Neurobiology For Dummies. Frank Amthor

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the memory “trace” back in those areas of the neocortex.

The finding that the neocortex represents both original sensory input and its memory has profound implications for understanding what memory is. Many neuroscientists now believe that memory is intrinsically reconstructive — a hallucination, if you will. This is a very different metaphor from the token look up and address model taken from computer science. One important aspect of the reconstructive aspect of memory is that the act of reconstruction can distort the memory. Suggestions, guesses, and events after the memory can affect the reconstruction such that they become part of, and indistinguishable from, subsequent reconstructions.

      The neurobiology of memory depends both on modifiable synaptic weights, such as with NMDA receptors in hippocampus and cortex, and the creation of new neurons in memory areas such as the hippocampus. The discovery of the birth of neurons in the adult hippocampus overturns the old idea of zero neurogenesis in the adult brain. Some senile dementia and even depression appear to be associated with failure of this mechanism.

      The frontal lobes and executive brain

      The frontal lobes are responsible for planning and executing behavior. Generally speaking, the output of the frontal lobe is in its most posterior portion, the primary motor cortex. Neurons in primary motor cortex send their axons down the spinal cord (or out some cranial nerves) to drive motor neurons that cause muscles throughout the body to contract.

      Anterior to the primary motor cortex are the supplementary motor area and premotor cortex that organize the firing of groups of muscles. Anterior to those areas are the frontal eye fields and other areas called prefrontal cortex (even though they are in the frontal lobe) that are involved in more abstract aspects of planning.

      It is generally held that there is relative expansion of the frontal lobe compared to the rest of the brain in humans compared to other primates, and primates compared to other mammals. Some exceptional non-primate mammals such as the echidna have large frontal lobes, however. This has led to debate among neuroscientists about whether these frontal areas are really homologous across mammalian species. Whatever the result of that debate, we know that damage to prefrontal cortex in humans produces distinctive cognitive deficits such as impulsive behavior and profound changes in affect.

      Language, emotions, lateralization, and thought

      True grammatically ordered language distinguishes humans from all other species on earth. Recent evidence has suggested an important role for a gene called FOXP2 in generating language capability, although how this gene changes the brain to allow language isn’t clear.

      The capacity for learning language is built in, but neuroscience does not now know how. One clue may be brain lateralization, however. Left- versus right-side specialization for some types of audio processing and production exists in other mammals, and even some birds, but is nowhere near as extensive as in humans.

      

A similar association exists with right-hand dominance, driven by the left side of the brain, which is more extensive in humans than any other animal. Chimpanzees, for example, may be relatively right- or left-hand preferring, but most have no overall tendency to be strongly right-handed or left-handed, the way humans do.

      Neuroscience’s view of emotions has changed markedly in the last decades. Earlier views regarded emotions as leftovers from our evolution from non-rational species. Star Trek’s Mr. Spock could be taken as a model of a superior, more evolved humanoid. However, we now know that emotions are a means of nonverbal communication within our brains. Hunches and anxiety in certain situations are signs of danger and the need to be cautious.

      

We see the usefulness of this nonverbal information in people with damage to the orbitofrontal cortex or amygdala. They may gamble recklessly or commit social faux pas because they lack internal feelings about the mistakes they’re making.

      One of the most important reasons to understand neurobiology is to understand mental disorders and treatments. The good news is that great progress is being made in this field now. We know the genetic bases of many developmental disorders, such as Fragile X and William’s syndrome. The bad news is that many disorders remain that we do not know about, and, even among disorders with known genetics, how the gene alteration produces the disorder, and what to do about it, are not clear. Chapters 15 through 18 discuss the background and current treatment approaches (if any) of many common neurological disorders.

      Developing the brain and nervous system

      

A useful metaphor is an ant hill or termite mound. No master ant or termite knows how to build a hill or mound and directs the other insects. Instead, ants and termites respond to each other, and to the environment, by digging holes and gluing arches together. Some holes and arches reach a critical mass that causes nearby insects to concentrate on those structures and related structures, which triggers the completion of the insect home as though its builders were following a design.

      Developing cells have genetically coded responses to substances they detect by their membranes or ingest, including cell identity and brain location marker molecules. Cell responses include movement, division, and secretion of other markers and agents. The interactions among cells that have these responses in the embryological environment builds the brain.

      Much of the genome is only expressed extensively during development, a time when the organism is also particularly susceptible to toxins that mimic or interfere with these markers and agents. The result of this interference is the construction of an improperly set-up brain, which is typically much worse than inferring temporarily with a properly constructed brain later in life, which often can be reversed.

      Movement disorders and symptoms

      Movement disorders can originate with brain damage that compromises the control of movement, or neurons that drive muscles, or the muscles themselves. Chapter 16 discusses some of the most common movement disorders. Cerebral palsy and epilepsy typically involve brain damage. Multiple sclerosis is caused by demyelination of axons of motor and other neurons. Myasthenia gravis is an autoimmune disease involving the cholinergic receptors on muscle cells.

      Some well-known movement disorders, such as Parkinson’s and Huntington’s diseases, occur only later in life. Neither of these diseases

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