neuro test 3

  1. the development of the human brain is unique in one respect; it develops far more _____ than the brains of other species
  2. the last part of the human brain to reach maturity is the
    prefrontal cortex
  3. the postnatal growth of the human brain results from
    • 1) myelination
    • 2) synaptogenesis
    • 3) dendritic branching
  4. human cortical ___ matter grows slowly and steadily until early adulthood
  5. in general, the sensory and motor areas of cerebral cortex acheive maturity before the ____ areas
  6. _____ is the tendency to continue making a formerly correct response when it is currently incorrect
  7. the competitive nature of neurodevelopment has been demonstrated by the effects of early monocular deprivation on
    thes ize of ocular dominance columns
  8. many studies have shown that early experience influences the _____ of sensory cortex
    topographic maps
  9. adult _____ occurs in two areas of the mammalian brain
  10. substantial neurogenesis occurs in adult
    hippocampuses and olfactory bulbs
  11. new neurons that are added to the hippocampus of an adult mammal are created near the
  12. adult rats living in enriched environments produced 60 percent more _____ neurons
  13. autism core symptoms
    • neurodevelopmental disorder
    • apparent before age 3 does not become more severe after that point
    • 1) reduced abiity to interpret the emotions and intentions of others
    • 2) reduced capacity for social interaction and communication
    • 3) preoccupation with a single subject or activity
  14. other symptoms of autism
    • 80 % male
    • 60 % retardation
    • 35% epilepsy
    • risk of autism increases with the age of the father
  15. early signs of autism
    • delayed onset of language ability
    • delayed onset of social interaction
  16. reasons for rise in autism
    broadened diagnostic criteria, increased public awareness of disorder, improved methods of identifying cases
  17. heterogenous
    individual is impaired in some respects but may be normal or superior in others
  18. savants
    • intellectually handicapped individuals who display amazing and specific cognitive or artistic abilities; 1 in 10 autistics
    • -feats of memory
    • -naming day of the week for any future or past date
    • identifiying rime numbers
    • -muisc, art
  19. genetic basis of autism
    • environment/gene interaction
    • siblings have 5% chance of being autistic
    • twin- 60%
    • hoxa 1 gene
  20. neural mechanisms of autism
    • cerebellum, brain stem
    • abnormal reaction to faces /fusiform face area has less fMRI activity
    • mirror neurons/less activity
  21. william's syndrome
    • mental retardation/uneven pattern of disability and ability
    • 1 in 200000 births
    • sociable, empathetic, talkative people
    • language skills are remarkable despite low IQs
    • impairment in spatial cognition/health problems
    • thinnning of cortex an dwhite matter in orbitofrontal cortex
    • elfin
  22. neural plate
    the patch of tissue on the dorsal surface of the vertebrate embryo that develops into the nervous system; in human embryos it is first visible 18 days following conception
  23. neural groove
    groove develops down the center of neural plate
  24. neural plate
    fluid filled tube formed in vertebrate embryo when lips of neural groove fuse; develops into CNS
  25. neural crest
    vertebrate embryonics tructure that is dorsal and lateral to neural tube; formed from neural plate cells that brake away as neural tube is being formed; develops into PNS
  26. totiopotenial
    prior to development of neural plate, cells have the potential to develop into any kind of human cell. if they are transplanted after neural plate, they will develop into nervous system cells
  27. migration
    stage of neural development during which newly created neurons migrate from region of cell division to appropriate locations in developing neural tube
  28. radial glial cells
    temporary network of glial cells that exists in developing neural tube only during period of neuron migration travel outward from point of creation along glial network
  29. aggregation
    stage of neural developement during which developing neurons align themselves to form specific brain structures
  30. process growth and synapse formation
    stage of neural developement during which axons and dendrites grow and establish synaptic contacts
  31. growth cone
    ameba like structure at growing tip of axon and dendride; direct the growth of axons and dendrites to appropriate targets
  32. neuron death
    stage during which neurons die, typically those w/out effective synaptic contacts
  33. proliferation
    stage during which many new neurons are created by cell division in the region of neural tube adjacent to fluid filled inner canal
