Mirror neurons help us discriminate goals and discern other humans intentions, some researchers even think that such neural nets are involved in autism.
Because mirror neurons appear to be involved in social interaction, dysfunctions of this neural system could explain some of the primary symptoms of autism, including isolation and absence of empathy. Studies of people with autism show a lack of mirror neurons activity in several regions of the brain. Researchers speculate that treatments designed to restore this activity could alleviate some of autism’s symptoms. A complementary hypothesis, the salience landscape theory, could account for secondary symptoms of autism such as hypersensitivity.
People with autism show reduce mirror neuron activity in the inferior frontal gyrus, a part of the brain’s premotor cortex, perhaps explaining their inability to assess the intentions of others. Dysfunctions of mirror neurons in the insula and anterior cingulated cortex may cause related symptoms, such as the absence of empathy, and deficits in
the angular gyrus may result in language difficulties. People with autism also have structural changes in the cerebellum and brain stem.
How much our behavior could be explained by learning through mirror neurons (family and culture) and how much to Biological heritage? The answer to this question might. come at least, in part by the studies of Moshe Zif of McGill University.
Moshe Szyf, of McGill University in Montreal, studies the effect of maternal care on epigenetic imprinting. As he explained at this week’s meeting on Epigenetics and Neural Developmental Disorders, held in Beltsville, Maryland, imprinting might be a general mechanism whereby experiences are translated into behavior. If that turns out to be so, it will affect the understanding and treatment of mental illness.
The first indication of this came when Michael Meaney, one of Dr Szyf’s long-term collaborators, noticed that rat pups whose mothers spent a lot of time licking and grooming them grew up to be less fearful and better adjusted adults than the off spring of neglectful mothers. Crucially, these well adjusted rats then gave their own babies the same type of care in effect, transmitting the behavior from mother to daughter by inducing similar epigenetic changes.
When Dr Szyf looked at the brain of the two sorts of rats, he found differences in their hippocampuses. Among other jobs, the hippocampus is involved in responding to stress. Dr. Szyf discovered that better adjusted rats had, in their hippocampuses, more active versions of the gene that encodes a molecule called glucocorticoid receptor protein. Glucocorticoid is a hormone produced in response to stress and its job is to make the animal be have appropriately. But too much glucocorticoid is a bad thing, so there is also a way to switch off its production. When glucocorticoid binds to its receptor in the hippocampus, that activates the expression of genes which dampen further synthesis of the hormone. This feedback system is weaker in rats that have had little maternal care. As a result, they are more anxious and fearful, and show a heightened response to stress.
The researchers went on to study what is responsible for the difference in expression of the glucocorticoid receptor gene. They found that two types of imprinting are involved. One adds molecules called methyl groups to the DNA of the gene. This suppress gene expression. The other adds acetyl groups, which are slightly larger, to the proteins around which the DNA is coiled. This has the opposite effect, making gene expression easier. Rats that had experienced little maternal care showed high levels of methylation and low levels of acetylation of the glucocorticoid receptor gene and its neighbouring proteins. The opposite was true for those that had a more attentive upbringing.
This explains why levels of glucocorticoid receptor protein are different in the two groups of rats. But Dr Szyf still wanted to know what triggers epigenetic tagging in response to maternal care. He suspected a protein called NGFI-A, which is produced in response to stimulations such as licking and grooming. The more stimulation a rat pup receives, the more NGFI-A it produced.
This suspicion was confirmed when he found it is also the case that the more maternal care a pup receives, the more NGFI-A it has bound to its glucocorticoid receptor genes. Then, in a series of experiments on cell cultures, he showed that when bound to this gene NGFI-A attracts two enzymes involved in epigenetic tagging. The enzymes in question are histone acetyltransferase (which adds acetyl groups to proteins) and methylated DNA binding protein-2 (which removes methyl groups from DNA).
According to Dr Szyf, epigenetic modifications in response to maternal care occur during the first week of life after birth the so called critical period. The effects are stable, and persist into adulthood. Because this type of programming involves adding and removing chemical, groups to and from the DNA and its nearby protein molecules, the researches wondered whether reversing those reactions during adulthood would affect an animal’s behaviour. To test this, they used two chemicals. One, called TSA, inhibits the enzyme that removes acetyl groups. The other, called L-methionine, is a donor of methyl groups.
When injected into the brain cavity near the hippocampus, TSA increased both the amount of acetylation and the level of expression of the glucocorticoid receptor in adult rats that had little maternal care early in life. As a result, those rats became less anxious and fearful. By contrast, L-methionine increased the level of methylation and thus reduced the expression of the gene in animals with loving mothers, and led to fear, anxiety and a heightened response to stress.
And what about free will?
The equation genes(interacting with environment) + mirrors neurons (learning through interaction with culture and family) + context (where interaction occurs social and physical) = individual response to a certain event.
Should we add free will at the end of the left side of the equation?.