In my previous post I discussed the brain and an evolutionist wrote to me about this paper. Does it not reveal solid hypotheses for the evolution of the brain’s circuitry? Before we answer this question we need briefly to review the biology involved.
Our nervous systems contains a great many nerve cells, or neurons. Like wires in a machine, neurons carry electrical signals. And just as wires pass electricity to other wires, so too neurons pass their electrical signals to other neurons. Also, just as wires ultimately connect to a motor, or a sensor, or some other device, neurons ultimately connect not to another neuron, but to tissue. But this is where the similarity ends. The closer we look at neurons and their connections, the more profound are the discoveries we make. So first let’s review how the signal travels down the neuron and how it is transmitted.
Nerve cells have a long tail which carries an electronic impulse, called an action potential. The tail can be several feet long and its signal might be passed to another neuron, stimulate a muscle to action, control a gland, or report a sensation to the brain.
After years of research it was discovered that the signal is boosted by membrane proteins. First, there is a membrane protein that simultaneously pumps potassium ions into the cell and sodium ions out of the cell. This sets up a chemical gradient across the membrane. There is more potassium inside the cell than outside, and there is more sodium outside than inside. Also, there are more negatively charged ions inside the cell so there is a voltage drop (50-100 millivolt) across the membrane.
In addition to the sodium-potassium pump, there are also sodium channels and potassium channels. These membrane proteins allow sodium and potassium, respectively, to pass through the membrane. They are normally closed, but when the action potential travels along the nerve cell tail, it causes the voltage-controlled sodium channels to open quickly. Sodium ions outside the cell then come streaming into the cell down the electro-chemical gradient. As a result the voltage drop is reversed and the decaying electronic impulse, which caused the sodium channels to open, is boosted as it continues on its way along the nerve cell tail.
When the voltage goes from negative to positive inside the cell, the sodium channels slowly close and the potassium channels open. Hence the sodium channels are open only momentarily, and now with the potassium channels open, the potassium ions concentrated inside the cell come streaming out down their electro-chemical gradient. As a result the original voltage drop is reestablished.
This process repeats itself until the impulse finally reaches the end of the nerve cell tail. Although we’ve left out many details, it should be obvious that the process depends on the intricate workings of the three membrane proteins. The sodium-potassium pump helps set up the electro-chemical gradient, the electronic impulse is strong enough to activate the sodium channel, and then the sodium and potassium channels open and close with precise timing.
How, for example, are the channels designed to be ion-selective? Sodium is about 40% smaller than potassium so the sodium channel can exclude potassium if it is just big enough for sodium. Random mutations must have struck on an amino acid sequence that would fold up just right to provide the right channel size. That is an astronomical long shot.
The potassium channel, on the other hand is large enough for both potassium, and sodium, yet it is highly efficient. It somehow excludes sodium almost perfectly (the potassium to sodium ratio is about 10000), yet allows potassium to pass through almost as if there were nothing in the way. The solution seems to be in the particular amino acids that line the channel and their precise orientation. For potassium, moving through the channel is as easy as moving through water, but sodium rattles around—it fits in the channel but it makes less favorable interactions with the amino acids. Again, the amino acid sequence of the potassium channel is fine-tuned for the job.
Next, when the action potential reaches the end of the neuron it is passed on. First, the action potential causes voltage-controlled calcium channels, located at the end of the tail, to open. Positive calcium ions on the outside stream into the neuron through the open channels. The calcium ions influence special proteins just inside the neuron, which in turn cause small bubbles to dock with the cell membrane. The bubbles contain a neurotransmitter chemical which is released to the outside of the cell.
Very close to this end of the neuron is the other cell with which the neuron communicates. The tight junction between the two is called the synapse. In this case, the neurotransmitter chemical floats across the gap between the cells, and attaches to the other cell, setting off the desired action, which is another story. Again, we’ve left out many details. There are literally thousands of proteins working behind the scenes. As one writer explained:
The human brain is truly awesome. A typical, healthy one houses some 200 billion nerve cells, which are connected to one another via hundreds of trillions of synapses. Each synapse functions like a microprocessor, and tens of thousands of them can connect a single neuron to other nerve cells. In the cerebral cortex alone, there are roughly 125 trillion synapses, which is about how many stars fill 1,500 Milky Way galaxies.
Needless to say, this whole process occurs with great reliability and speed. Nerve cells are constantly firing off in your body. They control your eyes as you read these words, and they send back the images you see on this page to your brain. They, along with chemical signals, control a multitude of processes in our bodies. And new research continues to peel back the layers of this profound design. As one scientist recently explained:
One synapse, by itself, is more like a microprocessor—with both memory-storage and information-processing elements—than a mere on/off switch. In fact, one synapse may contain on the order of 1,000 molecular-scale switches. A single human brain has more switches than all the computers and routers and Internet connections on Earth.