  34. hippocampal formation
    role in spatial memory; ability to remember locations
  35. hippocampal pyramidal cell layer
    middle layer of hippocampus; composed of the cell bodies of pyramidal cells with place fields
  36. place fields
    pyramidal cells fire at a high rate when the subject is in a particular location- associated with ability to recognize familiar places
  37. CA1, CA2, CA3, CA4
    four regions of hippocampus numbered sequentially from subiculum to edge of cortex (cornu ammonis)
  38. hippocamal circuit
    circuit of hippocampal formation, runs from entorhinal cortex, to dentate, to CA3, to CA1
  39. medial diencephalon
    region of the thalamus and hypothalamus on either side of third ventricle; commonly damaged in patients w/ korkosaff's syndrome (deficiency in thiamine)
  40. mammilary bodies
    2 spherical nuclei of medial hypothalamus, visible on inferior surface of brain behind pituitary, key memory structures
  41. mediodorsal nuclei
    large nuclei of medial dorsal thalamus, damage is associated w/memory impairment
  42. basal forebrain
    group of cholinergic structures at base of forebrain in anterior commisure, includes medial septum, band of Broca, nucleus basislis of meynert
  43. neurobrils and amyloid plaques
    found in alzheimer's patients; threat like tangles in cytoplasm and scar tissue composed of degenerating neurons and an abnormal protein called an amyloid
  44. medial septum
    medial region of septal nucleus, located in basal forebrain between lateral ventricles
  45. diagonal bands of Broca
    major tracts of basal forebrain, composed of axons of medial septal nuclei neurons coursing to medial temporal lobes and contain cholinergic neurons (release acetylcholine)
  46. nuclei basilis of meynert
    a pair of chloinergic basal forebrain nuclei below anterior commisure
  47. three ideas about cerebral localization of language
    • 1) more areas than wernicke-gershwind model are involved in language (including areas of right cerebral crtex and subcortical structures)
    • 2) various aspects of language are controlled by diffuse and intermingled neural networks
    • 3) cerebral organization o flanguage abilities often differs substantially between individuals
  48. four most frequently indicated areas ivolved in reading
    • 1) posterior prefrontal cortex
    • 2) superior temporal cortex
    • 3) angular gyrus
    • 4) visual word form area
  49. three standard psychophysiological bases for defining stages of sleep
    electroencephalogram (eEG), electroculogram (EOG) , neck electromyogram (EMG)
  50. four stages of sleep EEG/waves
    • alpha waves: waxing and waning bursts of 8-12 hz punctuate low voltage, high frequency waves of wakefullness
    • stage one sleep EEG: low voltage, high frequency signal similar to active wakefulness
    • 2, 3, 4: increase in EEG voltage, decrease in EEG frquency
  51. k complexes
    single large negative wave
  52. sleep spindle
    one to two second waxing and waning burst of 12-14 hz waves in stage 2 sleep
  53. delta waves
    • stage 3 sleep: largest and slowest EEG waves
    • stage 4: predominance of delta waves
  54. initial stage 1 EEG v. emergent stage 1 EEG
    first period of stage 1 EEG not marked by any striking changes, where emergent is accompanies by REMs and loss of tone in muscles of body core
  55. sleep cycle
    90 minutes long; as night progresses more time is spent in emergent 1 an dless is spent in other stagse. brief periods where subject is awake
  56. REM sleep
    • associated with emergent stage 1 EEG; rapid eye movements
    • loss of core muscle tone, low amplitude high frequency EEG, REMs, cerebral activity increases to waking levels in brain structures, increase in autonomic nervous system activity, occasional twitching and erection
  57. NREM sleep
    all other stages of sleep
  58. slow wave sleep
    stages 3 and 4 together because of delta waves
  59. common beliefs about dreaming
    • - external stimuli can become incorporated into dreams
    • -dreams run on real time
    • -most people dream though cannot remember
    • -erections are no more complete during dreams with sexual content than those without
    • -sleepwalking occurs during stage 3/4 sleep, never during dreaming
    • -sleeptaking can occur during any stage but often during a trnasition to wakefulness
  60. activation synthesis theory
    information supplied to cortex during REM sleep is largely random and resulting dream is the cortex's effort to make sense of random signals; during REM sleep many brain stem circuits are active and bombard cortex with neural signals
  61. recuperation theries of sleep
    being awake dirupts homeostasi and sleep restores it.
