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Chapter5

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