Do “Some Brain Cells ‘Change Channels’ To Fine-Tune The Message”? Absolutely NOT!
From the story in Medical News Today , “Johns Hopkins researchers have identified the proteins that allow specific brain cells to “change channels,” a rare ability that tweaks what can come into the cell. The findings, described in the March 24 issue of Neuron, might let researchers harness the process, perhaps one day using it to protect cells that die in Lou Gehrig’s disease.”
No they have not. They have identifed the proteins that control pathway changes.
The brain is the most efficient machine in existence. It does not ‘change channels’ for any reason other than its function. That function involves the effecient use of neurons for many different pathways. The synchronous timing of neuron charging and firing, coupled with the difference in output direction allows a single neuron to act as as processor for many different pathways of varying senses.
Imagine you are on a train ride. As you approach a switching station the train does not take a different track in order to ‘fine tune’ your voyage. The different track is taken to get you to your destination.
So it is in the brain. There are hundreds of thousands of ‘tracks’ (pathways) of signals being processed in a synchronous and timed process. Many different data streams are working through neurons and being routed to their own pathway or track.
“Much as turning the television dial changes what comes into the living room, these brain cells are able to change what they allow in by swapping one kind of channel, or membrane opening, for another. Doing so lets the cells fine-tune their messages and adjust connections within the cerebellum, the brain region that controls fine motor skills.” 
Therein lies a major problem with neuroscience and it is not their fault. The brain works in comparisons. It is natural for a neuroscientist to observe something happening and the first logical comparison that ‘comes to mind’ wins as the purpose. The problem is: there is nothing that compares to the brain. The brain is responsible for making the things that neuroscience uses to compare it with.
“Although the cells’ channel-changing ability has been recognized for a few years, the key players controlling it hadn’t been identified. Now, by studying mice, the Hopkins team has identified two proteins, called PICK1 and NSF for short, that help replace channels that let charged calcium ions in with another kind of channel that keeps calcium out. If muscle-controlling nerve cells can do the same thing, forcing the swap might help protect them from a calcium overdose that can kill them in Lou Gehrig’s disease.” 
Here, the researchers are mixing two different issues. The chemical process that is used to direct traffic in the brain is involved in conditions that occur when it goes wrong. But they are not the same thing.
“So far, no one has really looked for the channel changing in other cells in the brain, he says, in part because the swapped channels are most common in these particular cells in the cerebellum (so-called stellate cells). But Huganir thinks the channel changing is going to be relatively common in the brain. ” 
The process is very common in the brain but it is not to change channels. It is to direct the traffic. When traffic is misdirected (as with some psychotropic drugs) the message intended to represent one input receptor is mixed with the traffic intended to represent another input receptor and the output of that pathway is confusing and indeed psychedelic.
“Whether through channel changing or other, more well-understood ways of fine-tuning its responsiveness, a brain cell’s activity level depends on its neighbors, the nerves and other cells that connect to it. Although they don’t physically touch, the cell and its neighbor are so close to one another at these connection points, called synapses, that molecules released from one cell travel immediately to the next. These molecules dock at specific places, or receptors, on the cell and trigger “channels” in the cell’s membrane to open. Depending on the receptor and the channel, in will flow sodium, calcium, chloride or other charged atoms that then keep the communication process going.” 
This brings to ‘mind’ (comparisons at work) another main issue with neuroscience’s accepted perspective on brain function.
The brain is NOT a neural net. As data is sent from one ‘node’ to another in a neural net it is ‘fine tuned’. That is not at all what is happening in the brain. The brain’s data is sent from input receptors: individual receptors located in the eyes, ears, nose, tongue, skin, etc. As each input receptor ‘fires’ its data takes that clocking pulse as its position in traffic. It stays in that position as it is processed deeper and deeper into the pathway. Since the process is synchronized it nearly approaches the appearance of a hologram where the system contains many different perspectives of the same essential input. Each ‘perspective’ is another pathway and they all share many of the same neurons to process the data.
“To learn more about how this takes place, the Hopkins researchers studied brain cells from genetically engineered mice. Through their experiments, the researchers determined that the PICK1 and NSF proteins are both required for the calcium-forbidding channel to move into place at the synapse. Exactly how they help the channels move is still unknown, as is why the cells change their channels.” 
The cells are changing the output pathway in time with the pulse of the input receptor to retain the same perspective in the same pathway in the same time frame. They are not ‘changing channels like a television set’.
“Part of the answer is likely to be self-preservation: Too much calcium inside nerve cells can kill them. But Huganir points out that calcium does a lot of things inside cells, suggesting that the channel swap might be accomplishing more than just keeping the cell alive.” 
Mixing topics again. Yes. It would be a bad thing to have too much calcium inside nerve cells. No. The changes do not happen to make sure too much is not in nerve cells. The changes happen to execute the system. When something goes wrong, then there might be too much calcium in nerve cells.
“In some cases, protection might be enough of a goal. In people with Lou Gehrig’s disease, or amyotrophic lateral sclerosis (ALS), some muscle-controlling nerve cells die because too much of the brain chemical glutamate binds to the cells’ AMPA receptors, and so too much calcium gets inside. If these threatened nerve cells can swap their calcium-allowing channels for the kind that keeps calcium out, it might be possible to harness that switch to prevent the cells from dying.” 
Since the research was funded by “the Robert Packard Center for ALS Research at Johns Hopkins, the National Institute of Neurological Disease and Stroke, and the Howard Hughes Medical Institute,” and “under a licensing agreement between Upstate Group Inc. and The Johns Hopkins University, Richard Huganir, Ph.D., professor of neuroscience and a Howard Hughes Medical Institute investigator in Johns Hopkins’ Institute for Basic Biomedical Sciences is entitled to a share of royalty received by the University on sales of products used in this research.”
But if Huganir develops a product that stops neurons from sending data to the right pathway, it will serve as a nice new street hullucinogen. If Huganir develops any product that does more than regulate functions back to ‘normal’ it will have been a bad comparison to blame.