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Chapter 9

Chapter 9 Textbook - PSYC2410 Fall - Choleris

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PSYC 2410
Elena Choleris

Chapter 9 – PSYC2410 Three general points are emphasized: i. The amazing nature of neurodevelopment ii. The important role of experience in neurodevelopment iii. The dire consequences of neurodevelopment errors 9.1 Phases of neurodevelopment  Induction of the Neural Plate o 3 weeks after conception tissue to develop into NS is a neural plate: a small patch of ectodermal tissue on the dorsal surface of the developing embryo. The ectoderm is the outermost of the 3 layers of embryonic cells: ectoderm, mesoderm, and endoderm. o Development of the neural plate is the first major stage of neurodevelopment in all vertebrates induced by chemical signals from an area of the underlying mesoderm layer (an organizer area). o When the neural plate develops, its cells lose some of their potential to become different kinds of cells. They still have the potential to develop into most types of mature NS cells, but not other types. They are said to be multipotent, rather than totipotent (can develop into anything). o Cells of the neural plate often referred to as embryonic stem cells: they have a seemingly unlimited capacity for self-renewal if maintained in an appropriate cell culture, and they have the ability to develop into different types of mature cells. Then develop into neural stem cells and glial stem cells. o The neural plate folds to form the neural groove and then the lips of the neural groove fuse to form the neural tube the inside of which becomes the cerebral ventricles and spinal canal. o By 40 days, 3 swellings at anterior end of human neural tube which become: forebrain, midbrain, hindbrain  Neural Proliferation o After formation of neural tube, cells begin to proliferate o This doesn’t occur spontaneously or equally in all parts of the tube, most cell divisions occurs in the ventricular zone (region adjacent to the ventricle). o The cells proliferate differently between species. It is controlled by chemical signals from two organizer areas in the neural tube: the floor plate (runs along the midline of the anterior surface of the tube) and the roof plate (runs along the midline of the dorsal surface of the tube).  Migration o Once created in the ventricular zone of the neural tube, cell migrate to their target locations  Radial migration: from ventricular zone outward in a straight line toward the outer wall of the tube  Tangential migration: occurs at a right angel to radial migration – parallel to tube’s walls  Somal translocation: an extension grows from the developing cell in the general direction of the migration; the extension seems to explore the immediate environment for attractive and repulsive cues as it grows. Then, the cell body itself moves into and along the extending process, and trailing processes are retracted.  Glia-mediated migration: once the period of proliferation is well under way, a temporary network of glial cells (radial glial cell) appears in the developing neural tube. Cells move along the radial glial network.  Radial pattern of cortical development: inside-out pattern. Many cortical cells engage in long tangential migrations to reach their final destinations, and the patterns of proliferation and migration are different for areas of the cortex.  Migration of interneurons complex  Neural crest: structure situated just dorsal to the neural tube. Formed from cells that break off from the tube when it is being formed. These cells develop into the neurons and glial cells of the PNS  Many chemicals that guide migrating neurons have been discovered, some are released by glial cells. o Cells are still in an immature form, lacking processes (axons, dendrites) o Two major factors governing migration:  Time  location Chapter 9 – PSYC2410  Aggregation o Once migrated, cells must align with other cells in the area to form the structures of the NS o Both migration and aggregation are through to be mediated by cell-adhesion molecules (CAMs) which are located on the surfaces of neurons and other cells. Elimination of just one CAM in a knockout mouse has a devastating effect on brain development. o Gap junctions play a role in migration and aggregation  Axon Growth o Once migrated and aggregated, dendrites and axons begin to grow and must grow to the right targets. o Growth cone: amoeba-like structure at the tip of a growing axon or dendrite which extends or retracts fingerlike cytoplasmic exntesions called filopodia. o Chemoaffinity hypothesis: each postsynaptic surface in the NS released a specific chemical label and each growing axon is attracted by the label to its postsynaptic target during neural development and regeneration. However, fails to account for the discovery that some growing axons follow the same circuitous route to reach their target in every member of a species, rather than growing directly to it. o Revised hypothesis: growth cones seem to be influenced by a series of chemical signals along the route from