Neuroplasticity: loose association, medium-level association, strong association
July 25, 2013 | James Kohl
In the context of addiction, a supranormal stimulus, and neuroplasticity, a correspondent asked “…how do we distinguish between a “loose” association, a “medium-level” association, and a “strong” association?”
Neuroscientists do this by linking the epigenetic effects of sensory input directly to gene activation in hormone-secreting nerve cells of brain tissue that is consistently linked to affects on behavior via brain imagery and every other means currently at our disposal (including model organisms). Medical laboratory scientists like me then link the behavior back to gene activation because reciprocal relationships are required to demonstrate cause and effect in the context of adaptively evolved behaviors.
For example, in a 2011 article, Berreby states “…behavioral epigenetics has yet to connect all its levels of analysis. It needs, and doesn’t yet have, at least one slam-dunk demonstration of all the links in a chain from behavior to neural activity to gene expression and back out again. How, for example, do biochemical events at a neuron’s nucleus affect the synaptic signaling between neurons that is the basis for all behavior?” Since then, based on what we included about molecular epigenetics in our 1996 review, I have linked the epigenetic landscape to the physical landscape of DNA via the effects of olfactory/pheromonal input on intracellular signaling, internuclear interactions and alternative splicings, which were placed into the context of cause and effect by Teresa Binstock in From Fertilization to Adult Sexual Behavior. “Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation in at least two species, Drosophila melanogaster and Caenorhabditis elegans (Adler and Hajduk, 1994; de Bono, Zarkower, and Hodgkin, 1995; Ge, Zuo, and Manley, 1991; Green, 1991; Parkhurst and Meneely, 1994; Wilkins, 1995; Wolfner, 1988). That similar proteins perform functions in humans suggests the possibility that some human sex differences may arise from alternative splicings of otherwise identical genes.”
Examples from different model organisms clearly show that nutrient-dependent pheromone-controlled alternative splicings of otherwise identical genes contribute to sexual differentiation in every species that reproduces sexually. The conserved molecular epigenetics of sexual differentiation provide more than merely a ‘strong’ association. For contrast, brain imagery from human subjects provides the loosest association I can imagine given the context of a well-detailed gene-cell-tissue-organ-organ system pathway. See for example: Understanding the bases of sex differences (1981). Focus on the gene, cell, tissue, organ, organ system pathway is echoed in SWHR’s efforts that ‘…led to the 2001 ground-breaking report by the National Academies of Science’s Institute of Medicine… The report recommended that research on sex differences be conducted at every level –gene, cell, tissue, organ, and organism — and that sex differences be studied at every stage of life, from conception through death.’
Since 1981, despite Naftolin’s clear directive in the context of Understanding the bases of sex differences, and despite the SWHR’s recommendation that “…research on sex differences be conducted at every level — gene, cell, tissue, organ, and organism — and that sex differences be studied at every stage of life, from conception through death’ what I have seen is that the same people who ignored Teresa Binstock’s insights have ignored the works that detailed the involvement of epigenetic effects on the gene-cell-tissue-organ-organ system pathway that link olfactory/pheromonal input to hormones and their affects on behavior via the molecular mechanisms conserved in species from microbes to man and exemplified in the hormone-organized and hormone-activated behavior of invertebrates and vertebrates. Despite what might have been a degree of doubt in the context of cause and effect even in 2001, we have since seen ~10,000 papers published on the nutrient-dependent microRNA / messenger RNA balance, which is responsible for pheromone-controlled reproduction in species from microbes to man.
Yet my reception in different discussion groups has been roughly the same as the reception Teresa Binstock’s comments received elsewhere (in the late 1990s) from the same people. It’s past time for others to speak up, or learn about cause and effect so that they can contribute to discussions rather than limit discussions and drive away those who do not agree with their approach to the study of human sexuality.