U.S. scientists say they're zeroing in on a small area of the brain responsible for seasonal affective disorder or SAD, a kind of depression linked to the same season every year.
It most commonly strikes people in the short, gray days of winter, leaving them tired, irritable, depressed and experiencing trouble concentrating until spring and its brighter, sunnier days arrives.
It has been well-established that the amount of sunlight a person is exposed to, and the resultant effect on their circadian rhythm or body clock, plays a key role in the condition.
Neurotransmitters in the brain including serotonin and melatonin are also thought to be involved, but up until now efforts to identify the basic neurobiological mechanisms responsible for SAD have been unsuccessful.
Now researchers at Vanderbilt University, writing in the journal Current Biology, report they've tracked the seasonal light cycle effects linked to SAD to a small area of the midbrain known as the dorsal raphe nucleus.
The finding comes from experiments with mice, an animal model commonly used to study human depression.
In both mice and people, the dorsal raphe nucleus is the location for many special-function neurons that regulate serotonin levels throughout the rest of the brain, the researchers say.
Those neurons play a significant role in adjusting an individual's mood, they explain, since high concentrations of serotonin have been linked to feelings of happiness and well-being while lower levels are associated with depression.
In the experiment headed by graduate student Noah Green, the mice were divided into three groups, each born and raised in a different light/dark cycle: summer, winter, and spring/fall.
Other than the light/dark cycles, the environments in which the mice were born and lived were identical.
Subsequent tests showed the group living in the summer light cycle showed less depression-like behavior than either the spring/fall or the winter-cycle groups.
Examination of the mouse brains showed serotonergic neurons firing faster in the summer-cycle mice, which elevated their levels of serotonin, something borne out in the prior behavioral testing, the researchers said.
"Before, we thought serotonin was probably involved," says Douglas McMahon, chair of the university's Biological Sciences department. "Now we know that serotonergic neurons are definitely involved," which strongly points a finger at the dorsal raphe nucleus, he says.
One unexpected finding was that when mice born during summer light cycles were moved to a winter cycle, their increased firing of serotonin neurons persisted for several months as they grew into adulthood.
"This showed that early life seasonal photoperiods can have enduring effects on the serotonin neurons," says Mcmahon. "If such an effect occurs in humans, and is long-lasting, it could contribute to the season of birth modulation of SAD risk," said McMahon, citing previous research suggesting a correlation between a person's season of birth and their propensity to develop SAD.
