Top Stories - Posted by Bill Snyder-Vanderbilt on Sunday, December 26, 2010 19:23 - 2 Comments 
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(No Ratings Yet) Loading ...Flu funk may have ties to depression
This confocal microscope image of the midbrain section shows serotonin-releasing raphe nuclei (in green), the serotonin transporter (stained orange), and immunoreactivity to serotonin (in red). (Credit: Randy Blakely, Vanderbilt)
VANDERBILT (US) — The bad mood that often comes with the flu may be triggered by the same immune system mechanism linked to depression.
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Scientists were able to produce “despair-like” behavior in mice by activating the immune system. Details are reported in the journal Neuropsychopharmacology.
“Many people exhibit signs of lethargy and depressed mood during flu-like illnesses,” says Randy Blakely, a professor of pharmacology and psychiatry at Vanderbilt University. “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.”
Blakely and colleagues previously reported that inflammatory cytokines can enhance the activity of the serotonin transporter (SERT), which regulates the supply of the neurotransmitter serotonin in the synapse, or gap between nerve cells.
Prozac (shown as purple discs) increases the amount of serotonin in the synapse by blocking serotonin reuptake by the serotonin transporter. (Credit: Randy Blakely, Vanderbilt)
Elevations in SERT activity remove serotonin from brain synapses at an enhanced rate and, based on studies in animal models and humans, would be predicted to increase the risk for mood and anxiety disorders. Indeed, a class of antidepressant drugs called selective serotonin reuptake inhibitors (SSRIs)—such as Prozac and Zoloft—work by blocking the ability of SERT to eliminate serotonin.
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 behavior 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,’” Blakely says.
In their paper, the researchers 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,” Blakely says.
Identifying genetic variations in the SERT activation pathway, for example, might suggest additional sources of genetic risk for depression. “Our work suggests that novel therapies targeting inflammation-linked pathways may be of use in the treatment of mood disorders,” he adds.
More news from Vanderbilt: http://news.vanderbilt.edu/
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2 Comments
Mike Johnson
Andy Leisinger
A long-term sufferer of depression and anxiety, I was fascinated by this assertion regarding Cytokines, SERT and depletion of synaptic serotonin. Without fail, when I am struck down by a flu or very heavy viral infection of the chest and head, I find myself battling against acute symptoms of depression and anxiety. And this whilst on Venlafaxine, which has provided me with much long-term stability. It is as if the cytokine toxin just eliminates all efficacy of the AD, rendering me incapable of normal function.
I began to study MS to understand a friend. It may be that research is pointing toward virus generated immune responses in the CNS. I am thinking of neurophilic viruses perhaps of the herpes group. Certainly any virus might cause this including influenza. Perhaps flu simply removes synaptic serotonin causing depression along one path. Another path might be herpes related leading towards mania and depression.
I am thinking about herpes sores being one cause of demyelination and the difficulties caused by MS. The long term would be recurrent CNS herpes lesions that heal incompletely and scar. Eventually the healing and rewiring system is overwhelmed with the behavior or symptoms related to the lesion sites.
Genes are important but what are the causes of CNS autoimmune activity? There will be many pathways because the diagnostic categories are broad and based originally on external observation. To make real progress we will need to identify why a given individual is ill. That we do not yet reliably detect the agents is not a reason to rule them out. Look at the faint but persistent scarring on the lips of the herpes patient and visualize the same type of scarring in the CNS perhaps not on the exterior surfaces.