There’s a name for the inability to take pleasure in activities you once found enjoyable, the subject of countless commercials for depression medications: anhedonia.
In a study published Thursday in the journal Science, scientists stimulated the brains of rats to induce feelings of anhedonia, helping to explain how the phenomenon arises in the brain.
Hopefully, this understanding could one day lead to better treatments for depression and other related mood disorders.
Pleasure in the brain
Normally when we experience pleasure, the neural signaling chemical dopamine floods a part of our brain’s reward center called the striatum.
Previous research suggests anhedonia may be linked to lower activity in a part of the brain called the medial prefrontal cortex (mPFC), which may act as a kind of conductor for the brain’s reward system. But we still don’t understand exactly what’s going on.
To investigate further, Stanford neuroscientist Emily Ferenczi and her colleagues used brain imaging and stimulation techniques to induce anhedonia in rats.
First, they stimulated dopamine neurons in the animals’ midbrains (where dopamine exerts its effects) by shining light on light-sensitive nerve cells, a technique known as optogenetics. This caused a boost in activity in the reward area or striatum, which was measured by functional magnetic resonance imaging (fMRI), a technique that detects blood flow in the brain.
Next they stimulated neurons in the rats’ mPFC, and found that it decreased activity in the striatum. In one experiment, the stimulation made the animals lose their interest in drinking sugar water, which they normally prefer over plain water. In another experiment, stimulating the mPFC made rats less social when presented with another young rat.
Finally, stimulating the mPFC strengthened its connections to other areas of the brain, while weakening connections to some regions involved in depression and schizophrenia, the researchers report in the study.
The results suggest that anhedonia causes its effects via the mPFC, which controls the release of dopamine in wide-ranging parts of the brain.
These findings are in line with those of several previous studies of anhedonia.
In a small 2003 study in the journal Neuroreport, researchers scanned the brains of 14 women — seven who had been diagnosed with major depression and seven healthy women — while showing them positive or neutral images. Compared to the healthy subjects, the depressed women had lower activity in the mPFC.
And scientists have had some success in treating depression by targeting this region with deep brain stimulation, a technique that involves zapping brain cells with small amounts of electricity. A 2005 study in the journal Neuron found that four out of six patients with depression who received stimulation in the mPFC went into remission.
Taken together, this research reveals how our brain circuitry can go awry and suck the enjoyment out of life — and point toward a possible way to counteract the problem.