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Biopsychology Test 2 (How the Sensory Systems Work (Visual (What is…

- - - - stimulus
        
        odorants: particles in the air (volatile substances with molecular weights of 15 to 300 Daltons)
        
        can recognize up to 10,000 odorants (good at recognizing bad at identifying)
        
        no primaries discovered
      - anatomy of the nose: 1 inch square mucous membrane, cilia (dendrites) of olfactory bipolar neurons protrude through mucous (1 month survival because of the hostile environment)
      - transduction: 7-8 molecules are needed to stimulate receptors on olfactory cilia, Golf, increases cAMP, opens Na+ and Ca2+ channels, opens Cl- channels, depolarizes olfactory cell, action potential
      - pathway: olfactory cilia -> through cribiform plate -> ipsilateral olfactory bulb -> pyriform cortex and entorhinal cortex... and amygdala, hippocampus, orbitofrontal cortex (pathway is both ipsilateral and contralateral)
        
        topographically organized (olfactotopic)
        
        different odors = different pattern of glomeruli (thus olfactory cortex) activation
        
        binding problem: how do we know which odors go with which?
      - anosmia: the complete loss of smell (1% very rare)
    - - animals: finding/attracting a mate, identifying enemies/competition
      - humans: can alter skin temperature and other ANS response (e.g. hypothalamic activity), male sweat -> secretion of cortisol in females, McClintock effect: synchronization of menstrual cycles, men can identify menstrual stage by smell, women cycle faster in the presence of men, effects are unconscious
      - anatomy envolved
        
        animals: comeronasal organ (VNO) - located near olfactory receptors, very few and very specific (will hardly respond to other odors), does not adapt
        
        humans: humans do not have receptors on the VNO - VNO appears to be vestibular
      - pheromones: a chemical released by animals that affects the behavior of others in its species
    - - the VNO is an organ that responds to very few and very specific stimulus (pheromonones)
    - - what does it mean to be a "primary" taste?
        
        primary tastes mix to make flavors
        
        these are the items we need to be able to function
        
        salt: NaCl (cation with anion)
        
        transduction: Na+ channels open, action potential
        
        sweet: sugars, but also some amino acids
        
        transduction: G protein coupled receptors (sometimes gustducin) which leads to an increase in cAMP (then activates K+ channels) or increase Ip3 causing depolarization
        
        bitter (alkaloids, toxic compounds), detect things that are not very good for us
        
        transduction: variety of ways, some involving G protein coupled receptors, actually need a certain amount of toxicity, balance with sensitivity and ability to detect many kinds of poisons
        
        sour: H+ (hydrogen with anion)
        
        transduction: close K+ channels, action potential. H+ enter through cations
        
        umami: glutamate and amino acids (meaty, savory)
        
        transduction: G protein coupled receptors, receptor can sense sweet or umami but not both
        
        fat? we do not have a taste receptors for fat, but researchers have found some in rats
        
        there are different receptors for these tastes - taste depends on (temporal) pattern of responses across neurons as well as the rhythms of action potentials
      - describe the anatomy of the tongue
        
        where are receptors located?
        
        there are no taste receptors no the middle of the tongue
        
        nature doesn't like to waste resources
        
        papillae: often on sides (taste buds are embedded in them), sometimes on the top
        
        taste buds
        
        fungiform papillae: up to 8 taste buds
        
        foliate papillae: up to 1300 taste buds
        
        about 50 microvilli per taste bud
        
        survive about 10 days (new one grows in its place
        
        quick adaptation
      - how do the gustatory and olfactory systems interact?
        
        these two systems work together to create a sense of taste
      - gustatory pathway (mostly ipsilateral): nucleus of tractus soltarious (medulla) -> pons -> lateral hypothalamus -> amygdala -> somatosensory cortex (tongue stimulation) -> ventral posteromedial thalamic nucleus -> primary gustatory cortex (insular cortex) -> secondary gustatory cortex
      - gustatory damage:
        
        ageusia (loss of sense of taste) - rare
        
        non-taster, taster, super-taster: number of fungiform papillae near tip of tongue
        
        estradiol: know to increase your sensitivity to foods, an advantage for pregnant women
  - - - stimulus: pressure, temperature, tissue damage/nocxious stimuli, body position/movement of joints/tendons/muscles, lining of organs
    - - C fibers
        
