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Chapter 13

Chapter 13 - Neural Development and Developmental Disorders.doc

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University of Toronto Scarborough
Ted Petit

Chapter 13: Neural Development and Developmental Disorders The brain has not completed its developmental journey at birth, and there is long period of extended development that may be completed only sometime in adulthood. Many of the striking behavioural changes that occur childhood correspond w/ periods of brain growth or reorganization. Module 13.1 Neural Development Early Development Early in embryonic life (approximately three weeks after conception), neural plate (patch of cells that on the dorsal surface of embryo, which eventually becomes nervous system) forms from ectoderm of embryo. Cells of the dorsal ectoderm in neural plate are stem cells (embryonic cells that develop into any type of cell in body) that are pluripotent (cells that can develop into different types of cells), meaning have potential to develop into different types of nervous system cells. As development progresses, neural plate start to form groove, which by embryonic day 24 fuses to form neural tube. Different sections of neural tube become different parts of nervous system, w/ interior surface of neural tube becoming ventricles and central canal of spinal cord. Between third and fifth months of gestation, rapid cell proliferation and neural migration are dominant events. Cells of neural tube w/in ventricular zone are rapidly dividing through process called proliferation. Embryonic day 40, there are three prominent bumps on anterior portion of neural tube. Bumps eventually form forebrain, midbrain and hindbrain of central nervous system (CNS). Cells migrate from interior ventricular zone to final location by following certain types of glia. Beginning second month of gestation, telencephalon undergoes tremendous growth, developing from cortical plate. Deepest layer of neurons develop first and subsequent layers of neurons migrate through already established neurons to reach their destination. Once neurons migrate, begin grow axons and dendrites and differentiate into final form. Development of axons and dendrites occurs both prenatally and postnatally, cell differentiation essentially complete at birth. Exact mechanism underlying how axons grow toward their target not known, tips of growing axons and dendrites follow chemicals, arranging themselves in orderly fashion in position relative to initial place on cortical plate. Problems w/ any phase of development can lead to significant abnormalities in CNS. Particularly vulnerable during last four to five months of gestation, failures at any point in CNS development have significant impact on final form of brain. Adverse events can originate from problems w/in neurons themselves, or can be introduced by external factors. External events include intrauternine trauma or exposure to toxins. Effects of these disruptions often depend on nature, duration and extent of disruption. Type of CNS malformation give us clue as to when disruption occurred. One of more common congenital malformations of CNS occurs when neural tube fails to close. Complete failure of closure of neural tube is fatal, resulting in condition known as craniorachischisis, characterized by CNS appearing as groove in top of head and body. Syndrome ranging spina bifida to anencephaly result from partial closure of neural tube. Anencephaly occurs when rostral part of neural plate does not fuse and is characterized by general absence of cerebral hemispheres. Anencephaly is generally fatal, not all neural tube defects are fatal. Spina Bifida is disorder that caused by failure of neural tube to close completely. Number of diff. subtypes of spina bifida, symptoms of which depend on part of neural tube that did not close. By seventh month of prenatal development, most neurons migrated and differentiated into their final forms. Neurons undergo long period of synaptogensis and dendritic branching, producing more synapsis and dendrites than needed in adult brain. Synaptogensis and dendrite branching occur after birth, some cases into adulthood. Dendritic branching occurs slowly, w/ initial dendrites appearing as simple extensions exiting cell body of neuron. W/ time, dendrities become more complex, adding branches and spines. It is on dendritic spines that most dendritic synapses occur. Early embryonic life, synaptogenesis, or synapse formation, relatively sparse and occurs relatively independent of experience. Period extending from shortly before birth to about 2 years of age, synapse formation enter period of rapid growth. Thereafter, period of synapse reduction begins occur. Appears that about 50% more neurons produced in developing brain required in adult brain. Death actually normal and critical feature of development, which occurs predictable waves. Much neural death is apoptotic, or planned, programmed cell death. Unclear what triggers apoptosis, clear that apoptotic changes controlled by genes. Synapses that do not make functional connections or make incorrect connections are especially likely to die, leaving room for other synapses to sprout. Postnatal Development Most striking features of any babys early development is emergence of behaviors such as sitting, walking, or speaking. These behaviors are correlated w/ extensive growth in cortical areas of brain, which increase its volumes by four times between birth and adulthood. Possible to approach question from number of different perspectives. Plastic change is ability of CNS to alter itself in response to environmental stimuli. There are critical periods of plastic change in which environment can have maximal effect on CNS. Duration and timing of these critical periods vary by species, although appear that longer-lived animals exhibit prolonged critical periods that often occur later in life, well beyond prenatal period. Plasticity during critical periods occur response to experience-expectant or experience-dependent plasticity phenomena. Experience-expectant plastic changes are those CNS changes that dependent on experience(s) during critical period for specific synapses to develop as they should. Much of sensory cortex appears have these experience-expectant critical periods, and studies demonstrated organism does not experience sensory stimulation during critical period, long-lasting impairments in sensory modality occur. Experience-dependent plastic changes are idiosyncratic experiences that occur during critical periods that also affect brain development. Musical training in childhood have long-lasting changes on size of auditory cortex in adulthood BUT these changes were most profound for individuals who began practicing their instrument of choice before they were 9 years old. Critical periods during which musical training can have maximal effects on cortex. These changes are not random. Volumes of cortical grey matter increase until 4 years of age w/ much of postnatal growth and plastic change that occurs in brain resulting from synaptogensis, myelination of axons and dendritic branching. Synaptogensis and dendrtic branching maximal during critical periods. Brains ability to engage in plastic change often reduced as we age, especially once critical period has passed. Plastic areas change in response to significant environmental events. Factors underlying plastic change not completely understood, appear
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