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  1. 1. Chapter 5 Development and Plasticity of the Brain
  2. 2. Development of the Brain <ul><li>Plasticity of the brain refers the the idea that the brain is constantly changing throughout the lifetime. </li></ul><ul><li>Development of the brain is due to both experience and physical maturation. </li></ul><ul><li>Rapid development especially occurs early in life. </li></ul><ul><ul><li>Prefrontal cortex develops rapidly between 7 and 12 months (allowing for object permanence). </li></ul></ul>
  3. 3. Fig. 5-1, p. 122
  4. 4. Fig. 5-2, p. 123
  5. 5. Development of the Brain. <ul><li>The human central nervous system begins to form when the embryo is approximately 2 weeks old. </li></ul><ul><ul><li>The dorsal surface thickens forming a neural tube surrounding a fluid filled cavity. </li></ul></ul><ul><ul><li>The forward end enlarges and differentiates into the hindbrain, midbrain and forebrain. </li></ul></ul><ul><ul><li>The rest of the neural tube becomes the spinal cord. </li></ul></ul>
  6. 6. Fig. 5-3, p. 123
  7. 7. Development of the Brain <ul><li>The fluid-filled cavity becomes the central canal of the spinal cord and the four ventricles of the brain. </li></ul><ul><ul><li>The fluid is the cerebrospinal fluid. </li></ul></ul>
  8. 8. Development of the Brain <ul><li>At birth, the human brain weighs approximately 350 grams. </li></ul><ul><li>By the first year. the brain weighs approximately 1000 grams. </li></ul><ul><li>The adult brain weighs 1200-1400 grams. </li></ul>
  9. 9. Development of the Brain <ul><li>The development of neurons in the brain involves the following four processes: </li></ul><ul><ul><li>Proliferation </li></ul></ul><ul><ul><li>Differentiation </li></ul></ul><ul><ul><li>Myelination </li></ul></ul><ul><ul><li>synaptogenesis </li></ul></ul>
  10. 10. Development of the Brain <ul><li>Proliferation refers to the production of new cells/ neurons in the brain primarily occurring early in life. </li></ul><ul><li>Early in development, the cells lining the ventricles divide. </li></ul><ul><li>Some cells become stem cells that continue to divide </li></ul><ul><li>Others remain where they are or become neurons or glia that migrate to other locations. </li></ul>
  11. 11. Development of the Brain <ul><li>Migration refers to the movement of the newly formed neurons and glia to their eventual locations. </li></ul><ul><li>Migration occurs in a variety of directions throughout the brain. </li></ul><ul><li>Migration occurs via cells following chemical paths in the brain of immunoglobins and chemokines. </li></ul>
  12. 12. Fig. 5-6, p. 127
  13. 13. Development of the Brain <ul><li>Differentiation refers to the forming of the axon and dendrite that gives the neuron its distinctive shape. </li></ul><ul><li>The axon grows first either during migration or once it has reached its target and is followed by the development of the dendrites. </li></ul><ul><li>Neurons differ in their shape and chemical component depending on their location in the brain. </li></ul>
  14. 14. Development of the Brain <ul><li>Myelination refers to process by which glia produce the fatty sheath that covers the axons of some neurons. </li></ul><ul><li>Myelin speeds up the transmission of neural impulses. </li></ul><ul><li>Myelination first occurs in the spinal cord and then in the hindbrain, midbrain and forebrain. </li></ul><ul><li>Myelination occurs gradually for decades. </li></ul>
  15. 15. Development of the Brain <ul><li>Synaptogenesis is the final stage of neural development and refers to the formation of the synapses between neurons. </li></ul><ul><li>Occurs throughout the life as neurons are constantly forming new connections and discarding old ones. </li></ul><ul><li>Synaptogenesis slows significantly later in the lifetime. </li></ul>
  16. 16. Development of the Brain <ul><li>Although it was originally believed that no new neurons were formed after early development, recent research suggests otherwise: </li></ul><ul><li>Two Examples: </li></ul><ul><li>Stem cells are undifferentiated cells found in the interior of the brain that generate “daughter cells” which can transform into glia or neurons. </li></ul><ul><li>New olfactory receptors also continually replace dying ones. </li></ul>
  17. 17. Development of the Brain <ul><li>Animal research has also shown the development of new neurons occurring in other brain regions. </li></ul><ul><ul><li>Example: songbirds have a steady replacement of new neurons in the singing area of the brain. </li></ul></ul>