        smaller diameter than A delta fibers, unmyelinated, but slower
        
        dull, aching pain
      - A delta fibers
        
        larger, myelinated, faster
        
        sharp pain
    - - touch pathway: receptors -> dorsal column of white matter -> decussate at level of medulla -> at ventral posterior MEDIAL nucleus of thalamus -> primary somatosensory cortex (too deep pressure, too light touch on skin) -> secondary somatosensory cortex
      - pain pathway: decussate at level of spinal cord -> ventral posterior LATERAL nucleus (thalamus) -> primary and secondary somatosensory cortices + midline thalamic nuclei -> reticular formation, superior colliculus, the central gray, the hypothalamus, amygdala, anterior cingulate cortex, insula (emotional aspects of pain)
    - - anterior cingulate cortex: manipulating the anterior cingulate cortex, you can decrease pain intensity, ibuprofen can actually decrease emotional pain
      - congenital insensitivity to pain with anhidrosis
        
        born with it
        
        difficulty in regulating temperature
        
        you do not have an automatic alert system to alarm you of painful stimulus
        
        generally people with this condition do not live very long and have deformities
      - Melzack and Wall's gate control theory
        
        gate in spinal cord
        
        there must be gates that can be closed when need preventing pain stimulus from being transmitted
        
        2 triggers
        
        CNS trigger: when your brain realizes that this is not the time to focus on the pain
        
        opiates inhibit PAG interneurons thus disinhibiting other PAG which release enkephalins...
        
        Enkenphalins to exited raphe nucleus (medulla) neurons to release
        
        5-HT (serotonin) in the spinal cord
        
        stimulating spinal cord interneurons to release enkephalins which prevents release of substance P
        
        PNS trigger: when you rub the skin around an injury stimulating A beta fibers then stimulating the opioid neurotransmitters
        
        based on this, would it make sense to listen to your favorite music when in the dentist's office? yes, any kind of distraction works to prevent pain
      - chemicals
        
        decrease pain:
        
        endogenous opioids: slower pain
        
        endorphins (e.g. beta endorphins)
        
        enkephalins
        
        dynorphins
        
        inescapable pain, sex, thrilling music, acupuncture, placebo - inhibits cingulate gyrus and increases opiate release(but NOT hypnosis)
        
        cannabinoids (periphery): helps pain differently from opioids
        
        capsaicin: depletes substance P (burn first and then prolonged pain relief... icy hot, bengay)
        
        NSAIDs: block prostaglandins (type of chemical released because of tissue damage)
        
        estradiol: facilitates opiate activity
        
        increase pain:
        
        nocebos (anxiety)
        
        damage tissue -> histamine, nerve growth factor
        
        strong, repeated stimulation -> sensitization (potentiation)
  - - - semicircular canals: represent the 3 lanes in which you exist (sagittal, transverse, horizontal)
      - has hair and fluid like the auditory system
      - vestibular hairs are embedded in a gelatinous membrane
      - vestibular sacs
        
        utricle (tilting of head)
        
        saccule (movements up and down; forward and back)
        
        otolithic membrane with otoconia... can become dislodged
        
        depolarization, no action potentials
    - - balance, keeps head upright, focus, adjusting eyes while moving
  - - - sound localization is dependent on time of arrival, phase difference and intensity (loudness)
    - - stimulus
        
        condensing and rarefying of molecules in varying mediums, waves of vibration of air molecules (15-20,000 Hz)
        
        properties
        
        wavelength = pitch
        
        amplitude = loudness
        
        long wavelength = low frequency, short wavelength = high frequency
        
        timbre = purity
      - pathway: pinna -> external auditory canal -> tympanic membrane -> ossicles (increases force - malleus, incus, stapes) -> oval window -> cochlea (fluid-filled) -> organ of corti (basilar membrane with hair cells and tectorial membrane - transduction occurs here) -> 8th cranial nerve
      - auditory cortex
        
        topographically arranged
        
        core region: primary cortex
        
        belt region: first level of association cortex
        
        parabelt region: highest level of processing
    - - conductive deafness: damage to the ossicles -> hearing aid, when you get older you use your ability to detect high frequency sounds
      - nerve deafness: damage to the cochlea/hair cells -> cochlear implant
    - - frequency theory (50-400Hz): action potentials are fired at the frequency of sound
      - frequency theory with Volley principle (300-4000Hz): when action potentials cannot fire fast enough, so they now fire as a group and collectively represent the frequency
      - place theory (4000+ Hz): when neurons on the basilar membrane prefer specific frequencies. Neurons that prefer higher frequencies are closer to the oval window
      - perceiving loudness
        