  62. circadian theories of sleep
    sleep is the result of an internal 24 hour timing mechanism because sleep protects us from accident and predation during the night
  63. comparative analysis of sleep
    • all mammals and birds sleep; sleep serves an important physiological function
    • function of sleep is not a special high order function
    • large b/w species difference in sleep time suggestss that it is not needed in large quantities
    • no relationship b/w sleep time and activity, body size, or temperature
  64. circadian rhytms
    sleep wake cycle; each day bodies adjust in ways to meet demands of night and day.
  65. zeitgebers
    environmental cues that can entrain circadian rhythms; possible to lengthen or shorten circadian cycles through adjusting light and dark
  66. free running rhythms/free running period
    • circadian rhythms in constant environments, duration
    • are not learned but are innate
    • related to body temperature (sleep during falling temperature and awake during rising)
  67. internal desynchronization
    when subjects are housed in constant environments, sleep wake and temperature cycles break away from one another
  68. jet lag/shift work
    zeitgebers that control phases of rhythms are accelarated or delayed/zeitgebers stay the same but worked are forced to adjust natural schdule- produce sleep disturbances, fatigue, malaise,
  69. three consistent effects of sleep deprivation
    1) sleep deprived subjects display an increase in sleepiness 2) disturbances n various written tests of mood 3) poorly on tests of vigilance
  70. kinds of tasks affected by sleep loss
    • negatively affected by sleep loss: executive function
    • immune to effects: logical deduction, critical thinking
  71. physical effects of sleep loss
    • 1) periods of sleep deprivation up to 72 hours have no effect on strength or motor performance
    • 2) time to exhaustion was reduced in subjects who has 36 hrs of sleep deprivation, but no cardiovascular or metabolic measures were negatively afected
    • 3) no significant effect of 24 hours of sleep deprivation on strength, work rate, heart rate
  72. microsleeps
    brief periods of sleep occuring after 2 or 3 days of sleep deprivation;
  73. effects of REm sleep deprivation
    • with each successive night of deprivation, greater tendency for subjects to initate REM sequences
    • REM rebound/compensation
    • REM has a special function and is regulated seperately
  74. default theory
    difficult o stay continuously in NREM sleep, so brain switches from one to the other. if there is abodily need, brain switches to wakefulness, if there are no needs, brain switches to REM sleep. REM sleep is more adaptive when there are no immediate bodily needs
  75. sleep deprivation increases sleep efficiency
    sleep has higher proportion of slow wave sleep; which is the main restorative function
  76. the most convincing evidence that REM sleep deprivation is not seriously debilitating comes from the study of patients taking certain
    antidepressant drugs
  77. in contrast to the prediction of the recuperation theories of sleep, when a subject stays awake longer than usual under free running conditions, the flowing period of sleep tends to be
  78. two areas of the hypothalamus involved in sleep
    • posterior hypothalamus: wakefulness
    • anterior hypothalamus: sleep
  79. reticular activating system and sleep (cats)
    • 1) cats with a midcollicular transection displayed continuous slow wave sleep in EEG
    • 2) lesions at the midcollicular level that damaged core of reticular formation but left sensory fibers intact protuced continuous slow wave slep
    • 3) electrical stimulation of reticular formation desynchronized EEG and awakened cats
    • 4) cats with a transection of caudal brain stem displayed a normal sleep wake cycle of cortical EEG
    • a wakefulness producing area was located in reticular formation
    • low levels of activity in RF produce sleep
    • high levels in RF produce wakefulness
  80. caudal reticular formation and sleep
    REM sleep; controlled by same area that controls wakefulness. several sites responsible for core muscle tone, EEG desynchronization, rapid eye movements, etc.
