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Psychology (9,697)
PSYB65H3 (479)
Ted Petit (185)
Chapter 16

chapter 16 psyb65

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Ted Petit

Psyb65 – chapter 16 Recovery of function  The normal adult brain produces new neurons and that neural death is a normal part of brain development  Understanding why and how recovery occurs is the best hope to cure brain damage  Understanding neural degeneration, regeneration and organization in the intact central nervous system will provide us with possible treatments and therapy to improve the quality of life of brain damage Neural degeneration, regeneration and reorganization  Autopsy means to see for oneself. Its where the death rejoices to teach those who live  It gives researches valuable information about how various disease and conditions affect the body which could result in possible treatment  Many neurological disease are cause by dearth of neurons or glia Degeneration:  All cells, including neurons die in one of 2 ways 1. Necrosis: when there is an overwhelming failure to maintain homeostasis within the neuron 2. Apoptosis: programmed neural death, the neuron uses its own machinery to ensure its own death (neural suicide)  Necrosis: o When they lose their ability to regulate their internal environment, swelling and membrane bursting occur. o The membranes that encase the organelle and vesicles also burst. o This burst is called the lysis and it spills the content of the neuron into the extracellular space, o It’s always an abnormal event, normally associated with damage that occurs rapidly such as 1. mechanical damage of neurons (tumors) 2. event that cause disruption to ion channel (anoxia) 3. results of infection (meningitis)  any disruption to homeostatic that cannot be compensated by the neuron results in necrotic cell death  Ischemia: disruption in blood flow that results from strokes of heart attacks  It can reduce or terminate ATP production in the neuron since the sodium potassium pumps relies on ATP to power its opening and closing, there is a stoppage of sodium potassium pump and inability to regulate their levels after action potential  If the neuron fails to regulate sodium and potassium it also fails to regulate water and calcium.  Failure to regulate intracellular calcium results in accumulation which is responsible for much of the damage that occurs after the initial ischemic event  Acquire injury such as traumatic brain injury: results in alterations in the release of glutamate, which is an excitatory amino acid neurotransmitter that is involved in fast excitatory event in the NS.  Glutamate is itself toxic to neurons: known as excitotoxicity: the ability to of specific compound to both excite neurons and kill them  Primary neural death: neurons death that occurs immediately after trauma, when glutamate is release in excess o Primary death can occur when the system itself exhausts the resources and overwhelms homeostatic mechanisms o High concentrations of excitotoxins can results in neurons exciting themselves to death  Calcium plays a major role in excitotoxic cell death: secondary neuronal death which is the death of neurons following the primary event is from a large-scale influx of calcium into the neuron  Excess release o glutamate can results in a sustained and excessive influx of calcium Apoptosis;  Programmed cell death the main difference between apoptosis and necrosis is that apoptosis is an active process that uses cellular energy to effect death  Apoptosis is characterized by dead cells I which the nucleus is condensed into a tangle of DNA fragments, and intact cell membranes  It’s a feature of normal development of neurons,  Some people think that neurons are on the verge of apoptotic cell death  It can be imitated in a variety of ways, including damage to the DNA of the neurons, damage cause by free radicals and withdrawal of tropic factors require for normal development  The presence of necrotic neurons can induce nearby neurons to go through apoptosis  It is regulated by genes, which trigger proteins known as caspases that are responsible for destruction got the neuron.  It has been observed following acute event such as stroke and TBI Regeneration  Most of the time in the CNS neurogenesis does not occur therefore there is permanent loss of neuron  Collateral sprouting: undamaged neurons sprout new axon collaterals to innervate targets  Regenerative sprouting: If the entire neuron is not damages, there is also the possibility that the damage potion could regrow Collateral sprouting:  When cutting one of the two main inputs the number of synapses in the septum returned to prelesion levels, owing to collateral spouting of the axons of the undamaged input.  The adult CNS was capable of producing new axons  Plasticity: ability to change in response to events underlies a number of normal processes, including development and somatosensory function,  There’s a critical period in which this plasticity can be exhibited, in many parts of the brain such as the sensory cortex, motor cortex, auditory cortex and hippocampus  It may be the basis for neural reorganization following injury Regenerative sprouting:  Mammalian species, regeneration usually occurs only within the peripheral nervous system,  Axotomy (cutting of an axon) in the PNS results in axon regrowth  The PNS often fully recovers from axotomy the CNS does not  Events that lead to CNS axotomy like spinal injuries result in permanent loss of the axons and a permanent loss of functions  What’s the difference between PNS and CNS? How come PNS neurons regenerate? o Theory: CNS axons are not capable of regeneration – they damage the dorsal roots of spinal nerves, since it begins in the CNS and ends in the PNS, when the dorsal root is damages in the PNS it regenerates o When the dorsal root is damaged I the spinal cord, it does not regenerate, meaning although the axon has the potential to regenerate, the environment of the CNS does not permit it to do so o One major difference between he axons in the PNS and those in the CNS is the type of glia cells that surround them  PINS are myelinated by Schwann cells, whereas axons in the CNS are myelinated by oligodendroctye.  If they transplanted the PNS nerve tissue into the CNS, it will regrow until it reaches the CNS tissue and it will stop  Both astrocytes and oligodendrocytes appear to actively inhibit axonal growth Neurogenesis  It was believed that neurogenesis in the adult mammalian CNS did not occur  Much of the enurogenesis occurs before birth, during the second half of he embryo’s life  Even when neurogenesis occurs following birth, it’s restricted to the prenatal period (immediately after birth)  2 areas of the mammalian CNS that demonstrate neurogensis in adulthood: o 1. The neurons of the olfactory bulb o 2. Neurons in the dentate gyrus of the hippocampus  The rate of neurgoeneis appears to be inhibited by age and by stress  Suggested that the decrease in neurogenesis is related to the steroid hormone “corticosterone” commonly associated with stress responses  Steroids hormones are important factors in inflammatory responses  Neurons are postmitoris : it cannot use mitosis to divide and produce new copies of themselves  New neurons appear to come from populations of stem or precursor cells in the brain  Stem cells are cells that can become any type of cell in the body, whereas progenitor cells are committed to stem cells o They come from stem cells and are committed to becoming a specific type of cell, o Stem cells have been found within the sugranular later of the hippocampus and the floor and walls of the lateral ventricles o Some migrate a short distance to the dentate gyrus wh
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