Fundamental neurotransmission is not that simple

This is the kind of discovery that leads scientists to say, "What's happening is not a simple, monolithic process."

http://www.sciencedaily.com/releases/2011/08/110823154038.htm?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+sciencedaily%2Fmind_brain+%28ScienceDaily%3A+Mind+%26+Brain+News%29#.TlVjSrO9LIE.mailto

And when they say that, you know they're starting to pay attention. 

This fascinating discovery is a matter of function, not form. I gripe about the simplistic, even boneheaded science that seeks to uncover neurology by approaching it with a backhoe. This is one example of the more productive & telling approach, using the scientific equivalent of brushes and trowels. Good stuff, intelligent and apt. 

The radical new idea is this: the little blobs of neurotransmitters that sit between the nerve endings are not identical little blobs, but are in two separate sets of blobs. 

So what do they do?

The smaller group of blobs is the "recycling" set, called that because they get used and restocked each time the nerve fires. The larger group of blobs hangs back out of the way, and occasionally a blob takes off but not because the nerve just fired. Due to their relaxed attitude, these are called the "resting" set. 

In the article, the blobs are referred to as sacs (or "vesicles," in med-speak.) They're sacs in precisely the same way that the drop of water rolling across the hood of your car is a sac. The blobs have a sort of "skin" created by molecules gathering more densely at the surface, but nothing more. 

It's an important layer of molecules, though, since the detectable difference between the "resting" blobs/sacs and "recycling" sacs is the proteins that gather on their surfaces. 

Now, to discover what those proteins mean ... That's another study. I look forward to it. 

Scared of the wrong things: depressive chemistry and danger

Funny how the whole delicate neurological/neurochemical structure is so interwoven:

http://www.sciencedaily.com/releases/2011/08/110810133127.htm?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+sciencedaily%2Fmind_brain+%28ScienceDaily%3A+Mind+%26+Brain+News%29#.TkPZJ2TGXNQ.mailto

"...The researchers suggest that the strange defensive behavior exhibited by the enzyme-deficient mice may actually reflect a limited range of adaptive responses and lack of emotional flexibility -- the mice may only have one gear for fear."

We've all known people who make exaggerated choices around danger that make no sense to ourselves. (Having heard my mother and my sometime partner on the subject of my riding motorcycles, I'm pretty sure of that.) However, only at my most desperately depressed have I engaged in unsafe sex, which is the second stupidest risk I can think of (the first having nothing to do with motorcycles.) 

The role of MAO-A and depressive neurotransmitters, combined with the dopamine-deficient sense of hopelessness and diminished executive function, make that make sense: 

"Monoamine oxidase A is the main enzyme in the brain that breaks down serotonin, norepinephrine and dopamine..."

Which makes me think that it's possible, in humans in vivo, to be deficient in both MAO-A and in dopamine, serotonin, etc. It would explain a lot about certain mental states, even though it seems chemically tautological at first glance to be both Big 3-deficient and MAO-A deficient. As I've learned, though, deficiency and dysregulation do have additive effects, they don't cancel each other out. 

I'd like to see more studies which monitor serum and brain levels of these key chemicals together, preferably in humans. Science tends to take the simplest possible approach, which is rarely the most realistic and not necessarily the most telling. It does get funded and it does make it simpler to design the studies. 

I look forward to having more sophisticated thinkers (and funders) get into this branch of psychoneurology, since all these lively lovely tiny bits of info won't come together in a meaningful way until we can look at them in concert with a higher degree of exactitude and completeness. I suppose I'll have to be patient. And careful. 

Good medicine

Long silence. It's not that I've been uninspired by recent medical science.

I've been traveling, spending a lot of time with people I haven't seen in many years. They've turned out to be the kind of people who, as the body get more chewed up, the personality gets richer and smoother. Proud to love them. Delighted to be with them.

Now that's good medicine.

Mechanisms of the special neurologic destruction caused by blast injuries

This is absolutely thrilling:
"Bioengineers identify the cellular mechanisms of traumatic brain injury; New hope for treatment of TBI in veterans wounded by explosions"
http://www.sciencedaily.com/releases/2011/07/110722213427.htm?utm_source=feedburner&utm_medium=email&utm_campaign=Feed%3A+sciencedaily%2Fmind_brain+%28ScienceDaily%3A+Mind+%26+Brain+News%29

These scientists discovered the answers to two frustrating questions that have been blocking effective treatment of blast-related head injuries (TBI, or Traumatic Brain Injuries.)

1. What happens to the brain's axons? Why do the vital communication-arms of the brain's nerve cells just disappear?

2. Why does TBI from explosions cause the brain's blood vessels to shut down and turn themselves off, even though the the injury doesn't seem that bad?

The horrific health cost to our soldiers on active duty has included being blasted by explosives. These cause profound and persistent brain injuries that seem too severe for the amount of shock experienced by the brain.

1. The axons are part of an interlocked structure that's woven together by cells and intracellular "glues." This structure is shaken apart by explosive shock. Axons have to release their connections and shrink, retreating into the body of the cell. This destroys the physical functional structure of the brain. The person instantly loses memories and processing power, as well as a pervasive host of brain tasks.

2. The vessels undergo a mechanical stretch caused by the explosive force pushing through the gelatinous mass of the brain, and then, as a result of that stretch, they become super-sensitive to the chemical messenger that tells them to snap shut and then stop acting like vessels at all.
Normally, #2 only happens in the case of severe hemorrhagic (that is, bleeding) stroke. However, we now know that it also happens in blast injuries that otherwise cause less apparent damage.
Clinical note: Blast injuries to the brain are uniquely insidious. They cause diffuse injury that's invisibly disabling and incredibly hard to manage, let alone recover from significantly. Behavioral issues and so forth are mechanically and chemically imposed on the soldier's brain; they are not wilful choices on the soldier's part.

A lot of fundamental retraining has to be done, because emotional, cognitive and social skills have to be significantly rebuilt and rewired. The wiring that the soldier has built on since childhood has been torn up on duty.

Thanks to our present understanding of neuroplasticity, there's hope and a path to develop, but it takes time. On top of psychological trauma and the damage that causes to the amygdala and sometimes the hippocampus, it's a hell of a lot for any layperson to grasp, let alone try to handle.

One of the truly thrilling things about these findings is the discovery of a process that keeps the axons from pulling back in the first place. At present, it works in a Petrie dish if given within 10 minutes of injury; hard to see how that could work in combat.

If it could be formulated to be used in a person, it would still have to be administered extremely fast. Maybe send each soldier out with an inhaler of the stuff? Or a nose spray? A 50-cent bottle apiece to save millions in treatment, lost wages, cost of care, incidental costs on the family, for each injured soldier. Seems like a bargain!