        high frequencies: rate of firing action potential
        
        lower frequencies: number of firing cells
  - - - stimulus -> anatomy of the eye -> retina -> photoreceptors -> bipolar cells -> horizontal and amacrine cells -> ganglion cells -> optic disk -> optic chiasm -> lateral geniculate nucleus -> optic radiations -> occipital lobe
      - transduction: in the retinal (bent molecule) inside of the rhodopsin (protein) inside of the rod
    - - cones: concentrated in the fovea, far less than rods, necessary for color perception, less active in dim light
      - rods: spread out amongst the periphery of the retina, respond to faint light, responsible for telling us whether light is present
    - - visual transduction tells the brain that there is light stimulus by turning off the rods
      - light enters the eye, passes through the retina, comes in contact with a rod. Within this rod is the protein rhodopsin and within that the molecule retinal, if the light happens to hit this molecule it will change the confirmation (shape) from bent to straight. Transducin then breaks off of the retinal and binds to cyclic GMP. PDE converts GMP to cyclic GMP and when there is a shortage it closes sodium gates, hyperpolarizing the rod (turning it off)
    - - blindspot: area in the back of the retina where the optic nerve exits, it is devoid of photoreceptors
      - we are not usually aware of our blindspots because the brain fills in the gap and anything in the blindspot of one eye is visible to the other eye
    - - retina (photo receptors--> bipolar cells --> ganglion)--> optic chiasm --> lateral geniculate nucleus -> striate cortex
    - - located within the calcarine fissure
    - - stimulus that hits the nasal side of the eye is processed contralaterally (crosses the optic chiasm) in the right primary cortex. Stimulus that hits the temporal side of the eye is processed ipsilaterally (does not cross the optic chiasm) in the left primary cortex
    - - V1 or Broadmann's area: first place in the sensory system where the information is processed, it only receives information from that system (involves the first 6 layers of the brain), most basic, fundamental and deep analysis
      - modules: responsible for the analysis portion of the visual field
        
        ocular dominance columns: move in a different direction, different cells used, same line orientation in column
        
        orientation columns: across V1 with different line preferences (perpendicular to the ocular dominance)
        
        hyper column: visual info from a specific area of the visual field (binocular input), blobs that analyze color input
      - feature detectors: detect a certain feature within the visual field
        
        simple cells: simple cells: have long square receptive fields that depend on orientation and location. more light --> a larger response. have opponent fashion receptive fields (part inhibitory and part excitatory in fixed areas). also sensitive to sine waves. smallest
        
        complex cell: depend on the motion and orientation of a stimulus within its receptive field. doesn't have an opponent fashion receptive field (no fixed excitatory and inhibitory regions). rectangular.
        
        hypercomplex cells: depend on orientation, movement, and direction within a definite inhibitory zone on one side -> stimulus must be a certain length
    - - What? ventral stream: inferior temporal cortex- complex shape analysis, damage = visual agnosia - inability to recognize objects despite otherwise satisfactory vision , prosopagnosia - impaired ability to recognize faces, lack of shape constancy, V4 - color constancy, visual attention, damage = loss of color constancy , MT (aka V5) - motion of objects or still photographs implying motion, damage = akinetopsia (still images)
      - where? dorsal stream: parietal cortex - location of objects especially in relation to your body
    - - association area - can work on higher functioning processing and receives more information from one sense, sophisticated analyses
      - primary cortex: the first place in the sensory system where the information is processed, it only receives information from that system
    - - receptive field: area in visual space that excites or inhibits the brain
      - bipolar cells: have a co-centric receptive field. At the edges of an on center cell it would be stimulated even more. All of the center is illuminated, while only part of the inhibitory surroundings are. The next bipolar cell would not be excited, so there is a big contrast.
      - lateral inhibition: an activated bipolar cell sends information to horizontal cells, which inhibit their neighbors. Inhibition strength decreases with distance because the signal cannot be inhibited when being transferred from receptor to bipolar cell (amplifies the message). Inhibition is greatest in the center of the excited area and least at the borders. Inhibition is even greater on the non-stimulated border cells
    - - Lateral inhibition: the retina's way of sharpening contrasts to emphasize the borders of objects
      - the receptors send messages to excite the closest bipolar cells and send messages to slightly inhibit them and the neighbors to their sides. The net result will be to heighten contrast.
      - decrease in inhibition that results in net excitation
      - Mach bands: an optical illusion that exaggerates the contrast between edges of the slightly differing shades of gray as soon as they come in contact with each other, triggering lateral inhibition (Ernst Mach)
    - - opponent process theory: suggests that we perceive color in terms of paired opposites
        
