Whether disappointment is prompted by big setbacks or small mishaps, the feeling originates from within the brain. Now, scientists have identified a part of the brain that controls the processing of sensory and emotive information that results in this feeling.
This discovery could have major implications in the future treatment of mood disorders such as depression, as the researchers’ findings expand upon what is known about how the human body registers negative life events.
“The idea that some people see the world as a glass half empty has a chemical basis in the brain,” said Dr. Roberto Malinow, senior author of the study published in Science. “What we have found is a process that may dampen the brain’s sensitivity to negative life events.”
According to the Centers for Disease Control and Prevention (CDC), an estimated 1 in 10 adults in the US report experiencing depression.
Scientists believe that people with depression process negative experiences more strongly than others, and so the study’s findings could help researchers toward understanding what causes the condition and how it can be treated.
Through experiments with rodents, the researchers from the University of California, San Diego, discovered that neurons connecting to an area of the brain called the lateral habenula (LHb) were producing both glutamate and GABA; the former being an excitatory neurotransmitter and the latter being an opposing inhibitory neurotransmitter.
Neuronal firing is promoted by excitatory neurotransmitters and suppressed by inhibitory neurotransmitters. While glutamate and GABA are relatively common throughout the brain, neurons tend to specialize in producing one rather than both kinds of neurotransmitter.
“Our study is one of the first to rigorously document that inhibition can co-exist with excitation in a brain pathway,” says lead author Steven Shabel. “In our case, that pathway is believed to signal disappointment.”
The LHb is located within the epithalamus region of the brain and has been previously implicated with the regulation of pain responses, psychosis and a variety of motivational behaviors.
Tests conducted on primates have led to it being associated with disappointment, when activity within the LHb was noted to increase when a reward was expected by monkeys but not received.
Experts have also linked depression with hyperactivity in the LHb, but prior to these new findings, there had been limited empirical evidence for why healthy individuals did not succumb to overstimulation in this area. Previous assumptions were that there was a lack of inhibitory neurons in this area of the brain.
The authors of the study hypothesize that this area of the brain may be moderated via this unusual co-releasing of neurotransmitters in order to allow for a more subtle control of signalling, rather than through a direct conflict between two opposing neurons.
The findings also have implications for the understanding of how antidepressants work. Rodents in which aspects of human depression had been developed were found to produce less GABA in relation to their glutamate levels. When given an antidepressant to boost their serotonin levels, the levels of GABA also increased. Shabel explains:
“Our study suggests that one of the ways in which serotonin alleviates depression is by rebalancing the brain’s processing of negative life events vis-à-vis the balance of glutamate and GABA in the habenula. We may now have a precise neurochemical explanation for why antidepressants make some people more resilient to negative experiences.”
However, recent research has cast doubt over the role of serotonin within depression. Medical News Today recently reported on another rodent study that suggested that serotonin may not play as influential a role in depression as previously believed.
Be that as it may, this study could be the next step on the road to a true understanding of what is the leading cause of disability worldwide, affecting more than 350 million people across the globe – depression.