  18. 18. Development of the Brain <ul><li>Axons must travel great distances across the brain to form the correct connections. </li></ul><ul><li>Sperry’s (1954) research with newts indicated that axons follow a chemical trial to reach their appropriate target. </li></ul><ul><li>Growing axons reach their target area by following a gradient of chemicals in which they are attracted by some chemicals and repelled by others. </li></ul>
  19. 19. Fig. 5-7, p. 127
  20. 20. Development of the Brain <ul><li>When axons initially reach their targets, they form synapses with several cells. </li></ul><ul><li>Postsynaptic cells strengthen connection with some cells and eliminate connections with others. </li></ul><ul><li>The formation or elimination of these connections depends upon input from incoming of axons. </li></ul>
  21. 21. Fig. 5-8, p. 129
  22. 22. Development of the Brain <ul><li>Some theorists refer to the idea of the selection process of neural connections as neural Darwinism. </li></ul><ul><li>In this competition amongst synaptic connections, we initially form more connections than we need. </li></ul><ul><li>The most successful axon connections and combinations survive while the others fail to sustain active synapses. </li></ul>
  23. 23. Development of the Brain <ul><li>A neurotropin is a chemical that promotes the survival and activity of neurons. </li></ul><ul><li>Axons that are not exposed to neurotropins after making connections undergo apoptosis , a preprogrammed mechanism of cell death. </li></ul><ul><li>Therefore, the healthy adult nervous system contains no neurons that failed to make appropriate connections. </li></ul>
  24. 24. Development of the Brain <ul><li>Nerve growth factor (NGF) is a type of neurotrophin released by muscles that promotes the survival and growth of axons. </li></ul><ul><li>The brain’s system of overproducing neurons and then applying apoptosis enables the exact matching of the number of incoming axons to the number of receiving cells. </li></ul>
  25. 25. Development of the Brain <ul><li>The elimination and period of massive cell death is part of normal development and maturation. </li></ul><ul><li>After maturity, the apoptotic mechanisms become dormant. </li></ul><ul><li>Neurons no longer need neurotrophins for survivals, but neurotrophins increase the branching on axons and dendrites throughout life. </li></ul>
  26. 26. Development of the Brain <ul><li>Early stages of brain development are critical for normal development later in life. </li></ul><ul><li>Chemical distortions in the brain during early development can cause significant impairment and developmental problems. </li></ul>
  27. 27. Development of the Brain <ul><li>Fetal alcohol syndrome is a condition that children are born with if the mother drinks heavily during pregnancy. </li></ul><ul><li>The condition is marked by the following: </li></ul><ul><ul><li>Hyperactivity and impulsiveness </li></ul></ul><ul><ul><li>difficulty maintaining attention </li></ul></ul><ul><ul><li>varying degrees of mental retardation </li></ul></ul><ul><ul><li>motor problems and heart defects </li></ul></ul><ul><ul><li>facial abnormalities. </li></ul></ul>
  28. 28. Fig. 5-9, p. 130
  29. 29. Development of the Brain <ul><li>The dendrites of children born with fetal alcohol syndrome are short with few branches. </li></ul><ul><li>Exposure to alcohol in the fetus brain suppresses glutamate and enhances the release of GABA. </li></ul><ul><li>Many neurons consequently receive less excitation and exposure to neurotrophins than usual and undergo apoptosis. </li></ul>
  30. 30. Development of the Brain <ul><li>Children of mothers who use cocaine during pregnancy show a decrease in language skills, a slight decrease in IQ scores and impaired hearing. </li></ul><ul><li>Children of mothers who smoked during pregnancy are at increased risk for low birth weight, sudden infant death syndrome, ADHD, long term intellectual deficits and impairments of the immune system. </li></ul>
  31. 31. Development of the Brain <ul><li>The brain has the limited ability to reorganize itself in response to experience. </li></ul><ul><ul><li>Axons and dendrites continue to modify their structure and connections throughout the lifetime. </li></ul></ul><ul><ul><li>Dendrites continually grow new spines. </li></ul></ul><ul><li>The gain and loss of spines indicates new connections and potentially new information processing. </li></ul>
  32. 32. Fig. 5-10, p. 131
