Paraphrased from the article linked (below):
Approximately 10,000 neurons in 26 different brain areas appear to transmit signals directly to GnRH neurons, which appear to transmit signals to as many as 30,000 or more neurons in 34 brain areas. This allows GnRH neurons to modify diverse functions that coordinate the internal state of organisms with behavior that optimizes reproductive success.
How did the complexity of this neuronal network arise?
An abysmal lack of conceptual understanding in the context of neuronal networks became known to me after I announced the publication of Howard Bloom’s new book: “The God Problem: How A Godless Cosmos Creates” on the evolutionary psychology yahoo group. What Bloom thinks is “creation” is what I think was best addressed by the current director of the National Institutes of Health in “The Language of God: A Scientist Presents Evidence for Belief” by Francis S. Collins.
Dr. Collins makes it clear that genes are the language of God, science, and faith. The problem for faithless atheists; for agnostics; and even for intelligent non-scientists and authors, like Bloom, is this: They need to tell us how genes first appeared in cells that somehow create new genes. That way, we can all continue to write and to speak about God while using His language. For example, if there is a “language gene” in our genome, how did it get there? Why is our genetically predisposed language ability not found in other organisms? Was the language gene created by a godless cosmos?
Did the cosmos create any other genes? If so, when did this Godless cosmos create the first gene, and how did that gene lead to the creation of other genes? The concept of genes in cells that – in a godless cosmos — create new genes in other cells seems absurd. For comparison, a bio-logical explanation details how new (de novo) genes result from epigenetic effects of nutrient chemicals (e.g., on duplications) and how the epigenetic effects of pheromones control reproduction and speciation.
The nutrient chemicals metabolize to pheromones and both may cause electrostatically-driven changes in intracellular signaling and stochastic gene expression, which leads to the expression of new olfactory receptor genes. That’s how “Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.“
New nutrient chemicals in novel environments are ingested by organisms that recognize the difference between conspecifics and heterospecifics. When ingestion benefits individual survival, the nutrient chemicals are metabolized to pheromones that control reproduction and species survival. Ingestion of nutrient chemicals, however, is a receptor-mediated event, and the epigenetic effect of pheromones is also receptor-mediated.
For example (from Kohl, 2012): “A [new] gene that codes for the mammalian olfactory receptor, OR7D4, links food odors to human hunger, dietary restraint, and adiposity (Choquette et al., 2012). [In addition] OR7D4 exemplifies a direct link1 from human social odors to their perception (Keller, Zhuang, Chi, Vosshall, & Matsunami, 2007) and to unconscious affects2 on human behavior associated with human olfactory-visual integration (Zhou, Hou, Zhou, & Chen, 2011); human brain activation associated with sexual preferences (Savic, Heden-Blomqvist, & Berglund, 2009), human learned odor hedonics; and motor function (Boulkroune, Wang, March, Walker, & Jacob, 2007).
Many people will recognize how the unconscious affects of new olfactory receptor genes could support adaptive evolution via the cellular learning and memory required for ecological, social, neurogenic, and socio-cognitive niche construction. Others may not yet grasp the concept of niche construction. In any case, these 4-stages of our evolved niche construction support the more detailed notion that theistic Creation proceeds via the “…epigenetic tweaking of immense gene networks in ‘superorganisms’ (Lockett, Kucharski, & Maleszka, 2012) that ‘solve problems through the exchange and the selective cancellation and modification of signals (Bear, 2004, p. 330)’.” The honeybee is the model organism that exemplifies this cause and effect via epigenetic effects of the queen’s diet on her pheromones and neuroanatomy of the worker bees’ brains. These epigenetic effects appear to have their origins as choices in the first unicellular organisms, which led to the advent of nutrient-chemical dependent sexual reproduction.
Does the language of God predict the importance of food choice and mate choice for sexual reproduction? Many believers in Biblical Genesis would probably say that it does. For contrast, does evidence for conservation of gonadotropin releasing hormone (GnRH) across 400 million years of vertebrate evolution (and diversification of its receptor) help biologists to refute any theories that random mutations cause adaptive evolution? If so, does the evolutionary history of the GnRH molecule as a yeast species alpha-mating pheromone at the advent of nutrient-dependent sexual reproduction help with those refutations?
