Morphine shows promise against post-traumatic stress disorder

Studies find that troops who got the powerful painkiller when injured were about 50% less likely to develop PTSD than those who didn't. The findings offer hope for preventive treatment.

Early administration of morphine to military personnel wounded on the front lines during Operation Iraqi Freedom appears to have done more than relieve excruciating pain. Scientists believe it also prevented hundreds of cases of post-traumatic stress disorder, the debilitating condition that plagues 15% of those who have served in Iraq and Afghanistan.

That conclusion is based on findings published today in the New England Journal of Medicine. They suggest that a simple treatment can stop a single horrifying event from escalating into a chronic, incapacitating illness.

Small clinical trials and observational studies have hinted that opiates and other medications could disrupt the way the brain encodes traumatic memories, thus preventing the incidents from being recorded with too much intensity. The new findings -- troops who received morphine within a few hours of their injuries were about 50% less likely to develop PTSD than those who didn't get the powerful painkiller -- are a strong endorsement of that theory.

The results underscore the potential for preemptive treatment not just for soldiers, but for victims of war, natural disasters, physical abuse, violent crimes such as rape, and traumatic accidents.

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Old Antidepressant Offers Promise in Treating Heart Failure

A team of Johns Hopkins and other researchers have found in animal experiments that an antidepressant developed over 40 years ago can blunt and even reverse the muscle enlargement and weakened pumping function associated with heart failure.

In a report to be published in the Jan. 8 edition of the journal Circulation Research, the international team of U.S. and Italian heart experts describes in a dozen key laboratory experiments in rodents how the antidepressant clorgyline, which is no longer in use in humans, blocks the action of enzyme monoamine oxidase-A (MAO-A) and stops its breakdown of a key neurohormone. Norepinephrine, as it is called, controls the pace of blood pumping and makes the heart pump harder and faster in response to stress.

The latest study results, they say, are believed to be the first evidence showing how elevated MAO-A activity biochemically drives heart failure and that its dangerous downstream effects can be stalled by drug therapy.

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Antidepressant Gatekeeper - Structural and functional studies point to tricyclics' mechanism of action

AN IMPORTANT CLASS of drugs-tricyclic antidepressants (TCAs)—binds in a surprising place. That finding, based on studies with a bacterial protein, could influence the design of new drugs for depression.

According to two new studies, TCAs seal off a molecular passageway in a bacterial counterpart of human neurotransmitter transporter proteins (Nature, DOI: 10.1038/nature06038 and Science, DOI: 10.1126/science.1147614). The work indicates a molecular mechanism of action for this compound class.

Since the 1950s, TCAs such as desipramine (Norpramin and Pertofrane) have been prescribed to treat symptoms of depression. They prevent reuptake of serotonin and norepinephrine by binding to corresponding membrane-spanning neurotransmitter transporter proteins

READ MORE @ CHEMICAL & ENGINEERING NEWS