The other day I found an article that seemed all too perfect. Development. Neurology. Zebrafish. For those of you who don’t know, these little fishies are not only PZ’s specialty but are also currently taking over our lab (You will be missed, fishies in tank #3).
In zebrafish, the sleep-wake cycle is regulated by hypocretin neurons (HCRT). These neurons also play a major role in mammals as well and if damaged can lead to narcolepsy. The researchers labeled these neurons in zebrafish with a presynaptic marker synaptophysin (SYP) attached to a fluorescent dye. Now the researchers can look at activity across the span of a day to visually quantify changes in baseline function or artificially produced by various conditions (e.g. sleep deprivation). So, they irritated fish for several hours after normal sleeping time until the fish were nice and sleep deprived.
The sleep deprived fish showed homeostatic influences on the number of HCRT synapses. Why is this important? The fish showed that upon sleep deprivation more synapse terminals were created to maintain cellular balance. Yet, simultaneously, the natural circadian rhythm began to decrease the number of synapses from the point of initial sleep deprivation. Homeostatic effects are estimated to be a mere 17% and this result appears only after six hours of deprivation. Essentially, as the day wears on the brain winds up more and more. The circadian rhythm counteracts this by gradually resetting the system back to baseline. A portion of this study showed that as the system tries to reset, sleep deprivation will weakly offset efficacy leading to impairment in memory retainment (and overall cranky fish).
*Professor, I would have gotten that question right but the course workload created homeostatic effects which led to faulty memory retainment!*
Last week, Current Biology released an article about structural differences between sexes in Drosophila melanogaster. It may not be about a human brain, but it’s still neurology and at least semi-related to developmental biology this time.
While the “model” organism displays distinct behavioral differences between sexes, the overall anatomy in regards to dimorphism has been essentially neglected. Previously, the only discernible difference was in the olfactory system. Male olfactory systems have a 25 – 60% larger volume than female flies. Coincidently the male pheromone cVA attracts females while repelling males (however no credible correlation can be made).
Pretty picture! This is one of many from a collage presented in the article and most interesting to myself as it visibly shows the gender difference in brain size. Magenta is larger in females and green is larger in males.
The article proceeds to explain the fine tunings of specific proteins (fruitless, sex lethal, and transformer) and their effect on dimorphism in a manner that is, quite frankly, far beyond my level of comprehension.
Overall, sexual dimorphism does exist in the Drosophila brain and may influence behavior as a result. A key example of this lies in the activation of fruM (the male version of the fruitless protein) in females and the resulting behavior of courting other females. Now that the anatomical groundwork has been laid the researchers are able to pursue behavioral consequences in future research.
Last week I received a request from MarkNS asking about cerebral palsy therapy when viewed from neuroplasticity. Sounds good, let’s look at that.
I did not know much about cerebral palsy prior to this post, but strangely I do know an ultimate fighter with it… Cerebral palsy is a multi-faceted disorder that comes in all shapes in sizes, many of which are outside the scope of this post. When looked at with a simplistic view, cerebral palsy is a movement disorder caused by damage to the motor cortex of the brain.
Brain damage. “Irreversible. Permanent.” <–Wrong! The most common form of brain damage associated with neuroplasticity is in stroke patients. This is where the greater body of research can be found. It would seem that for many years all signs pointed to “you’re screwed”. That is, until Edward Taub came onto the scene.
Taub, through deafferentation experiments on monkeys, invented a new form of therapy, Constraint Induced (CI) Therapy (Simple or Advanced explanation, I recommend the advanced if you have the time as I will only touch lightly on it). The premise of this therapy focuses on a phenomenon called “learned non-use”. In essence, after losing a degree of control in one limb you then compensate with the other to pick up the slack. (e.g. after a stroke affecting the left side, you would use your right side that much more.) When this compensation occurs the neural pathways begin to weaken, leading to even further non-use.
So we know how to lose it, now how do we get it back? CI Therapy essentially forces the affected limb to switch roles. By restraining the “good” limb and using only the “bad” one, the patient begins to build motor control on the weaker side. It turns out this not only builds character but rebuilds the pathways!
So that’s all fine and dandy for strokes, but what about cerebral palsy? There’s an app for that. Unfortunately the only data I could find was done on children with hemiparesis associated with cerebral palsy. The good news is that the children responded amazingly well to the therapy and sustained the results afterwards. The range of effectiveness is still limited for the moment. CI Therapy has come a long way and it would be a safe assumption that it will continue on.
I have had in my possession for quite some time a copy of The Brain that Changes Itself by Norman Doidge, M.D. I first picked it up in my beginning days as an undergrad. The remarkable thing was how easy it was to follow. Written for the layman and directed at instilling the wonder of biology.
Now, I’ve picked it up again as a Senior. A little older, hopefully a little wiser. It would seem this turn around I’m beginning to see potential that went unnoticed previously.
The premise of the book revolves around Neuroplasticity, the ability for neurons to change. By itself, this concept is enough to marvel at. Doidge assembles a myriad of research affected by neuroplasticity ranging from the cochlear implant to porn addiction.
The most fascinating piece (IMHO) would be the effectiveness of rehabilitation on late adulthood cognitive decline. Focusing on the work of Dr. Michael Merzenich, he addresses the cognitive problem of “everything is progressively going to hell”. The interesting part is the method in which rehabilitation is carried out. Merzenich and others created the computer Fast ForWord that exercises and sharpens key neural pathways.
In their first study, they compared the results of two groups of children (it becomes relevant to adults in later studies) with learning disabilities. The first group used Fast Forword, while the second used a similar computer game but without training in temporal processing. The first group was able to score higher and maintain test scores longer than those of group two.
From this type of therapy, Merzenich and his colleges saw a bleeding effect into other areas. In fact, visual processing increased with temporal processing despite no intervention directed towards it. When this same type of therapy is applied to adults the same results appear. It would seem the brain has no age limit on growth, even in late adulthood, and the therapies used function similarly.
Overall, this was a good Pop Sci book on a common misconception of the human brain. Use it or lose it still applies, but once it’s gone it still can come back. I would recommend this to anyone for a bit of awesome light reading.