  81. circadian clock location
    superchiasmatic nuclei of medial hypothalamus: lesions disrupt circadian cycles
  82. retinohypothalamic tracts
    leave optic chiasm project to suprachiasmatic nuclei- mediate the ability of light to entrain photoreceptors WITHOUT rods or cones. the photoreceptors are neurons, rare retinal ganglion cells, which sacrifice the ability to respond quickly and briefly to light changes in favor of the ability to respond consistently to slowly changing levels of illumination. photopigment is MELANOPSIN
  83. tau, clock
    • mammalian circadian gene
    • 1) circadian genes evolved early in evolutionary history
    • 2) mechansm of rhythms: transcription of proteins by circadian genes
    • 3) most cells contain a genetic circadian clock but are normallly entrained by neural or hormonal signals from SCN
  84. hynotic drugs
    increase sleep; benzodiazepines; tolerance develops, cessation causes insomia, addictive, distort normal pattern of sleep by decreasing stage 4 and REM and increasing stage 2
  85. 5 HTP
    precursor to serotonin, readily pases through blood brain barrier. injections reduce insomnia but have no benefit in treatment of hman insomnia
  86. antihypnotic drugs
    • stmulants/tricyclic antidepressants
    • increase catecholamines
    • can supress REM sleep
  87. melatonin
    • hormone synthesized from serotonin in pineal gland
    • can shift the timing of circadian cycles (chronobiotic)
  88. insomnia
    • many are iatrogenic (physician created) because of sleeping pills
    • effectie treatment: sleep restriction
    • caused by sleep apnea (obstruction or central)
    • periodic limb movment disorder
    • restless leg syndrome
  89. hypersomnia
    • narcolepsy: severe daytime sleepiness, repeated naps, cataplexy
    • sleep paralysis
    • hypnagogic hallucinations
  90. down syndrome
    • .15% of births- extra chromosme 21 is created in the egg
    • disfuigurement and retardation
  91. apoptosis
    cell death- plays a role in brain damage . more adaptive than necrosis because apoptosis is slow and there is no inflammation or damage to nearby cells
  92. epilepsy
    1% characterized by spontneous seizures. can be in the form of convulsions or subtle changes in thought, mood, or behavior . can be caused by genes or injury. associated with faults at inhibitory synapses that cause neurons to fire in bursts. diagnosed from EEG
  93. epileptic auras
    psychological changes before a convulsion in the form of smell, thought, feeling of familiarity, hallucination, tightness in chest. the nature of the auras is a clue to the location of the epileptic focus. also, the epileptic auras are similar from attack to attack.
  94. partial seizures
    do not involve the entire brain; epileptic neurons at a focus begin to discharge together in bursts which produces in epileptic spiking in the EEG. not usually accompanied by total loss of consciousness or equilibrium.
  95. simple partial seizures
    partial epilepsy; smptoms are primarily sensory or motor or both.
  96. complex partial seizures
    partial epilepsy; restricted to temporal lobes; patient engages in compulsive, repetitive, simple behaviors and in more complex behaviors that appear almost normal
  97. generalized seizures
    involve the entire brain; grand mal- loss of consciousness, equilibrium, convulsion, hypoxia. petit mal: not associated with convulsions but a disruption of consciousness which is associated with a cessation of behavior, vacant look, fluttering eyelids. most common in children in puberty
  98. hypoxia
    symptom of grand mal generalized seizure. shortage of oxygen supply to tissue that can cause brain damage
  99. 3 per second spike and wave discharge
    EEG of a petit mal seizure. bilaterally symettrical
  100. parkinson's disease
    .5% of population. more prevalent in males. initial symptoms are mild but increase in severity. tremor that is pronounced during inactivity but not voluntary movement or sleep, muscular rigidity, difficulty initiating movement, slwones of movement, masklike face. no single cause
  101. where is parkinson's located?
    sbstantia nigra- midbrain nucleus whose neurons project via the nigrostriatal pathway to the striatum of the basal ganglia. little dopamine in parkinson's patients.
