage of sodium ions into heart cells and/or stimulating the release of the neurotransmitter norepinephrine, which can lead to irregular heartbeat, or arrhythmia, Vokow asserts.

She and her colleagues also found that large concentrations of cocaine bind to the aorta, the major artery carrying blood from the heart. This, they say, may account for some of the blood vessel damage associated with cocaine overdose. Volkow reported the findings last week at the annual meeting of the Society of Nuclear Medicine in Washingtoin, D.C.

In a separate study described at the meeting, Volkow's team and collaborators at the State University of New York at Stony Brook examined human brain scans highlighting nerve-cell receptors for the neurotransmitter dopamine.

Normally, dopamine spills into the gap, or synapse, between the "prosynaptic" neuron that released it and a neighboring, "postysnaptic" neuron, staying there just long enough to stimulate receptors on the second neuron. The dopamine then returns to the storage compartments of the presynaptic cell, a process known as reuptake. But cocaine blocks reuptake, leaving dopamine in the synapse to repeatedly bombard the post-synaptic receptors, contributing to a temporary feeling of euphoria.

The number of postsynaptic receptors can fluctuate with changes in stimulation levels. To assess cocaine's effect on receptor abundance, the researchers gave trace amounts of a radioactively tagged compound that binds selectively to post-synaptic dopamine receptors to 10 healthy volunteers and 10 cocaine addicts who had not taken the drug for one month or less.

Addicts who had been off the drug for one week or less showed about 30 percent fewer dopamine receptors than the healthy volunteers, Volkow and her colleagues found. Those who had abstained for a full month had about the same number of receptors as the healthy controls, the researchers note in the June AMERICAN JOURNAL OF PSYCHIATRY.

Volkow conjectures that the decreased number of dopamine receptors reflects the body's attempt to balance a system gone out of control: As cocaine floods synapses with dopamine, postsynaptic receptors dwindle in number to avoid excess stimulation. But when addicts stop taking cocaine, the receptor looss can leave them temporarily starved for dopamine and craving the drug, Volkow suggests, noting that most relapses occur during the first weeks of treatment.

Other researchers have proposed similar scenarios for cocaine's influence on dopamine receptors. But until now, Volkow says, tests of those theories in humans have relied only on indirect measurements, such as correlating cocaine use with blood levels of prolactin, a dopamine-regulated hormone. The new study, which directly measured receptor abundance, suggests recovering addicts may have fewer relapses and less craving for cocaine if they receive compounds that mimic or enhance their natural supply of dopamine during the first few weeks of treatment.

"Timing is essential. Giving a dopamine-like drug after the first weeks may not help," she says, because dopamine receptors may have bounced back to normal values by then. Volkow stresses that while such drugs might aid in treatment, they cannot cure the underlying addiction.

Dean Wong of the Johns Hopkins University in Baltimore says he finds Volkow's theory reasonable and awaits further work to verify her preliminary findings. Wong and Godfrey D. Pearlson of Hopkins have begun a more detailed imaging study of postsynaptic dopamine receptors among people receiving cocaine in a nose spray.

For several years now, Charles A. Dackis of Hampton Hospital in Westampton, N.J., has experimentally treated cocaine addicts suffering severe withdrawal symptoms with a dopamine-mimicking compound called bromocriptine. Dackis says it has helped ease withdrawal cravings, and he attributes the effect to bromocriptine's ability to replace the dopamine stimulation once provided by cocaine. In a departure from Volkow's scenario, he suggests his patients respond to bromocriptine because they have developed an excess of postsy naptic receptors. Citing evidence from animal studies, he proposes that this excess arises from the dopamine-starved brain's attempt to capture every drop of the neurotransmitter.
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Author:Cowen, Ron
Publication:Science News
Date:Jun 30, 1990
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