why ketamine makes you happy
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Why Ketamine Makes You Happy
by Sarah C.P. Williams on 15 June 2011, 1:00 PM | 0 Comments
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Happy drug? Ketamine helps combat depression.
Credit: Psychonaught/Wikimedia
When psychiatrists write a prescription for a typical antidepressant such as Zoloft or
Paxil, they don't expect their patients to show much improvement for a few weeks.
Clinical trials, however, have shown that low doses of a drug known as ketamine, which
is used at higher doses as an anesthetic and is taken recreationally as a hallucinogen
(sometimes called "Special K"), can ease the symptoms of depression within hours.
Now, scientists have figured out how ketamine works in the brain. In the process,
they've uncovered a new molecular pathway involved in clinical depression.
Neuroscientist Lisa Monteggia and her colleagues at the University of Texas
Southwestern Medical Center in Dallas began their work on ketamine by verifying what
other scientists have shown: 30 minutes after receiving a dose of ketamine, mice prone
to depression show an easing of their symptoms. When put in a tub of water, mice
considered depressed quickly give up escape attempts and instead float motionless.
After receiving ketamine treatment, such mice swim for a longer period of time in the
water.
Monteggia's team then moved toward understanding how the drug affects the brain.
Scientists already knew that ketamine binds to, and blocks, a receptor in the brain calledNMDAR, which triggers its anesthetic effects, so Monteggia's group used other
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compounds to block NMDARs in mice. As the water test revealed, the animals
depression once again lessened, so the researchers knew that ketamine's antidepressant
effects also depended on NMDAR. Next, the team studied how levels of certain proteins
in the brain changed when mice were given ketamine. Blocking NMDARs with other
compounds turns off production of some proteins, but ketamine causes the neurons to
make more of a protein called BDNF (brain-derived neurotrophic factor), theresearchers report online today inNature. The findings suggest a new set of molecules
that ketamine and NMDAR affects, and that means a new set of molecules involved in
depression.
Live Chat: Are We Training Too Many Scientists? Thursday 3 p.m. EDT
"There was no precedent for this," Monteggia says. "We had no idea why blocking an
NMDAR would produce protein." There are two ways of activating NMDARs. Some
turn on when the specific neurons fire to accomplish a taskbe it learning, memorizing,
or thinking. But other NMDARs are activated simply as background noise in the brain.
Ketamine, the researchers showed, doesn't block the brain from activating NMDARswhen it's using them to send a specific message. But it does block them from creating
that background noise. Although scientists have long known about the brain's
spontaneous level of background nerve firing, Monteggia's study is the first to suggest a
link between such background noise and depression.
"What we're suggesting is that this background activity is important," Monteggia says.
She says that the link between spontaneous nerve firing and depression could also
explain why electroconvulsive therapy (also known as "electroshock therapy") eases
depression--perhaps ECT and ketamine reset the background brain activity.
Furthermore, Monteggia's group identified a new molecule that carries out NMDARs'
effects on spontaneous brain activity. When the researchers activate this protein, called
eEF2, in mice, they see the same fast-acting antidepressant action. A drug that targets
eEF2 instead of NMDARs could treat depression, Monteggia says.
Carlos Zarate, a psychiatrist at the National Institute of Mental Health, in Bethesda,
Maryland, who led many of the initials studies of ketamine as an antidepressant, says
that the study goes far in uncovering a new pathway involved in depression. "It brings
about a new series of targets for drugs that has not been pursued at all."
Although ketamine is used for short-term depression treatment in humans, its potential
for abuse keeps doctors from prescribing it for the long term. A drug that targets theketamine pathway in another way could offer antidepressants without the same potential
for abuse. The next questions, Zarate says, are whether eEF2 is a safe drug target in
humans and what other pathways are involved in depression.
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