        possible mechanism for the theory is that bipolar cells are excited by one set of wavelengths
        
        part of the trichromatic theory - color perception occurs through the relative rates of response by three types of wavelengths - suggests that negative afterimages result from fatiguing a response by opponent process cell
      - retinex theory: the cortex compares each of the inputs to determine the brightness and color perception for each area
      - the trichromatic theory cannot account for all aspects of color perception
        
        brightness constancy: tendency for a visual object to be perceived with the same brightness under different conditions of illumination
        
        color constancy: the ability to recognize color despite changes in lighting
    - - retinal disparity: difference in the retinas that gives us a clue to the location of an object (binocular cue)
      - when objects are closer to you the disparity is greater than when it is farther apart
      - your brain needs coordinating action from both of your eyes to calibrate an objects location
      - monocular cues - ways that you judge object location
    - - top-down: uses background knowledge to influence perception. THEORY DRIVEN. Gestalt perspective
      - bottom-up: stimulus influences what we perceive. If you absolutely nothing about some (no preconceived information about it), the stimulus is influencing your perception. DATA DRIVEN. Binding problem can occur. Retina -> visual cortical cells -> parietal/temporal cortical cells
    - - how plastic is it when an infant is born?
        
        extremely plastic when born
        
        if you were to cover both eyes for 3 weeks after birth the brain could recover. If you cover 1, some axons would beat others causing a permanent lack of use of that one eye (patch in kids)
      - Are we hard-wired to see certain types of stimuli more than others?
        
        we are immediately drawn to motion, but infants prefer faces over other stimuli (visual attention and motor control)
      - what is a "critical period"?
        
        when the nervous system is especially sensitive to stimuli
        
        exposure to limited array of patterns: astigmatism - blurring of vision in certain areas of your visual field
- - - - process: light enters the eye at the pupil and goes to the retina. The retina has rods and cones - these are really important because they take the light and convert it into neural impulses. The photo-transduction cascade (turning light on or off) occurs as soon as light hits a rod or cone.
        
        rods are super sensitive light and very good for night vision. Found in the periphery of the eye allowing you to see on the sides.
        
        normally rods are turned on, but when light hits it the rod turns off. This turns on the bipolar cell, which turns on the retinal ganglion cell. The ganglion cell goes into the optic nerve and from there to the brain.
        
        inside of a rod there are optic disks (thousands in an individual rod)
        
        rods do not produce color vision
        
        100 times more sensitive to light than cones... responsible for telling us whether light is present
        
        rods have a very slow recovery time... as soon as a rod is activated by a ray of light, it takes a lot longer to fire another action potential than cones (reactivated and reset)
        
        there are a lot less cones than rods. They are important for because they are necessary for color vision. Red, Green, and Blue cones each sensitive to their specific colors of light. Cones are centered in the fovea (almost no rods in the fovea) - the part of the eye that lets us see very fine details.
        
        cones also have optic disk with proteins embedded in them... in cones the protein is photopsin
        
        cones also have a photo-transduction process
        
        result in color vision
        
        cones have a quick recovery time
        
        photoreceptor distribution in the fovea
        
        blindspot: right in front of where the optic nerve exits the back of the eye, there are no photoreceptors here
        
        rods are found mostly in the periphery of the eye
        
        cone are found throughout the fovea (really high concentration here) there are very few cones found spread out throughout the eye
        
        the retina dimples in where the fovea is because these photoreceptors are connected to other neurons which all have axons
    - - visual field processing
        
        a ray of light coming from the left visual field will hit the nasal side of the left eye and the temporal side of the right eye
        
        a ray of light coming from the right visual field will hit the nasal side of the right eye and the temporal side of the left eye
        
        the optic nerve from each eye converges at the optic chiasm and then breaks off again
        
