The process of learning requires morphological changes in the neuronal connections and the formation of new synapses. The key mechanism by which different forms of memory are encoded, processed and stored in the brain is modulated depending on the activity, strength and structure of specific synaptic connections. Long-term memory requires changes in genetic expression, which induce the growth of new synaptic connections.
Due to the importance of memory and learning in our species, some authors had suggested that the synaptic plasticity in a number of association areas is higher in the human brain than in the other primates.
Cortical neurons in mammals are characterized by higher metabolism and synaptic plasticity and activity during development and the juvenile stage than in the adult.
In Homo sapiens, brain development is retarded compared with other primates, especially in some association areas, and the rate of brain growth in humans in the postnatal period is much higher than the rate of cerebral growth in non human primates, including chimpanzees. The prolongation of cerebral growth and fetal growth rates during infancy and childhood explains the large brain size in Homo sapiens.
Some association areas in the human brain are characterized by the presence of neurons, which remain structurally immature throughout their lifespan and show an increase in the expression of the genes which deal with metabolism and the activity and synaptic plasticity in the adulthood. High degrees of synaptic plasticity and activity in association areas of the adult human brain seem to have been retained through an increase in the expression of certain genes, many of which are related to cerebral development and, to a lesser extent, through the positive selection of certain genetic variants. Adult human beings are similar to juvenile chimpanzees in terms of their cerebral genetic expression profiles. Neotenic changes only affected a limited group of genes expressed in the brain, which suggests mosaic evolution.
Prefrontal cortex
Aerobic glycolisis in the adult human brain, which seems to be related to an increase in synaptic activity and plasticity, is significantly elevated in certain areas of the cortex of association which have undergone considerable modification during the evolution of human species, as the dorsolateral prefrontal cortex, which is associated with working memory, and a group of areas that make up the brain’s default mode network, which display elevated activity when the individual is at rest and is related to autobiographical memory, planning, and functions related to social interaction and navigation, such as theory of the mind and moral decision making.
Neurons belonging to certain areas of the human cerebral cortex exhibit a higher metabolism and a higher degree of synaptic plasticity and activity in adulthood than the cortical neurons of other mammals. So it appears that human neurons belonging to particular association areas retain juvenile characteristics throughout adulthood, which suggests that a neuronal neoteny has occurred in Homo sapiens, which allows the human brain to function, to a certain degree, like a juvenile brain during adult life.
The increase in the aerobic metabolism in these neurons may lead, however, to higher levels of oxidative stress, therefore favouring the development of neurodegenerative diseases which are exclusive, or almost exclusive, to humans, such as frontal dementia and Alzheimer’s disease, which may be, in part, the result of the retention of juvenile characteristics in adulthood in neurons associated with learning, memory and other complex cognitive functions, and the price our species pay for our elevated cognitive capacity, our longevity and our advanced social intelligence.
For further information:
Bufill, E., AgustÃ, J., Blesa, R., 2011. "Human Neoteny Revisited: The Case of Synaptic Plasticity". American Journal of Human Biology. 23: 729-739-284.
Bufill, E., AgustÃ, J., Blesa, R., 2011. "Human Neoteny Revisited: The Case of Synaptic Plasticity". American Journal of Human Biology. 23: 729-739-284.
Contact
Enric Bufill
ebufill@telefonica.net
Enric Bufill
ebufill@telefonica.net