Now, having reviewed the biology, let us consider the evolutionist’s paper. It is a review of the origin and evolution of synapses. Given the molecular biology of synapses, the neuron, action potentials, and associated machinery, you might think random mutations and the like creating all this would be unlikely. And indeed the paper has its share of caveats and uncertainties. Here are some examples:
It is conceivable that the first protein–protein interaction that led to synaptogenesis would be homophilic.
we postulate that these molecules originated before the evolution of synapses …
Cadherins may therefore be important for cytoskeletal rearrangement in choanoflagellates and may represent a precursor to synapse formation.
heterophilic transynaptic protein interactions probably evolved later.
… implying that they may form a protosynaptic complex involved in sensing environmental stimuli and that they could represent an evolutionary precursor to synaptic sites.
But this is only the beginning. In fact nowhere does the paper explain in scientific detail how the synapse and associated machinery could have arisen on its own. How did the massive protein machines, with their intricate and fine-tuned functions arise? How did evolution establish the right ionic concentrations inside and outside of the cell? How did the finely-tuned action potential initiation and transmission mechanisms evolve? How did the neurotransmitter chemical concentrations, complete with bubbles and associated proteins arise? And none of this would function without the finely-tuned receptors on the receiving cell. It also would not function without the right mechanisms for replenishing the neurotransmitter chemical, as well as the calcium, potassium and sodium concentrations. And how did evolution bundle the neurons, and connect them to the right receptors, implementing trillions of synapses. How did evolution provide both memory-storage and information-processing elements to the synapse?
Aside from vague speculation the paper provides no such details. Instead, such problems are, in typical fashion, pushed back. The protein machines, for instance, are said to have “originated before the emergence of classical morphological synapses and have been co-opted for synaptic roles.”
Indeed synapse designs are so widespread amongst the species that the paper must conclude that “Many mammalian synaptic components existed before the appearance of synapses.”
It is not surprising that evolutionists would be unable to provide scientific details for the evolution of the synaptic components. But when not failing to provide such foundational data, the paper is decidedly confident and certain. It states in no uncertain terms that evolutionary studies “point to an ancestral molecular machinery in unicellular organisms — the protosynapse — that existed before the evolution of metazoans and neurons”
Similarly, the reader learns that this protosynapse consists of “synaptic components that were present before the emergence of synapses.” Were present? It is remarkable that evolutionists can know such details.
Here is another example of how the paper confidently presents detailed evolutionary histories as fact:
In general terms, the evolution of synaptic genes at the eukaryote–metazoan and metazoan–chordate boundaries preceded their expression in different populations of neurons and synapses and thereby allowed diversity of function in nervous systems that have emerged later, in evolutionary terms, and that are generally larger.
Again, these evolutionary conclusions are amazing. What powerful scientific methods do evolutionists possess that can yield such detail and certainty?
A breach of ethics
The answer, it seems, is none. Reading further we see only weak justifications for these sweeping conclusions. In fact the paper’s conclusions are largely based on various genetic comparisons. Here is an example:
If we can deduce the composition of the last common ancestor of all synapses, the ursynapse, then we should be in a position to address the question of how and why the first synapse originated. We approach the question of the composition of the ursynapse by taking synaptic proteins identified in vertebrate model organisms and searching for orthologues in the genomes of two categories of organism.
Searching for orthologues? That may sound sophisticated, but it amounts to nothing more than searching for similar genes in different species. That’s it. Evolutionists search for these and other genetic similarities, and from those make sweeping conclusions and present them as new truths.
One of the ever-present themes in the evolution genre is that similarity mandates evolutionary relationship. If two species share a common design, such as similar genes, it must have arisen from a common ancestor. This is not a scientific premise, and it is an example of how metaphysics makes its way into science under the guise of the scientific method. Searching for orthologues certainly sounds scientific. But in the hands of evolutionists it is religiously-driven science.
Evolutionists insist that evolution is a scientific fact every bit as much as is gravity or the roundness of the earth. That is a misrepresentation of science that goes far beyond a simple mistake. For centuries evolutionary thinkers have issued unlikely speculation as undeniable truth, and the gap is only becoming wider. Today, the certainty they insist upon is prima facie absurd. Evolution has degraded to a religiously-driven junk science making, what are frankly, silly claims. But the manipulation of science is no joke. Misleading the public with inexcusable misrepresentations is a serious breach of ethics. Religion drives science, and it matters.