        all light that hits the temporal side of the eyeball does not cross the optic chiasm (ipsilateral)
        
        all light that hits the nasal side of the eyeball crosses the optic chiasm (contralateral)
      - feature detection (color, form, motion)
        
        color = cones (trichromatic theory)
        
        form = boundaries from the background (parvo pathway - high spatial resolution, poor temporal resolution, color) STATIONARY
        
        motion = movement in relation to a background (magno pathway - high temporal resolution, poor spatial resolution, no color)
    - - electromagnetic waves of light - part of a large spectrum (gamma rays to AM/FM radio waves)
      - ranges from violet (400nm) to red (700nm)
    - - photo-transduction cascade (refers to rods): set of steps that takes the rod and turns it off, turning on the other cells and telling the brain that there is light
        
        rods are made up of disks which have multiple proteins spread out amongst it - rhodopsin - inside of rhodopsin a bent molecule sits - retinal . Light comes in and hits the retinal... it causes a change in confirmation (from bent to straight)
        
        when the retinal changes shape it also causes the rhodopsin to change shape
        
        transducin made up of alpha and beta
        
        transducin breaks off from retinal and binds to a particle called cyclic GMP. PDE takes GMP and converts it into cyclic GMP... this is important because it in order to have open sodium channels the neurons need a bound cyclic GMP
        
        when there is a decrease in cyclic GMP, there is less sodium in the cell causing it to hyperpolarize. This turns off the rods
        
        without light, the sodium channels are open and the rods can create action potentials
        
        bipolar cells
        
        on center (on when the rod is turned off) vs off center cells (off when the rod is turned on)
    - - lateral geniculate nucleus: looks like a knee. This is where the majority of ganglion cell axons go - from there it sends axons to other parts of thalamus and the visual cortex (the other parts send it back after processing)
    - - opponent process theory: idea that we perceive color in terms of opposites
      - trichromatic theory (Young-Helmholtz theory): theory that color is perceived through the relative rates of response by three kinds of cones, each one maximally sensitive to a different set of wavelengths
      - retinex theory: concept that the cortex compares information from various parts of the retina to determine the brightness and color for each area
- - - - somatosensory and verbal ability > occipital lobe
      - intense transcranial magnetic stimulation
    - - musicians
      - focal hand dystonia and writer's cramp
  - - - countrecoup
        
        concussion
        
        disturbance of consciousness
        
        vital to give the brain rest and recovery
        
        multiple concussions is believed to cause dementia and motor disorders
        
        contusion: lesioning of circulatory system (bleed)
        
        usually a contrecoup injury: when you hit your head and your brain hits the opposite side
        
        what happened to Mohammad Ali? punch-drunk syndrome aka pugilistic Parkinson's syndrome
      - stroke
        
        cause
        
        3rd most common cause of death
        
        ischemia: obstruction, cutting off blood supply to neurons... atherosclerosis (build up of plaque in your blood) > embolism (blockage)
        
        hemorrhage
        
        penumbra: dead and dying neurons secreting chemicals that kill surrounding neurons
        
        treatments
        
        tPA (tissue plasminogen activator)
        
        break up clots
        
        toxic to neurons
        
        cannot be used for hemorrhagic stroke
        
        cooling brain
        
        makes the molecules move slowly
        
        issues: hypothermia, damages membranes because of expansion
        
        glutamate inhibitor
        
        marijuana?
        
        anti-oxidant or anti-inflammatory properties?
        
        first it increases glutamate activity, decrease glutamate (eventually)
        
        it may overstimulate and then become a problem
        
        omega-3 fatty acids: blocks apoptosis
        
        bats
        
        there is a class of bats that suck blood
        
        they release an anti-coagulant (prevents clots)
        
        it is not toxic in the brain!
        
