Do these changes mean anything in terms of adolescent behavior? The answer is clearly no—or at least, not yet. From a cellular/molecular point of view, however, they suggest a great deal. Alterations in cortical volume are sometimes associated with the changes in synaptic pruning, for example, usually couched as density measures. (It’s a familiar developmental idea: synaptic connections that are overproduced during childhood need to be pruned to achieve their final mature state.) Do these changes in cortical volume indicate changes in synaptic pruning during adolescence?
The answer, interestingly enough, is “No.” There certainly are changes in synapse number in a variety of cortical regions during adolescence. But clear data now exist which show that the decrease in synaptic density is insufficient to account for the observed dramatic changes in volume.
What then accounts for these changes? Although speculation abounds, the real answer is that we just don’t know. One interesting explanation attempted to take into account the simultaneity of the developmental patterns of both gray and white matter. Because white matter usually indicates an increase in the myelination of nerve fibers, it was thought that a processive myelination pattern was being observed. (As you recall, myelin is the fatty sheathing that provides an electrical insulating function for the conduction of neural signals. An unmeylinated neuron can conduct a signal at about 1 meter per second. A myelinated one can conduct an impulse at about 100 meters per second).
Were myelination patterns really being observed? Researchers took this into account and then combined the idea with the gray matter volume data. It was possible that less gray matter was being observed simply because these neural tissues were in the process of being “whitewashed” (myelinated). Covering over gray matter with white would explain the loss of gray matter volume while simultaneously explaining an increase in the white. There is some empirical support for this myelinating notion, particularly with intracortical fibers, which are processively myelinated throughout brain development in the early years.
It turns out that this explanation, satisfying as it may be, does not tell the whole story. Data exist that challenge the notion that myelin has any involvement in the observed developmental changes. There are other ways to measure myelin than just looking for white matter (using a technology whose metric is termed the MTR [magnetization transfer ratio] index). When these technologies are deployed, one sees there is actually a decrease in the amount of myelin per unit volume in the developing brain—even while the amount of white matter is increasing. Sound contradictory? It is the reason I said “we don’t know” in attempting to hypothesize relevant mechanisms.
Regardless of our ignorance, it is clear that understanding puberty-associated changes in brain structure is not as simple as saying “lots of things happen to it at puberty.” To be sure, lots of things are happening to brain structure during adolescence, but changes are observed throughout the brain’s developmental narrative. Indeed, the final chapter in white matter growth does not end until the third decade of life, giving the human brain an odd trophy: it is the last organ to finish its postnatal developmental program.
Functional Changes
Things have not been helped by the creation of what some in the popular press euphemistically call the “teenage brain.” You may have heard of this near-mythological idea, which has been mostly an attempt to explain the erratic behavior of many adolescents. It is usually couched in terms of the developmental regulation of executive function. As you may recall, executive function is a suite of behaviors involved in such disparate activities as planning, foresight, impulse control (actually, inhibition), and aspects of working memory (Figure). Risk-taking and sensation-seeking behavior, especially among males, has also been mentioned as being part of the story of the teenaged brain—behaviors adolescents are known for having in short supply. From a neurological perspective, the story usually goes something like this:
• Executive function is mediated by areas in the prefrontal cortex.
• These areas are not functionally connected to other regions of the brain that are involved in emotional regulation, risk taking, or sensation seeking. (The limbic system and the nucleus accumbens are the usual suspects.)
• The regions involved in emotional reactions do not begin to form functional connections with regions mediating executive function until the child is well into adolescence.
• We should therefore understand that certain types of “foolish” adolescent behavior occurs as a result of immature or non-existent connections in these brain structures.