  102. lewy bodies
    clumps of proteins in the surviving dopaminergic neurons of the substantia nigra in parkinson's patients
  103. l-dopa
    chemical from which dopamine is synthesized; can relieve symtoms of parkinson's but is rarely a permanent solution and has side effects
  104. deep brain stimulation
    treatment for parkinson's- low intensity electical stimulation is continuously applied to the brain through th esubthalamic nucleus. high frequency electrical stimulation blocks the function of the target structure and alleviates symptoms
  105. Huntington's disease
    progressive motor disorder, 1 in 10,000. strong genetic basis, associated with dementia. increased fidgetiness. death about 15 years after first symptoms
  106. huntingtin
    dominant gene that is mutated in huntington's disease; huntingtin protein protects neurons from apoptotic cell death. abnormal huntingtin protein is produced in all parts of the brain, but brain damage is restricted to the striatum and cerebral cortex
  107. multiple sclerosis
    progressive disease that attacks the myelin of axons in the CNS. microscopic areas of degeneration on myelin sheaths. areas of hard scar tissue develop in the CNS. visual disturbances, weakness ,numbeness, tremor, ataxia
  108. alzheimer's disease- two main indicators
    10% of population over 65, 35% over 85. progressive, terminal. neurofibrillary tangles and amyloid plaques and neuron loss
  109. the two major categories of epileptic seizures
    partial and generalized
  110. simple repetitive responses that occur during complex partial seizures
  111. the disorder characterized by tremor at rest
  112. parkinson's disase is associated with generation in the ____-
    nigrostriatal dopamine pathway
  113. disease passed from generation by a single dominant pathway
  114. genetic studies of parkinson's and alzheimer's have focused on what?
    early onset familal forms of the disorder
  115. experimental autoimmmune encephalomyelitis is an animal model of
    multiple sclerosis
  116. the most common cause of dementia
  117. two major neuropathologiacl symptoms of alzheimers
    neurofibrillary tangles and amyloid plaques
  118. learning v. memory
    • learning: how experience changes the brain
    • memory: how these changes are stored and ractivated
  119. H.M
    man who had the medial portions of his temporal lobes removed for epilepsy; a bilateral medial temporal lobectomy and removal of the hippocampus, amygdala, and cortex. he suffered severe anterograde amnesia
  120. memory consolidation
    transfer of short term memories to long term storage
  121. explicit v. implicit memories
    • explicit: conscious memories
    • implicit: memories taht are expressed by improved test performance without conscious awareness
  122. medial temporal lobe amnesia
    menemonic deficits like HM, with preserved intellectual functioning, and evidence of medial temporal lobe damage
  123. why do we have two memory systems ? (implicit/explicit)
    implicit system is the first to evolve because it is more ssimple. the evolution of explicit memory systems provided for the flexible use of informaiton
  124. semantic v. episodic memories
    • semantic: explicit memories for general facts or information
    • episodic: explicit memories for the particular events or experiences of one's life
    • amnesics have difficulty with episodic emories
  125. cerebral ischemia
    an interruption of blood supply to the brain
  126. HM had his _____ lobes removed
    medial temporal
  127. the mirror drawing test, the rotary pursuit test, the incomplete pictures test, and the repition priming test are all tests of _____ memory
  128. HM appears incapable of forming new long term
    explicit memories
  129. suppport for the view that hippocampal damage can by itself cause amnesia comes from the study of RB who suffered _____ damage to the pyramidial cells of his CA1 hippocamal subfield
  130. the current view that damage to the __________ is responsible for most of the memory deficits of people with Korsakoff's disease
    medial diencephalon
  131. the gradual onset of korsakoff's syndrome complicates the study of the resulting __________
    retrograde amnesia
  132. the ____ nuclei are the medial diencephalic nuclei that have been most frequently implicated in memory
  133. alzheimers disease is associated with the degeneration of the basal forebrain and resulting depletion of
  134. posttraumatic amnesia can be induced with _____ shock, which is ued in the treatment of depression
  135. the transfer of a memory from short term to long term storage
  136. because some gradients of retrograde amnesia are extremely long, it is unlikely that memory consolidation is mediated by _____ neural activity, as hypothesized by Hebb
  137. the changes in the brain that store memories
  138. when does neurogenesis generally end?