        diaschsis
        
        decreased activity of surviving brain neurons after damage to other neurons
        
        if diaschisis contributes to behavioral deficits following brain damage, then increased stimulation should help
      - meningitis vs. encephalitis
        
        meningitis: inflammation of the meninges due to infection
        
        encephalitis: inflammation of the brain due to infection.... usually occurs after meningitis
      - herpes: transmitted through fluids and contact (virus)
    - - PNS vs. CNS
      - collateral sprouting: after a cell loses input from an axon, it secretes neurotrophins that induce other axons to form new branches
      - denervation and disuse supersensitivity
        
        denervation supersensitivity
        
        helps compensate for decreased input
        
        if a certain set of synapse becomes inactive, because of damage elsewhere in the brain, the remaining synapses become more responsive, more easily stimulated
      - upregulation of receptors
    - - deafferentation
        
        unilateral vs. bilateral
        
        if you damage nerves in one arm, the monkey chooses to use the other arm because it is uncomfortable to use the other
        
        if you damage nerves in bother arms, the monkeys will accommodate for the damage and use both arms
        
        this is what we want for physical therapy patients. To be able to strengthen the behaviors that you do have. These are effortful exercises that help to create new synapses
        
        implications of these studies
        
        study involving rats and damaged visual cortices
      - regrowth of axons
        
        a neuron of the PNS has its cell body in the spinal cord (motor neurons) or in a ganglion near the spinal cord (sensory), the axon extends into one of the limbs
        
        in the CNS axon regrwoth is inhibited. Scarring occurs, neurons on the two sides of the cut pull apart, the glia cells that react to CNS damage release chemicals that inhibit growth
  - - - suggests that the last neuro-signature that the body has was the limb in pain
      - what you should first do is decrease teh amount of pain, so that the last message to the brain is that "it's fine. I feel fine"
      - the illusion that you have the limb can help to change the neurosignature
- - - - neurons are born in the inner portion of the neural tube and then crawl out to the outer portion of the neural tube creating a new layer
    - - 6 layers
    - - layers of cells on the other surface of the cerebral hemisphere of the forebrain
    - - white matter: area of the nervous system consisting mostly of myelinated axons
      - gray matter: areas of the nervous system that are densely packed with cell bodies and dendrites
  - - - how does this occur?
        
        proliferation is the production of new cells... cells lining the ventricles of the brain divide to become either stem cells or primitive neurons/glia
        
        totipotent: within 36 hours, the zygote multiples into many stem cells that can become anything
        
        multipotent: 18 days after conception, the cells of the neural plate form
        
        pluripotent: the cells also differentiate, such that eventually, the embryo is composed of an endoderm, mesoderm, and ectoderm
        
        nearly all neurons form within the first 28 weeks of gestation
        
        symmetrical vs. asymmetrical division
        
        symmetrical: dividing one thing to create two (genetically identical)
        
        asymmetrical: dividing one thing to create two different things
      - does this happen postnatally at all?
        
        while neurogenesis is considered done by birth, there is evidence of a limited supply of new neurons (some in the olfactory bulb and hippocampal region - new memories
        
        learning and exercise have a great impact on neuron growth
        
        also evidence in dendritic branching
      - What is the neural tube?
        
        the brain and spinal cord begin as folding lips surrounding a fluid-filled canal
        
        the tube sinks under the skin. the forward end enlarges and becomes the hindbrain, midbrain, and forebrain. the rest becomes the spinal cord
        
        24 days after conception
        
        spina bifida: when the neural tube did not successfully submerge into the ectoderm
        
        anencephalic infant: when the anterior portion of the neural tube did not successfully submerge
        
        to prevent these defects, take folic acid
        
        environmental and genetic factors contribute
        
        eventually the neural tube fills with CSF
    - - theories
      - how?
        
        there are many guidance molecules that tell the neuron where to go
        
        cell adhesion molecules: tend to be on the surface of cells, sticky (connection)... immunoglobin
        
        neurotrophins: nourish immature neurons and help them survive (primary degree), guidance molecules (secondary degree)
        
        Nerve growth factor (NGF), brain derived neurotrophic factor that prevents apoptosis
        
        pathfinding by axons
        
        diffused molecules: sent out into the tissue
        
        fixed molecules in extracellular matrix: guidance molecules fixed in fluid, fibers etc. in the tissues. Some are attractive and some are repellant depending on interaction and reaction
        
        fixed molecules on cells (cell-surface molecules
      - What are...
        
        growth cones: tips of axons, dendrites
        
        filolodia
        
        lamellipodia
        
        growth cone follows many guidance molecules
        
        pioneer: usually have a special tip (cosa) that specializes into growth cones
        
        axons serve as a pathway for additional neurons that develop later in the embryo and direct them to their target
        
        pioneer cells are eliminated by apoptosis or programmed cell death
      - types
        
        tangential
        
        neurons move along the surface of the brain
        
        fasciculation: when a growing neuron follows along the path of other axon
        
        radial migration
        
        neurons move from the inside to the outside of the brain
        
        move perpendicular to the neural tube (Radial glia)
        
        somal translocation: slinky effect, moves around or up and down the neural tube
        
        glia-mediated migration: immature neurons move out from the central canal along radial glia cells
      - what did Sperry do and what was the implication of his study?
        
