Monthly Archives: February 2010

The Neurotransmitter Toolkit

We’ve just seen that many preadaptations for the evolution of neurons were in place. Calcium toolkit for secretion of neurotransmitters? Check. Post-synaptic scaffold? Check. Circuitry for neurogenesis? Check. But what about the neurotransmitters themselves?

Now, in principle, just about any molecule could serve as a neurotransmitter, as you simply need something that specifically binds to a receptor that triggers the opening of an ion channel. In fact, some amino acids, like glutamate, can moonlight as neurotransmitters.

Nevertheless, I decided to check up on two important neurotransmitters – acetylcholine and epinephrine. These neurotransmitters play key roles in your autonomic nervous system, the ancient system that maintains homeostasis through the regulation of all your body’s organs. What’s more, acetylcholine is the neurotransmitter used to stimulate muscle contraction.

The hypothesis of front-loading neurons would lead us to expect that these neurotransmitters exist in organisms that do no possess neurons. And sure enough, they do.

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Front-loading and the Nervous System

A neuron is a very fascinating cell. It is a cell that is specialized to detect changes in the environment, translate that environmental information into the language of membrane potential changes (electrical signals), and engage in long-distance communication by transmitting such electric signals to distant targets in a body. The key to this transmission is the synapse, where the axon of one neuron uses exocytosis to release neurotransmitters that can diffuse and bind to receptors on the dendrite of an adjacent neuron.

In essence, the synapse is a ‘decision point’ for determining whether or not the signal will proceed. It is the synapse which confers immense plasticity and potential for control to the whole circuit.

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Where is the “I”?

Over at the First Things blog, a standard “ID vs. Evolution” fight broke out involving some major players.  Unfortunately, I arrived late (as usual), but I decided to add my two cents to the kerfuffle anyway:

Over the years I have discovered a primary reason there is so much heated argument about this issue is that people employ numerous personal definitions for the concepts “intelligent design,” “evolution,” and “science.” Thus, I appreciate that Stephen Barr spells out his definition of ID: “The ID claim is that certain biological phenomena lie outside the ordinary course of nature.” If that is ID, then I would disagree. But ID can also mean something more modest, where one simply infers some form of intelligent influence on biological phenomenon, including evolution itself. For example, life itself could have been designed to shape subsequent evolution, thereby imparting some form of direction to evolution. This form of ID would not require evolution to fail or evolutionary mechanisms to be inadequate. On the contrary (!), this form of ID would more likely marvel at the success of evolution and try to develop a deeper understanding of why evolution succeeded.

I also added:

a clever designer could actually recruit and exploit the processes of random mutations and natural selection to carry out some purpose. After all, a common belief shared by both the ID people and their critics is that random mutations and natural selection are antithetical to purpose. I think that common belief is simply an assumption (or reflex response) that has become entrenched for historical and cultural reasons.

And:

design and evolution are not mutually exclusive. There may be ways to make intelligent use of randomness and natural selection such that they can carry out an objective. For example, scientists already make use of randomness when designing new proteins.

In response, someone proposed the following questions to me:

Can you (at least) provide a useful essential hint of how “intelligent use of randomness and natural selection … can carry out an objective”? What would INTELLIGENT mean, in such context?

This person hit on something very important.

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‘Fight or Flight’ Might be Ancient

One way to think about front-loading is that a lot of the “heavy-lifting” was done very early in evolution, such that it is all “down hill” from there.  Well, it looks like the basic logic of the autonomic nervous system, which allows organisms to shift between a non-stressed state and a state needed to respond to threats (adrenalin) was in place very early in evolution:

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Recursive front-loading

Since prestin represents a splendid example of convergent evolution at the molecular level, which in turn, supports the position that the blind watchmaker can be guided, one has to wonder about the origin of prestin itself.

To these ends, I have run across the following paper:

Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7690-5.

Expression of prestin-homologous solute carrier (SLC26) in auditory organs of nonmammalian vertebrates and insects.

Weber T, Gopfert MC, Winter H, Zimmermann U, Kohler H, Meier A, Hendrich O, Rohbock K, Robert D, Knipper M.

Prestin, the fifth member of the anion transporter family SLC26, is the outer hair cell molecular motor thought to be responsible for active mechanical amplification in the mammalian cochlea. Active amplification is present in a variety of other auditory systems, yet the prevailing view is that prestin is a motor molecule unique to mammalian ears. Here we identify prestin-related SLC26 proteins that are expressed in the auditory organs of nonmammalian vertebrates and insects. Sequence comparisons revealed the presence of SLC26 proteins in fish (Danio, GenBank accession no. AY278118, and Anguilla, GenBank accession no. BAC16761), mosquitoes (Anopheles, GenBank accession nos. EAA07232 and EAA07052), and flies (Drosophila, GenBank accession no. AAF49285). The fly and zebrafish homologues were cloned and, by using in situ hybridization, shown to be expressed in the auditory organs. In mosquitoes, in turn, the expression of prestin homologues was demonstrated for the auditory organ by using highly specific riboprobes against rat prestin. We conclude that prestin-related SLC26 proteins are widespread, possibly ancestral, constituents of auditory organs and are likely to serve salient roles in mammals and across taxa.

Fascinating.  So homologs of prestin have not only been identified in both other vertebrates and non-vertebrates, but are also expressed in their auditory organs.  Okay, so we can say that a prestin-like protein was already in place to carry out auditory function in the last common ancestor of mammals and insects.  That’s some pretty deep homology.  But does it go further?

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Driving biology to more and more complex forms

As I explained before, “The hypothesis of front-loading evolution would thus predict that significant transitions in evolution would depend on preadaptation.”

Recently, I discussed one such candidate – the origin of mitochondria.

A new paper has come out that strengthens this case for preadaptation:

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Protein nudges organismal evolution

We have seen that prestin is a motor protein found in the outer hair cells of the inner ear of the mammalian cochlea.  It vastly enhances auditory sensitivity by converting the energy from an ion gradient to force such that if you eliminate this protein in mice, there is a greater than 100-fold loss in auditory sensitivity.

Of course, what is most remarkable about this protein is its convergent evolution in certain bats and dolphins, where the prestin protein from both species share at least 14 independently derived amino acid sites. These changes apparently played key roles in the independent evolution of echolocation.  The molecular design of this protein seems to have facilitated the appearance of echolocation, which takes auditory sensitivity to the next level.  What’s more, there are other signs of convergent evolution at the anatomical level:

Echolocation requires exceptionally high frequency hearing and, though echolocating whales and bats generate their calls differently, their cochleae show multiple convergent anatomical features [4]. In particular, the cochlear OHCs in both taxa are shorter and stiffer than in other mammals [4], and this inferred adaptation for processing ultrasound is supported by audiograms that reveal correspondingly higher frequency thresholds [5].  (Yang Liu, James A. Cotton, Bin Shen, Xiuqun Han, Stephen J. Rossiter and Shuyi Zhang. 2009. Convergent sequence evolution between echolocating bats and dolphins. Current Biology Vol 20 No 2).

Prestin would thus appear to be a good candidate for something I describe in The Design Matrix.

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