    seventh month of prenatal developement
  139. what are the three methods of quadrupling brain volume
    1) synaptogenesis 2) myelination 3) dendritic arborization
  140. isocortex versus allocortex
    • isocortex: 6 layers, more complex connections. no reptilian homologues
    • allocortex: primitive 3 layered, homologues in reptiles (more ancient)
  141. what are sleep spindles and k complexes
    • stage two markers
    • spindles: mini seizure
    • k complexes: spike in activity
    • marks for cognitive condiiosn like dementia
  142. more alert- ___ amplitude, _____ frequency
  143. what is the difference b/w initial and emergent sleep
    • initial: rapid/retained muscle tone/no REM
    • emergent: expands each cycle/lack of muscle tone/REM
  144. general v. specific control over wake/sleep cycles
    • general : zeitgeiber (exposure to light)
    • specific: neurotransmitters
  145. three types of specific biological rhythms
    circadian rhythms (sleep/wake, temperature, hormones like cortisol, motor performance and learning) ANTERIOR HYPOTHALAMUS

    infraradian rhythms: occur in periods longer than a day (ovulation/menstruation)

    ultraradian rhythms: repeat more than once a day (cycling of sleep stages)
  146. what modulates temperature and the sleep/wake cycle
    anterior hypothalamus
  147. effect of light
    retinal ganglion cells w/ melanopsin photopigmen excited by light--- excite suprachiasmatic nucleus in hypothalaus-- inhibitory on pineal gland which releases little melatonin
  148. pineal gland
    • "seat of the soul"
    • releases melatonin
  149. what is the source of acetylcholine in rem
    peribrachial area of pons
  150. what nucleus is responsible for REM sleep
    magnocellular nucleus becomes active in REM sleep
  151. hypocretin
    • also orexin
    • stimulates basal forebrain and RAS
    • promotes wakefulness
  152. adenosine
    • accumulates during waking/hard thinking
    • more adenosine- more you inhibit excitatory neurotransmitters (more tired you become)
    • inhibits hypocretin (which stimulates excitatory NTs)

    caffeine blocks adenosine
  153. protein _____ makes receptors more sensitive/effective
  154. protein kinase does "____", a mechanism which causes cells to produce more ampa receptors
    up regulation
  155. the ____ action potentials a neuron participates, the more it will be able to react to ______ in the future
    more, glutamate
  156. _____ leaves dendritic spine and enters presynaptic neuron, increasing glutamate synthesis
    nitric oxide
  157. which 2 lobes are smaller in down's syndrome
    frontal and superior temporal lobes
  158. first neuron symtpom of alzheimers
    acetylcholine neurons become dysfunctional
  159. what are the neurological changes in alzheimers?
    • neurons produce amyloid precursor protein which are improperly cleaved
    • too many long proteins fold over, form beta-amyloid plaques, which attract inflammation
    • cilia release glutamate, which produces exototoxicity
    • this disrupts long term potentiation
  160. what accumulates in alzheimers
    beta-amyloid plaques
  161. neurofibrillary tangles are made of ____ proteins in _____
  162. parkinson's is a degeneration in the __________
    substantia nigra
  163. this treatment for parkinson's stimulates dopamine until neurons die
    J DOPA
  164. huntington's disease is linked to a degeneration in the ______ and ________ in basal ganglia
    caudate and putamen
  165. in anterograde amnesia, retrieval is ok but there is poor consolidation after the injury
    in retrograde amnesia
    there are retrieval problems but consolidation is ok
  166. damage to CA1=?
    damage to hippocampal formation=?
    damage to hippocampal formation and medial temporal lobe=?
    • ca1= no retrograde amnesia
    • hippocampal=10 yr. retrograde amnesia
    • hippocampal and temporal lobe=10-30 yr retrograde amnesia
  167. HM had severe ______ amnesia and 2 yrs of ______ amnesia after his bilateral medial temporal lobectomy
    • anterograde
    • retrograde
Card Set
neuro test 3
neuro test 3