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FSU PSB 2000 - Development and Plasticity

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Development and Plasticity• Brain development: 1. Primary germ layers are formed/ organized during gastrulation2. Endoderm (most internal germ layer) forms lining of gut/internal organs3. Mesoderm (middle germ layer) forms muscle/skeletal system/circulatory system4. Ectoderm (outer germ layer/contains nervous system) folds into what eventually becomes the brain5. 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 systemStrokes: -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) • • 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 synapsesBoth 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)• 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 around it)• Learning/training help: therapy can focus on practicing impaired skills from brain damageVision• Distance seen depends on distance light travels before hits eye(enters as light, processed as energy signal)• 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 receptors2. Receptor cells send messages to neurons called bipolar cells3. 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


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