guidance molecules which some attract, and some repel, as well as signals coming from adjacent growing axons. Pioneer growth cones (first growth cones to travel along a particular route) are presumed to follow the correct trail by interacting with guidance molecules, and then other growth cones on the same journey follow the routes blazed by the pioneers. o Fasciculation: tendency of developing axons to grow along the paths established by preceding axons o A lot of axonal development involves growth from one topographic array to another. Suggested that topographic maps evolved as a means of minimizing the volume of neural connections in the brain. o Topographic Gradient Hypothesis: axons growing from one topographic surface to another are guided to specific targets that are arranged on the terminal surface in the same way as the axons’ cell bodies are arranged on the original surface. The growing axons are guided to their destinations by two intersection signal gradients (anterior- posterior gradient, a medial-lateral gradient). o Guidance molecules: Ephrins: ephrin-A, ephrine-B define locations on the vertebrate retina  Synapse Formation o Takes coordinated activity between neurons to create synapses o Synaptogenesis depends on the presence of glial cells, particularly astrocytes that process, transfer and store information supplied by neurons o Neurons will form synapses with any cell in vitro, but if not used they are eliminated o Developing neurons need high levels of cholesterol during synapse formation which is supplied by astrocytes  Neuron death o About 50% more neurons are produced than needed o Necrosis: passive cell death. Necrotic cells usually break apart and spill their contents into the extracellular fluid, could be harmful inflammation o Apoptosis: active cell death (safer) DNA and other structures are cleaved apart and packed in membranes before the cell beaks apart then microglia eat them. however, if genetic programs for apoptotic cell death are locked, can result in cancer, if they are inappropriately activated could result in neurodegenerative disease. o Triggers:  Some cells are genetically programmed for early cell death once they have fulfilled their functions  Some seem to die because they fail to obtain the life-preserving chemicals that are supplied by their targets:  Neurotrophins (Nerve growth factor (NGF)) promote growth and survival of neurons, function as axon guidance molecules and stimulate synaptogenesis.  Synapse Rearrangement o Neurons that have established incorrect connections are particularly likely to die o Synapse rearrangement tends to focus the output of each neuron on a smaller number of postsynaptic cells, increasing the selectivity of transmission Chapter 9 – PSYC2410 9.2 Postnatal Cerebral Development in Human Infants  Postnatal Growth of the Human Brain o Volume of human brain quadruples between birth and adulthood; all the neurons that will compose the adult th human brain have developed by the 7 month of prenatal development. o Postnatal growth of human brain seems to result from 3 other kinds of growth: i. Synaptogenesis ii. Myelination of axons iii. Increased branching of dendrites o General increase in synaptogenesis in human cortex after birth th  In primary visual and auditory cortex there is a major burst of synaptogenesis in the 4 postnatal month and maximum synapse density (150% adult levels) is achieved in the 7 or 8 postnatal month; whereas in the prefrontal cortex it occurs at steady rate, reaching maximum density in the second year.  Myelination of areas roughly parallels their functional development. Myelinationg of sensory areas occurs in the first few months after birth, myelination of the motor areas follows after that, myelination of prefrontal cortex continues into adulthood.  Dendritic branching progresses from deeper to more superficial layers. Changes in dendritic shape can be observed during just a few seconds. o Some regression too. Once maximum synaptic density is reached, there are periods of synaptic loss at different times in different parts.  Synaptic density in primary visual cortex declines to adult levels by about 3 years of age  Synaptic density in prefrontal cortex decline to adult levels by adolescence  Suggested that overproduction of synapses may underlie the greater plasticity of the young brain o Cortical white matter grows slowly and steadily until early adulthood. o Cortical gray matter grows until it is larger than it will be in the adult brain; then decreases in size. o Sensory and motor areas reach their mature form before cognitive areas.  Development of the Prefrontal Cortex o Various parts of the adults prefrontal cortex seem to play roles in: i. Working memory ii. Planning and carrying out sequences of actions iii. Inhibiting responses that are inappropriate in the current context but not in others iv. Following rules for social behaviour o Perseverative error made between ~ 7 and 12 months of age, but not after o o o 9.3 Effects of Experience on the Early Development, Mai
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