  33. 33. Development of the Brain <ul><li>Rats raised in an enriched environment develop a thicker cortex and increased dendritic branching. </li></ul><ul><li>Measurable expansion of neurons has also been shown in humans as a function of physical activity. </li></ul><ul><li>The thickness of the cerebral cortex declines in old age but much less in those that are physically active. </li></ul>
  34. 34. Fig. 5-11, p. 132
  35. 35. Development of the Brain <ul><li>Neurons also become more finely tuned and responsive to experiences that have been important in the past. </li></ul><ul><li>This may account for the fact that blind people often have enhanced tactile senses and increased verbal skills. </li></ul><ul><ul><li>The occipital lobe normally dedicated to processing visual information adapts to also process tactile and verbal information. </li></ul></ul>
  36. 36. Development of the Brain <ul><li>Extensive practice of a skill changes the brain in a way that improves the ability for that skill. </li></ul><ul><li>For example, MRI studies reveal following: </li></ul><ul><ul><li>the temporal lobe of professional musicians in the right hemisphere is 30% larger than non-musicians. </li></ul></ul><ul><ul><li>thicker gray matter in the part of the brain responsible for hand control and vision of professional keyboard players </li></ul></ul>
  37. 37. Fig. 5-12, p. 133
  38. 38. Development of the Brain <ul><li>Part of the mechanism on increased ability due to experience is that attention to anything releases dopamine. </li></ul><ul><li>Dopamine acts on the cortex to expand the response to stimuli active during the dopamine release. </li></ul>
  39. 39. Development of the Brain <ul><li>Focal hand dystonia or “musicians cramp” refers to a condition where the reorganization of the brain goes too far. </li></ul><ul><li>The fingers of musicians who practice extensively become clumsy, fatigue easily and make involuntary movements. </li></ul><ul><li>This condition is a result of the area of the brain responsible for a specific finger movement growing and overlapping with others. </li></ul>
  40. 40. Plasticity After Brain Damage <ul><li>Survivors of brain damage show subtle to significant behavioral recovery. </li></ul><ul><li>Some of the mechanisms of recovery include those similar to the mechanisms of brain development such as the new branching of axons and dendrites. </li></ul>
  41. 41. Plasticity After Brain Damage <ul><li>Possible causes of brain damage include: </li></ul><ul><ul><li>Tumors </li></ul></ul><ul><ul><li>infections </li></ul></ul><ul><ul><li>exposure to toxic substances </li></ul></ul><ul><ul><li>degenerative diseases </li></ul></ul><ul><ul><li>closed head injuries. </li></ul></ul>
  42. 42. Fig. 5-13, p. 138
  43. 43. Plasticity After Brain Damage <ul><li>A closed head injury refers to trauma that occurs when a sharp blow to the head drives the brain tissue against the inside wall of the skull. </li></ul><ul><ul><li>One of the main causes of brain injury in young adults </li></ul></ul><ul><li>A stroke or cerebrovascular accident is temporary loss of blood flow to the brain. </li></ul><ul><ul><li>A common cause of brain damage in the elderly </li></ul></ul>
  44. 44. Plasticity After Brain Damage <ul><li>Types of strokes include: </li></ul><ul><li>Ischemia -the most common type of stroke, resulting from a blood clot or obstruction of an artery. Neurons lose their oxygen and glucose supply. </li></ul><ul><li>Hemorrhage -a less frequent type of stroke resulting from a ruptured artery. Neurons are flooded with excess excess calcium oxygen and other products. </li></ul>
  45. 45. Plasticity After Brain Damage <ul><li>Ischemia and hemorrhage also cause: </li></ul><ul><li>Edema -the accumulation of fluid in the brain resulting in increased pressure on the brain and increasing the probability of further strokes. </li></ul><ul><li>Disruption of the sodium-potassium pump leading to the accumulation of potassium ions inside neurons. </li></ul>
  46. 46. Plasticity After Brain Damage <ul><li>Edema and excess potassium triggers the release of the excitatory neurotransmitter glutamate. </li></ul><ul><li>The overstimulation of neurons leads to sodium and other ions entering the neuron in excessive amounts. </li></ul><ul><li>Excess positve ions in the neuron block metabolism in the mitochondria and kill the neuron. </li></ul>
  47. 47. Fig. 5-14, p. 139
  48. 48. Plasticity After Brain Damage <ul><li>A drug called tissue plasminogen activator (tPA) breaks up blood clots and reduces the effects of an ischemic strokes. </li></ul><ul><li>Research has begun to attempt to save cells in the penumbra or region that surrounds the immediate damage by: </li></ul><ul><ul><li>blocking glutamate synapses </li></ul></ul><ul><ul><li>opening potassium channels </li></ul></ul>
