Serotonin Transporter Gene

The serotonin transporter gene may affect neural circuits connecting the amygdala and the cingulate and cause depression.

People with anxiety disorders or depression complain not so much about the emotion itself as its unceasing nature, says Daniel Weinberger of the National Institute of Mental Health. Now he and his colleagues may have found why their experience is continuous, according to work published in the June issue of Nature Neuroscience. Scientists know that the serotonin transporter gene, which encodes a key protein for neurotransmission in the brain, comes in a long form and a short form. People who have the short form are susceptible to developing depression or anxiety, though the gene does not actually cause it.

To find out how the short form affects emotional health, Weinberger’s team looked at 94 healthy individuals, some who have each form. Using brain imaging techniques, they found that two regions involved in emotional responses, the amygdala and the cingulate, were smaller in people with the short gene. Also, the neural circuits connecting the amygdala and the cingulate were weaker in people with the short form than in those with the long one. That is important, says Weinberger, because the amygdala controls a person’s response to fearful situations, evaluating whether they should react or not, and then the cingulate vets the amygdala’s response. If a fear signal put out by the amygdala is not justified, the cingulate turns it off.

But in people with the short form of the gene, the cingulate is not able to perform this editing function as effectively, so it is as if the amygdala is going off all the time. “If you can’t shut off fear, it is much worse than just feeling it for the first time,” Weinberger says. The new evidence suggests that this phenomenon happens in people with the short gene, which would explain why they are more prone to depression and anxiety.

However, for the past several days, Doug has taken a turn for the worse and is again experiencing debilitating symptoms. He is very angry, depressed, and frustrated to say the least. He has no energy to move and even skipped out on going to a baseball game that someone gave him tickets to, which he was excited about just last week. I’ve been trying to motivate him to change his routine to no avail. We’ve talked, but all that comes out of his mouth is negativity and anger, which makes it very difficult to have a productive conversation.

Underneath it all, he knows and understands that it is the disease talking, and I get that too. But I won’t lie and say it’s easy to take. It’s not. I miss the real Doug, the one who had me in tears laughing when we recorded some of our silly bits in episode #13. I miss the Doug that I can talk to for hours about music and comedy. And I miss the Doug that is positive and thinking about how well he is doing fighting to get his life back. The Doug I’ve been talking to the last few days is a false one, taken over by an evil beast of a disease. The hardest parts are those fleeting moments where his true self bleeds through, if only for a sentence or two. Like he’s fighting to get a message out to me that says “don’t listen to him, that’s not me!”

I hear you, brother. And I’m still here for you, waiting.

In the meantime, I am trying to get an update recorded and added to our next show to explain to our listeners that the remission has decided to take a little break for now. Not sure what we’ll do for the show after that, but we’ll take it one day at a time.

Thank you all again for your continued support.