        Sperry cut the optic nerves of some newts (because it can grow back in this species of amphibian) in order to show how sensory axons find their way to their correct targets
        
        topographic organization vs. chemical gradients
        
        topographic organization: spatial organization
        
        chemical gradients: dorsal ventral gradient (front to back), rostral caudal gradient (differs from one side to another)
        
        as axons are growing, the target areas are also growing which helps the neurons make the most of the space
        
        need this when neurons need to know where they are in relation to other neurons... you're going to need a set of coordinates provided by chemical gradients
    - - what was the ferret study about and what was the implication of this study
        
        how plastic are primary cortices?
        
        damage: superior colliculus, occipital lobe, inferior colliculus
        
        retinal nerves - serving right visual field - have nowhere to go and the primary auditory cortex has not input
        
        ferrets are trained to turn right for visual stimulus and left for auditory stimulus using the intact side
        
        how do the cells of the temporal cortex differentiate?
        
        using the re-wired side
        
        will the brain area charge to process the visual stimulsu as visual or auditory
        
        automatically understood using the contralateral side
        
        the ferret turned the right way indicating that he synthesized the information as a visual signal
        
        brain plasticity decreases with age
      - when do axons vs. dendrites develop?
        
        axons grow first
        
        migrating neurons tow their growing axon along like a tail
        
        axon grows toward its target
        
        after the migrating neuron reaches its destination, its dendrites begin to form
    - - glia produce the insulating fatty sheaths that accelerate transmission in many vertebrate axons
      - myelin forms first in the spinal cord and then in the hindbrain, midbrain, and forebrain
      - unlike proliferation and migration, myelination continues through adolescence and early adulthood
    - - when does this occur? how does this differ from neurogenesis?
        
        synaptogenesis is the formation of synapses
        
        the process begins before birth and continues throughout life. Neurons form new synapses and discard old ones.
      - what is "Neural Darwinism"?
        
        knowing that if neurons are unable to make a successful connection, they are more likely to die
        
        PNS and CNS (more complicated)
      - what are "neurotrophic factors" and how are they involved with the synaptogenesis and overall survival of the neuron when the neuron is immature?
        
        they increase the likelihood of a neuron's survival
        
        as NGF, it attracts certain neurons (migration)
      - where do neurotrophic factors come from?
        
        glial cells, especially astrocytes
        
        target cells
        
        incoming axons
      - how do trophic chemicals differ from tropic chemicals?
        
        trophic: nourishes the cell
        
        tropic: guides the cell
      - how does alcohol interfere with proper development of the nervous system?
        
        inhibits glutamate and agonizes the GABA factor
        
        children born with fetal alcohol have both physical and mental disabilities. The babies even cry differently
        
        drinking as an adolescent can result in a lower IQ because it interferes with vital synapse of neurons during development
    - - what's the difference between apoptosis and necrosis?
        
        necrosis: unexpected cell death causing problems to nearby neurons (usually occurs because of brain injury)
        
        loss of oxygen and glucose
        
        impaired Na+K+ pump
        
        increase sodium inside neuron
        
        increased glutamate
        
        overstimulation
        
        blocks mitochondrial metabolism
        
        neuronal death
        
        microglial proliferation
        
        initially, 50% more neurons
      - is apoptosis a normal part of aging? using the prefrontal cortex, explain how so or not
        
        different areas go through apoptosis at different times
        
        normal... sign of maturation
        
        prefrontal cortex
        
        coordinates thoughts and actions
        
        function seem to include:
        
        working memory
        
        attention
        
        planning and carrying out sequences of actions
        
        inhibiting inappropriate action
        
        does not mature until the late teens (18 year of age... or later)
        
        based on what we have just learned, do you think 16 years of age is a good age to begin driving? why or why not?
        
        probably not because important decisions do need to be made
  - - - yes but limited
      - olfactory receptor stem cells: from layer adjacent to lining of lateral ventricles to olfactory bulbs
      - hippocampi
    - - increased dendritic branching
      - growth of spines