Q. Who need refutations of theories? A. People like Clarence ‘Sonny’ Williams, who participate in discussions of evolutionary psychology. Williams, and others, seem to think that different alleles result from random mutations or unknown natural mechanisms. Unlike Bloom, however, Williams is not capable of any critical thinking about Creation, genetics, theistic evolution, or the language that must be used to communicate accurate concepts to others. Indeed, as Francis S. Collins has clearly indicated, it is the language of God (i.e., DNA). What’s known about genetics must be used to tell others about how sensory input from the environment directly effects the molecular mechanisms that affect the evolution of behavior in organisms from microbes to man. Perhaps, when people like Williams stop pretending to know about DNA and genetics, progress can be made by those who understand the basic principles of biology and levels of biological organization. which are required to link sensory cause directly to effects on hormones and their affect on behavior.
A similar problem came up in discussion on the human ethology yahoo group, where John Angel participates as a self-described ethologist and canid researcher. I refer to him as an “animal trainer” because he has adamantly expressed his belief that “Behaviour is driven by consequences.”
It is clear to nearly everyone else that behavior is NOT driven by consequences. It is genetically predisposed and epigenetically affected by sensory stimuli from the environment. It is easy to counter the belief that behavior IS driven by consequences, by showing how obvious it is that behavior is driven by sensory input that epigenetically determines the result of genetically predisposed behaviors. Behaviorists, like John Angel and Glen Sizemore who are vocal discussants cannot seem to grasp this obvious fact. What is worse is that they seem to want others to believe an advanced academic degree is required to distinguish between operant conditioning and classical conditioning.
A shock paired with a tone exemplifies operant conditioning. A food odor paired with a tone exemplifies classical conditioning. After either of these paired associations has repeatedly occurred, the tone predicts the behavior in the absence of either the shock or the odor. That’s simple enough for most people without an advanced academic degree to understand! Isn’t it? Pavlov’s dog is the most commonly used example of classical conditioning, but Glen Sizemore has repeatedly misrepresented tone and shock pairing as if it exemplified Pavlovian/classical conditioning, which it obviously does not.
In mammals, for example, odors cause receptor-mediated changes in intracellular signaling and stochastic gene expression in hormone-secreting nerve cells of brain tissue, which is how olfactory/pheromonal input epigenetically alters the brain’s control of behavior. For contrast, electrical shocks elicit a response from pain receptors and reflex-like responses. No epigenetic effects are involved, which is why training does not alter genetically predisposed behavior during its development.
I did not say that training does not affect behavior. I am attempting to clarify that animal trainers can only train animals that are genetically predisposed to respond to sensory stimuli and that training does not cause the creation of new genes, which is why behavior cannot be driven by consequences. Is John Angel, like Glen Sizemore, a fool? A metaphorical representation of biological facts would be that a cart does not pull the horse. The horse, however, can be trained to pull the cart because it is genetically predisposed to respond to sensory stimuli associated with the training that are associated with changes in its behavior. The take-home message is that training does not epigenetically cause the creation of genes.
Olfactory/pheromonal input epigenetically causes the creation of new genes. That’s how sensory input is linked to genetically predisposed differences in the behavior of microbes — that must first find nutrient chemicals — to mammals that must first find nutrient chemicals, before either the microbe or the mammal can metabolize the nutrient chemicals to the pheromones that control their nutrient-dependent reproduction. This links the epigenetic effects of nutrient chemicals and pheromones via the creation of new genes to the language of God (DNA) and presents the God problem to those who seem unable to understand how He communicates.
 Saying “these are whole new genes, not just new alleles” makes no sense. An allele IS a gene, just an alternative form at a given locus in a chromosome.
 If you point to some circumstance where an animal learns something and none of the “major players” are chemical – say like a rat that freezes in response to a tone that has been “paired” with shock – Kohl will insist that this is junk (he would probably deride this as “training” even though the process is Pavlovian)