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Development and Plasticity Brain development 1 Primary germ layers are formed organized during gastrulation 2 Endoderm most internal germ layer forms lining of gut internal organs 3 Mesoderm middle germ layer forms muscle skeletal system circulatory system 4 Ectoderm outer germ layer contains nervous system folds into what eventually becomes the brain 5 CNS forms after 2 weeks neural tubes around fluid filled cavity Neural tubes forward end becomes fore mid hindbrain and rest becomes the spinal cord Fluid cavity becomes central canal of spinal cord and ventricles of brain Neural inducer genes that trigger development cordin noggin and sonic hedgehog directs proteins Stages of development 1 Proliferation production of stem cells divide or neurons glia 1st axon then dendrites don t divide 2 Migration neuron glia movement to location in brain using chemical paths through axon targeting 3 Differentiation forming of axon dendrite that gives neuron shape axon first then dendrites 4 Myelination glia produce myelin 1st in spinal cord reflexes then brain develops for decades 5 Synaptogenesis formation of synapses between neurons occurs throughout life but slows significantly Neurogenesis stem cells are homogenous can regenerate create new neurons Create new olfactory every 90 days differentiate in hippocampus and facilitate learning Axon targeting axons form correct connection by following chemical gradient path from postsynaptic cell immunoglobin chemokine some don t reach destination until adulthood Suicide cell more synapses between axons than needed so postsynaptic cells eliminate some connections Neurotophis chemicals that promote survival of axon secret handshake that link to certain neurons Neurons that do not get signal to stay from incoming axons die through apoptosis program cell death Problems with brain development Mutation possible for almost everything Malnutrition thyroid deficiency impaired proliferation low glucose impaired development Infection fever impairs neuron proliferation Toxins cocaine antidepressants cigs can increase risk of ADD fetal alcohol syndrome FAS alc suppresses glutamate enhances GABA less synapses between neurons connect than needed too many die in apoptosis causing hyperactivity impulsiveness and mental motor heart facial problems Neurons in diff brain parts differ in shape and chem component can rewire immature cortexes change ferret auditory cortex to respond to visual stimuli but not as well in older ones Axons and dendrites can modify from experience learning or physical activity thicker gray matter develops in areas of experience or constant exposure musicians have larger temporal lobe Focal hand dystonia lose independent muscle control when areas of sensory cortex reorganize overlap Antisaccade task more control of prefrontal cortex resisting impulses behaviors improves w age Plasticity ability of brain change from learning injury recovery use disuse dendrite branching dystonia Greatest in first 2 years and decreases with age everyone varies dramatically in old age decline Brain damage spinal cord damage tumor infection toxins stroke most common cause for old injury most common cause for young damage rely heavily on plasticity Brain controlled prosthetics for limb damage with ok nervous system Strokes Ischemia most common result of blood clot or artery obstruction neurons lose oxygen glucose supply Hemorrhage less common result of ruptured artery neurons flood w excess blood calcium oxygen Both cause 1 edema accumulation of fluid in brain increasing pressure 2 Disruption of sodium potassium pump triggers release of glutamate over stimulation of neurons leads to excess sodium other ions entering neuron and killing it Stroke treatments tPa drug that breaks up blood clots Research save neuron death by blocking glutamate synapses and calcium entry Brain cooling Cannabinoids to minimize cell loss after brain stroke more effective before stroke After brain damage surviving brain areas increase or reorganize activity Diaschisis decreased activity death of surviving neurons after brain damage Stimulant drugs stimulate activity in healthy brain regions after damage stroke After damage destroyed cell bodies can t be replaced but damaged axons can grow back Damaged PNS axons follow myelin sheath back to target grows back toward periphery Damaged CNS axons do not regenerate well in mature mammals scar tissue makes barrier to axon growth spinal cord damage permanent paralysis glia cells inhibit axon growth Denervation super sensitivity postsynaptic cells deprived of synaptic inputs develop increased sensitivity to neurotransmitter to compensate for decreased input destruction of incoming axon cause chronic pain Collateral sprouts denerved cells release neurotrophins that induce non damaged axons to form new branches with vacant receptors lost synapses around it Vision energy signal Phantom limb continuation of sensation of lost body part cortex reorganizes remaps vacant synapses and thus becomes responsive to stimulation of other parts Deafferentated limbs limbs that lost afferent sensory input can still be used but easier to work Learning training help therapy can focus on practicing impaired skills from brain damage Distance seen depends on distance light travels before hits eye enters as light processed as Each sense has specialized receptor sensitive to particular kind of energy vision light Receptors transduce convert energy into electrochemical patterns so the brain can perceive them Law of specific nerve energies activity by particular nerve always conveys same type of info to brain Light enters eye through pupil in the center of the iris is focused by the lens and cornea on surface of eye onto the retina rear surface of eye with visual receptors on opposite sides 1 Light passes through series of neural cells and hits visual receptors 2 Receptor cells send messages to neurons called bipolar cells 3 Bipolar cells send messages to ganglion cells closer to center of eye 4 Ganglion cells join one another to form the optic nerve that travels to brain Blind spot where optic nerve group of ganglion cells leaves back of eye to brain contains no receptors Retina rear surface of eye contains two types of receptors 1 Rods 120 mil per retina most abundant in periphery respond to faint light not good w bright lights contain photo pigment Rhodopsin which is better in the dark many rods share one line to brain 2 Cones 6 mil per retina mostly at fovea has iodopsin


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FSU PSB 2000 - Development and Plasticity

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