A flawed model: no tripartate synapse in the adult brain
Posted on January 15, 2013 by James Kohl.
Excerpt: “The tripartite synapse – a model long accepted by the scientific community and one in which multiple cells collaborate to move signals in the central nervous system – does not exist in the adult brain.”
Glutamate-Dependent Neuroglial Calcium Signaling Differs Between Young and Adult Brain [subscription required]
Excerpt: “The observations reported here do not call into question that astrocytes can be indirectly activated by neural activity. A number of transmitters, including endocannabinoids, purines, norepinephrine, and acetylcholine, as well as changes in extracellular Ca2+, can trigger astrocytic Ca2+ signaling (14, 18–21). Yet, activation of these pathways is typically limited to episodes of intense glutamatergic transmission or to the global release of neuromodulators that occur in the setting of arousal or awakening.”
My comment to the Science site (received on Thu, 10 Jan 2013 19:54): Epigenetic effects on the unicellular young and the multicellular adult brain.
Shall we eliminate the indirect effects of sensory input that never really altered intracellular signaling and stochastic gene expression in neurons? Can we then focus on the direct effects of nutrient chemicals and pheromones on gene expression? If so, will we see that learning and memory in unicellular yeasts is exemplified via epigenetically-effected changes in
gonadotropin releasing hormone (GnRH) secretion in young mammals?
Apparently, the research reported here links gene duplication and increased hexose transport / glucose utilization to genetically predisposed in utero development of the vertebrate GnRH neuronal system. This links glucose uptake to postnatal competition among conspecifics for nutrients that enable their metabolism of nutrients to pheromones, which signal species-specific reproductive fitness during the developmental staging / life history of species from microbes to man.
In yeasts, the epigenetic effects of glucose on the level of expression of the hexose transporter and receptor-mediated rate of glucose transport into the cell alters nutrient chemical-dependent pheromone-controlled reproduction at the advent of sexual reproduction. Presumably this occurs via the same nutrient chemical stress-altered and social stress-altered molecular mechanisms that epistatically effect the microRNA / messenger RNA balance in
hormone-secreting nerve cells of the mammalian brain, which control neurotransmission.
In my model, this nutrient chemical stress-altered and social stress-altered microRNA / messenger RNA balance facilitates hypothalamic GnRH pulse frequency and amplitude and 1) epigenetically effected, 2) nutrient chemical-dependent, 3) pheromone-controlled
reproduction via the hypothalamic-pituitary-gonadal (HPG) axis and HP-adrenal
Perhaps the failed promise of drug effects on astrocytes was due to the more powerful direct (i.e., epigenetic) effects of nutrient chemicals and pheromones on neurotransmission (e.g., as required for adaptive evolution and prenatal to postnatal developmental staging in mammals).
Addendum: For two decades, people have designed studies based on the wrong model of adult neurotransmission. The result is a failure to recognize the right model. The right model is the one where nutrient chemicals and pheromones change neurotransmission and cause adaptive evolution in species from microbes to man.
In mammals, we can see the epigenetic effects of food odors and pheromones manifested in neuroendocrine changes during the development of behavior. Hormone-organized behaviors lead to hormone-activated behaviors in vertebrate and invertebrate species. This means the same model for pheromone-controlled neurotransmission and insect behavior extends well to pheromone-controlled neurotransmission and mammalian behavior.
There is no need to separate the model for food odors that control behavior from the model for pheromonal control of behavior via ecological, social, neurogenic, and socio-cognitive niche construction. Food odors and pheromones organize and activate behavior via niche construction. Indirect activation of neural activity in astrocytes can now be viewed in the light of direct activation of neural activity by olfactory/pheromonal input, which links ecological epigenetics to niche contruction and downstream effects on the behavior of all organisms (i.e., from microbes to man). Behavior is nutrient chemical-dependent and pheromone-controlled with or without the involvement of neurotransmitters, but behavior is better controlled when niche construction leads to species-specific neurogenic and socio-cognitive niches.
Retired medical laboratory scientist
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