Injecting molecules from a sea slug that received tail shocks into one that didn’t made the recipient animal behave more cautiously.
Mice raised in isolation from their mothers developed cognitive deficits similar to those of babies raised in orphanages where physical contact is infrequent.
September 17, 2012|
Isolating mouse pups from their mothers early in development can reduce the insulation surrounding neurons of the brain, which leads to problems with memory and socialization, a study in Science reported last week (September 14). The study provides a molecular explanation for the cognitive deficits observed in children raised in orphanages where they are rarely touched.
“This is incredibly important data, because it gives us the neural mechanisms associated with the deleterious changes in the brain” that arise from neglect, Nathan Fox, a cognitive neuroscientist at the University of Maryland told Wired Science.
Researchers from Harvard University took mice that were 21 days old and kept them isolated from other mice for 1 month. Afterwards, they were put in cages with other mice that had been raised with others. Isolated mice spent less time interacting with others, and seemed content inspecting props in the cage. They also performed more poorly on memory tests.
Earlier studies had shown that human children raised in isolation or abusive conditions had less white matter in their prefrontal cortex—the part of the brain involved in memory, decision making, and social interactions. When the Harvard team looked at the brain cells of their isolated mice, they noticed that the myelin sheaths that insulate neurons and make them send and receive signals faster, were reduced in size. However, mice that were raised with other pups until 5 weeks of age, then put in isolation, did not show the same deficits, suggesting that myelin is formed during a critical early window in development.
(Hat tip ScienceNOW.)
September 17, 2012
Lowering stress, and thus cortisol production, promotes the
development of white matter via what would otherwise be a negative effect of
stress via cortisol suppression on the development and function of the
adaptively evolved mammalian hypothalamic gonadotropin releasing hormone (GnRH)
neurogenic niche, which is responsible for nutrient chemical-dependent and
pheromone-dependent brain development.
GnRH modulates luteinizing hormone (LH), and a quick glance through the extant
literature on neuroendocrine and neuroimmune system function in mammals would
show how both GnRH and LH are clearly involved in development of myelinized
white matter and gray matter. Stress, for example, negatively impacts both the
neuroendocrine and neuroimmune system, which are modulated by GnRH.
What a quick glance would not show is how the epigenetic effects of nutrient
chemicals and pheromones cause adaptive evolution and the development of the
mammalian hypothalamic GnRH neurogenic niche. For that, you have to look back
at the ecological and social niche construction that precedes neurogenic and
cognitive niche construction. Across the continuum of ecological, social,
neurogenic, and cognitive niche construction we have the conservation of GnRH
and diversification of its receptor.
Kochman 2012 has this to say about that: "The discovery of the fact that
one decapeptide molecule, among the GnRHs, was constructed perfectly at the
beginning of 400 million years evolution and that it is not possible to improve
its physiological potency using the any natural amino acid is, in my opinion,
important, fascinating and beautiful."
The role of GnRH is central to my model of how nutrient chemicals and
pheromones cause adaptive evolution via their effects on LH. The abysmal lack
of knowledge of current molecular biology that links the epigenetic effects of
nutrient chemicals and pheromones directly to the secretion of hypothalamic
GnRH in humans, and to LH secretion and myelinization in mammals via exposure
to food odors and pheromones that are important to brain development, seems
destined to delay the realization that human brain development is as dependent on
pheromones as it is on nutrient chemicals.
These results in mice extend requirement for mammalian pheromone-dependent
myelinization to human infants raised with minimal social contact because the
absence of social odors (the pheromones) shows up in behavior caused by the
otherwise â€œnormalâ€쳌 epigenetic effects of pheromones as measured in luteinizing
hormone during the first 2-3 years of life in human infants.
Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338.