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Your Encephalon On White Patato Chips

Or, to a greater extent than accurately, a rat's encephalon on tater chips.  Last week, PLoS One published a real interesting newspaper past times MD Tobias Hoch in addition to colleagues on what happens inward a rat's encephalon when it is exposed to a highly palatable/rewarding nutrient (1).  Rats, similar humans, overconsume highly palatable foods fifty-fifty when they're sated on less palatable foods (2), in addition to feeding rats a diverseness of palatable human junk foods is i of the most effective ways to fatten them (3).  Since the encephalon directs all behaviors, nutrient consumption is an appear of encephalon action patterns.  So what is the encephalon action designing that leads to the overconsumption of a highly palatable in addition to rewarding food?

Researchers have got already uncovered a large amount of data well-nigh this process.  In short, it centers around the activation of the mesolimbic vantage system, including precisely non limited to the ventral tegmental surface area (VTA; a major root of dopamine), the nucleus accumbens (NAc), the dorsal striatum, in addition to the lateral hypothalamus (LH; specifically orexin neurons).  Chemically manipulating the nucleus accumbens or lateral hypothalamus causes voracious feeding inward sated rats, replicating the natural conduct that is observed inward rats exposed to highly palatable nutrient (4, 5).  This is the arrangement that motivates you lot to attempt things that are desirable, including sure enough foods.

Here's a schematic of the rat encephalon showing some of the relevant structures, equally good equally dopamine pathways coming from the VTA in addition to the substantia nigra (image reproduced from the lab page of MD Jeremy Clark hither at UW; 6).  Many other connections in addition to neurotransmitter systems are non pictured**.

Most of the approaches used inward the past times to report reward-based feeding have got been invasive or involved chemic manipulations that complicate the interpretation of results equally they pertain to natural behavior.  Enter the recent study.  Dr. Hoch in addition to colleagues used a twist on an interesting technique called MEMRI*, which allowed them to monitor cumulative neuron action over a 7-day flow inward freely behaving rats.  Rats were divided into 2 groups, in addition to each received a dissimilar diet:
  1. Normal rat chow addition crushed rat chow.
  2. Normal rat chow addition crushed tater chips.  Score!
Rats, similar humans, dearest tater chips, in addition to equally expected grouping #2 grouping ate a lot of chips over the 7-day period, significantly increasing full calorie intake.

The changes inward encephalon action were striking.  Here's a cool prototype from the paper.  Regions inward cherry showed increased activity, spell regions inward bluish showed reduced activity:

The NAc, mayhap the most iconic reward/addiction-related construction inward the brain, was strongly activated inward grouping #2.  Other structures related to vantage also lit up, including the dorsal striatum in addition to LH.  Neuron action inward the VTA 'paradoxically' was suppressed.  This could likely endure explained past times somebody who knows to a greater extent than well-nigh the VTA than I, precisely I hit intend it's worth noting that some neurons dot past times firing less rather than more.

This is where the findings larn fifty-fifty to a greater extent than interesting.  Group #2 experienced a decrease inward the action of encephalon regions that regulate release energy homeostasis, including the arcuate nucleus inward the hypothalamus in addition to the nucleus tractus solitarius inward the brainstem, consistent alongside the possibility that consumption of a hyperpalatable nutrient may have got 'shut down' the mechanisms that unremarkably forestall excess nutrient intake.  We can't have got this line of reasoning also far, because each of these structures contains a diverseness of jail cellphone types doing dissimilar things, in addition to looking at global action patterns doesn't necessarily laissez passer on us a clear see of what's going on at the cellular level.  But it's an interesting hint nevertheless.

Also, they constitute changes inward encephalon regions related to slumber in addition to wakefulness, which is interesting given the emerging links betwixt circadian rhythms, sleep, nutrient intake in addition to obesity.

Since humans have got essentially the same encephalon structures equally rats, in addition to these structures serve similar purposes, this is likely roughly what happens inward the human encephalon during habitual consumption of highly palatable junk food.  The vantage arrangement gets revved up, in addition to the regions that would unremarkably oppose nutrient intake in addition to trunk fatness may endure near downward equally a consequence.

* Manganese-Enhanced Magnetic Resonance Imaging.  The basic see is that when neurons burn downward strongly, they have got inward calcium, which acts equally an intracellular second messenger.  Normally, this calcium is transported out of the jail cellphone after it has done its job.  However, manganese tin also brand it through these channels, precisely it isn't efficiently exported afterward.  So if researchers experimentally increment the concentration of manganese inward the brain, it accumulates inward neurons inward proportion to the amount each neuron has fired.  This accumulated manganese tin in addition to then endure detected past times MRI.  MEMRI has been around for a while, precisely the electrical flow authors improved on it past times using a gradual low-dose infusion rather than a large needlelike injection, which tends to brand the animals sick.

** Besides dopamine, neurons inward the vantage arrangement work endorphins, orexins, cannabinoids, glutamate, GABA, in addition to other signals.  Connections betwixt the VTA, the NAc, in addition to the LH are key to nutrient reward, though other areas are also important.  These connections are mediated primarily past times dopamine, orexin, GABA, in addition to glutamate signals.


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