  49. 49. Plasticity After Brain Damage <ul><li>One of the most effective laboratory methods used to minimize damage caused by strokes is to cool the brain. </li></ul><ul><li>A cooled brain (91-97° F) has less activity, lower energy needs and less risk of overstimulation. </li></ul>
  50. 50. Plasticity After Brain Damage <ul><li>Cannabanoids have also been shown to potentially minimize cell loss after brain damage be decreasing the release of glutamate. </li></ul><ul><li>Excess glutamate may result in the over-excitation of neurons. </li></ul>
  51. 51. Plasticity After Brain Damage <ul><li>Diaschisis refers to the decreased activity of surviving neurons after damage to other neurons. </li></ul><ul><li>Because activity in one area stimulates other areas, damage to the brain disrupts patterns of normal stimulation. </li></ul><ul><li>The use of drugs to stimulate activity in healthy regions of the bran after a stroke may be a mechanism of later recovery. </li></ul>
  52. 52. Plasticity After Brain Damage <ul><li>Damaged axons do grow back under certain circumstances. </li></ul><ul><li>If an axon in the peripheral nervous system is crushed, it follows its myelin sheath back to the target and grows back toward the periphery at a rate of about 1 mm per day. </li></ul>
  53. 53. Plasticity After Brain Damage <ul><li>Damaged axons only regenerate 1 to 2 millimeters in mature mammals. </li></ul><ul><li>Paralysis caused by spinal cord damage is relatively permanent. </li></ul><ul><li>Scar tissue makes a mechanical barrier to axon growth. </li></ul><ul><li>Myelin in the central nervous system also releases proteins that inhibit axon growth. </li></ul>
  54. 54. Plasticity After Brain Damage <ul><li>Collateral sprouts are new branches formed by other non-damaged axons that attach to vacant receptors. </li></ul><ul><li>Cells that have lost their source of innervation release neurotrophins that induce axons to form collateral sprouts. </li></ul><ul><li>Over several months, the sprouts fill in most vacated synapses and can be useful, worthless or harmful. </li></ul>
  55. 55. Fig. 5-16, p. 141
  56. 56. Fig. 5-17, p. 142
  57. 57. Plasticity After Brain Damage <ul><li>Gangliosides , a class of glycolipids formed by the combination of carbohydrate and fat molecules, also promote the restoration of damaged brains. </li></ul><ul><li>The mechanism of action of gangliosides is unknown but it is believed they adhere to neuron membranes and aid recognition of one neuron by another. </li></ul>
  58. 58. Plasticity After Brain Damage <ul><li>In laboratory mammals, female animals with high levels of the hormone progesterone have recovered better from frontal cortex damage. </li></ul><ul><li>Progesterone increases the release of neurotrophin BDNF which promotes axon sprouting and the formation of new synapses. </li></ul>
  59. 59. Plasticity After Brain Damage <ul><li>Ways the brain compensates for decreased input and to restores normal functioning include: </li></ul><ul><li>Denervation supersensitivity- the heightened sensitivity to a neurotransmitter after the destruction of an incoming axon and usually a result of increased receptors. </li></ul><ul><li>Disuse supersensitivity- the hypersensitivity to a neurotransmitter after a result of inactivity. </li></ul>
  60. 60. Plasticity After Brain Damage <ul><li>Phantom limb refers to the continuation of sensation of an amputated body part and reflects this process. </li></ul><ul><li>The cortex reorganizes itself after the amputation of a body part by becoming responsive to other parts of the body. </li></ul><ul><li>Original axons degenerate leaving vacant synapses into which others axons sprout. </li></ul>
  61. 61. Fig. 5-18, p. 143
  62. 62. Plasticity After Brain Damage <ul><li>Phantom limb can lead to the feeling of sensations in the amputated part of the body when other parts of the body are stimulated. </li></ul>
  63. 63. Plasticity After Brain Damage <ul><li>Deafferenated limbs are limbs that have lost their afferent sensory input. </li></ul><ul><li>Deafferented limbs can still be used but are often not because use of other mechanisms to carry out the behavior are easier. </li></ul><ul><li>The study of the ability to use deafferented limbs has led to the development of therapy techniques to improve functioning of brain damaged people. </li></ul><ul><ul><li>focus on what they are capable of doing. </li></ul></ul>