Researchers have identified an association between inflammatory response and depression. Vanderbilt University scientists found that depression may be activated by the same mechanism that enables the immune system to respond to any form of infections.
Chong-Bin Zhu, William Hewlett and colleagues activated the immune system in mice to produce "despair-like" behaviour that has similarities to depression in humans.
"Many people exhibit signs of lethargy and depressed mood during flu-like illnesses," said Blakely, of the Vanderbilt Center for Molecular Neuroscience.
"Generally these have been treated as just a consequence of being physically ill, but we think there is likely to be something more brain-centric at work here," he said.
Blakely and colleagues had previously reported that inflammatory cytokines could enhance the activity of the serotonin transporter (SERT), which regulates the supply of the neurotransmitter serotonin in the synapse, or gap between nerve cells.
In the current study in mice, the researchers triggered pro-inflammatory cytokine production. Within 30 to 60 minutes, SERT was activated in the brain and the animals displayed despair-like behavior.
Remarkably, this behaviour was not observed when cytokine production was triggered in mice lacking the SERT gene. Similarly, a drug that blocks inflammatory molecule signaling also prevented stimulation of SERT and the despair behavior.
"It's as if these inflammatory molecules are an 'anti-Prozac,'" said Blakely.
The researchers have cautioned that "we do not presume that changes in SERT activity alone are sufficient to induce the full spectrum of depression traits, nor that our animal model can reproduce all the elements of a complex neuropsychiatric disorder."
"Nonetheless, we were able to identify a mechanism that may be a engaged, even without inflammation, to impact risk for depressive illness," said Blakely.
The findings were published in the journal Neuropsychopharmacology.