I’m facinated by this “circuit-board” model of major depression–the connection between specific sets of nerve cells in different regions of the brain–explained by researchers like Helen S. Mayberg, M.D., professor of psychiatry and neurology at Emory School of Medicine.
And I’m intrigued by this not-so-new notion that depression is not just a chemical imbalance in the brain. It’s much more complicated and involved than that–which is why neurology and psychiatry have to work in tandem to figure out how best to treat it.
I tried to link an excellent “Psychology Today” article by Hara Estroff Marano, but it required a passoword, so I’ve excerpted the first part of her piece that clarifies so many confusing myths and concepts about depression that are simply out-dated based on the emerging field of neurobiology.

New research is challenging the assumption that the world’s most common mental ailment is just a chemical imbalance in the brain.
Melancholy is a fertile muse. No sooner had William Styron become the poet laureate of depression after describing his bout with madness in “Darkness Visible” when all manner of confessions followed. Mike Wallace. Art Buchwald. Dick Cavett lined up to disclose their own struggles with the disabling disorder. It quickly became acceptable, even chic, to publicly confide vulnerability to depression.
At the same time, the world was being made safe for depression, or at least public revelations of it, by another development, the 1988 advent of the so-called SSRIs—Prozac, Paxil and related drugs believed to specifically combat depression by beefing up serotonin and other neurotransmitters that ferry signals between nerve cells. The wild success of psychiatrist Peter D. Kramer’s thoughtful “Listening to Prozac” generated not only new respect for the effectiveness of Prozac but new appreciation of the disorder it was intended to treat. There followed hundreds of new book titles on depression, over 100 on Prozac alone, surely making it the most heralded drug on the planet. Depression chic cannot be dismissed as a passing fad because, it turns out, how the disorder is defined and popularized deeply shapes what patients are willing to do about it.

Despite the flood of Prozac prose, depression itself has remained, as Styron saw it, a mystery. One of science’s cruel ironies is that it can explain bizarre rare conditions, but common afflictions like depression—Western countries’ second most disabling ailment (after heart disease) and the world’s fourth—elude understanding. That, however, is changing.
Refined imaging techniques have begun providing an unprecedented look into the neurobiology of depression, showing what goes on in the brains of patients as they process positive and negative experiences. The work is forcing a radically revised view of depression, one that promises new treatments for the future. Among the findings:
* Regarding depression as “just” a chemical imbalance wildly misconstrues the disorder. “It is not possible to explain either the disease or its treatment based solely on levels of neurotransmitters,” says Yale University neurobiologist Ronald Duman.
* The newest evidence indicates that recurrent depression is in fact a neurodegenerative disorder, disrupting the structure and function of brain cells, destroying nerve cell connections, even killing certain brain cells, and precipitating cognitive decline. At the very least, depression sets up neural roadblocks to the processing of information and keeps us from responding to life’s challenges.

* Human emotions take shape in a neural circuit involving several key brain structures, including the hippocampus, the amygdala, and the prefrontal cortex. In depression, faulty circuitry fails both in generating positive feelings and inhibiting disruptive negative ones.
* Stress-related events may kick off 50 percent of all depression and early life stress can prime people for later depression. Ongoing research in animals and in people demonstrates that early strain can alter nerve circuits that control emotion, exaggerating later responses to stress and creating the neurochemical and behavioral changes of depression. In other words, the deeper researchers probe the brain, the more they validate the psychoanalytic view that early adverse life events can create adult psychopathology.
* Depression is not just a disorder from the neck up but a disorder involving many body systems. It both leads to heart disease in otherwise healthy adults and magnifies the deadliness of existing cardiac problems. What’s more, it accelerates changes in bone mass that lead to osteoporosis. “The lifetime risk of fracture related to depression is substantial,” researchers have declared in the “New England Journal of Medicine.”

* Just as nerve cell connections can be destroyed in depression, perhaps they can be rebuilt. The common denominator in effective antidepressant treatments, including electroshock, may be their ability to stimulate the sprouting of neurons in key brain regions, literally the forging of behavioral flexibility. An identified neurochemical pathway promises to revolutionize therapy by suggesting ways to do this better and faster.
* The adult brain has a degree of plasticity that is astonishing researchers. “The big news is the structural plasticity of the adult brain, the remodeling of neurons,” says neurobiologist Bruce McEwen, Ph.D., of Rockefeller University. “The idea that there are long-lasting, even permanent, changes in structure and function that can affect the way brains process information is the most important part of what we’re doing in the lab. We thought that after birth, the brain is a stable organ like a computer that just works away, and no more new nerve cells are produced. The emphasis was on chemical imbalances, as if the circuitry itself was fairly stable. All these changes–cell loss, atrophy of connections–that’s very new, and still catching people by surprise.”