neuro test 3

slowly

prefrontal cortex

• 1) myelination
• 2) synaptogenesis
• 3) dendritic branching

white

cognitive

perseveration

thes ize of ocular dominance columns

topographic maps

neurogenesis

hippocampuses and olfactory bulbs

hippocampus

hippocampal

• 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

• 80 % male
• 60 % retardation
• 35% epilepsy
• risk of autism increases with the age of the father

• delayed onset of language ability
• delayed onset of social interaction

broadened diagnostic criteria, increased public awareness of disorder, improved methods of identifying cases

individual is impaired in some respects but may be normal or superior in others

• 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

• environment/gene interaction
• siblings have 5% chance of being autistic
• twin- 60%
• hoxa 1 gene

• cerebellum, brain stem
• abnormal reaction to faces /fusiform face area has less fMRI activity
• mirror neurons/less activity

• 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

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

groove develops down the center of neural plate

fluid filled tube formed in vertebrate embryo when lips of neural groove fuse; develops into CNS

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

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

stage of neural development during which newly created neurons migrate from region of cell division to appropriate locations in developing neural tube

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

stage of neural developement during which developing neurons align themselves to form specific brain structures

stage of neural developement during which axons and dendrites grow and establish synaptic contacts

ameba like structure at growing tip of axon and dendride; direct the growth of axons and dendrites to appropriate targets

stage during which neurons die, typically those w/out effective synaptic contacts

stage during which many new neurons are created by cell division in the region of neural tube adjacent to fluid filled inner canal

role in spatial memory; ability to remember locations

middle layer of hippocampus; composed of the cell bodies of pyramidal cells with place fields

pyramidal cells fire at a high rate when the subject is in a particular location- associated with ability to recognize familiar places

four regions of hippocampus numbered sequentially from subiculum to edge of cortex (cornu ammonis)

circuit of hippocampal formation, runs from entorhinal cortex, to dentate, to CA3, to CA1

region of the thalamus and hypothalamus on either side of third ventricle; commonly damaged in patients w/ korkosaff's syndrome (deficiency in thiamine)

2 spherical nuclei of medial hypothalamus, visible on inferior surface of brain behind pituitary, key memory structures

large nuclei of medial dorsal thalamus, damage is associated w/memory impairment

group of cholinergic structures at base of forebrain in anterior commisure, includes medial septum, band of Broca, nucleus basislis of meynert

found in alzheimer's patients; threat like tangles in cytoplasm and scar tissue composed of degenerating neurons and an abnormal protein called an amyloid

medial region of septal nucleus, located in basal forebrain between lateral ventricles

major tracts of basal forebrain, composed of axons of medial septal nuclei neurons coursing to medial temporal lobes and contain cholinergic neurons (release acetylcholine)

a pair of chloinergic basal forebrain nuclei below anterior commisure

• 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

• 1) posterior prefrontal cortex
• 2) superior temporal cortex
• 3) angular gyrus
• 4) visual word form area

electroencephalogram (eEG), electroculogram (EOG) , neck electromyogram (EMG)

• 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

single large negative wave

one to two second waxing and waning burst of 12-14 hz waves in stage 2 sleep

• stage 3 sleep: largest and slowest EEG waves
• stage 4: predominance of delta waves

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

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

• 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

all other stages of sleep

stages 3 and 4 together because of delta waves

• - 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

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

being awake dirupts homeostasi and sleep restores it.

sleep is the result of an internal 24 hour timing mechanism because sleep protects us from accident and predation during the night

• 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

sleep wake cycle; each day bodies adjust in ways to meet demands of night and day.

environmental cues that can entrain circadian rhythms; possible to lengthen or shorten circadian cycles through adjusting light and dark

• circadian rhythms in constant environments, duration
• are not learned but are innate
• related to body temperature (sleep during falling temperature and awake during rising)

when subjects are housed in constant environments, sleep wake and temperature cycles break away from one another

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,

1) sleep deprived subjects display an increase in sleepiness 2) disturbances n various written tests of mood 3) poorly on tests of vigilance

• negatively affected by sleep loss: executive function
• immune to effects: logical deduction, critical thinking

• 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

brief periods of sleep occuring after 2 or 3 days of 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

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

sleep has higher proportion of slow wave sleep; which is the main restorative function

antidepressant drugs

shorter

• posterior hypothalamus: wakefulness
• anterior hypothalamus: sleep

• 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

REM sleep; controlled by same area that controls wakefulness. several sites responsible for core muscle tone, EEG desynchronization, rapid eye movements, etc.

superchiasmatic nuclei of medial hypothalamus: lesions disrupt circadian cycles

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

• 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

increase sleep; benzodiazepines; tolerance develops, cessation causes insomia, addictive, distort normal pattern of sleep by decreasing stage 4 and REM and increasing stage 2

precursor to serotonin, readily pases through blood brain barrier. injections reduce insomnia but have no benefit in treatment of hman insomnia

• stmulants/tricyclic antidepressants
• increase catecholamines
• can supress REM sleep

• hormone synthesized from serotonin in pineal gland
• can shift the timing of circadian cycles (chronobiotic)

• 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

• narcolepsy: severe daytime sleepiness, repeated naps, cataplexy
• sleep paralysis
• hypnagogic hallucinations

• .15% of births- extra chromosme 21 is created in the egg
• disfuigurement and retardation

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

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

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.

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.

partial epilepsy; smptoms are primarily sensory or motor or both.

partial epilepsy; restricted to temporal lobes; patient engages in compulsive, repetitive, simple behaviors and in more complex behaviors that appear almost normal

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

symptom of grand mal generalized seizure. shortage of oxygen supply to tissue that can cause brain damage

EEG of a petit mal seizure. bilaterally symettrical

.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

sbstantia nigra- midbrain nucleus whose neurons project via the nigrostriatal pathway to the striatum of the basal ganglia. little dopamine in parkinson's patients.

clumps of proteins in the surviving dopaminergic neurons of the substantia nigra in parkinson's patients

chemical from which dopamine is synthesized; can relieve symtoms of parkinson's but is rarely a permanent solution and has side effects

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

progressive motor disorder, 1 in 10,000. strong genetic basis, associated with dementia. increased fidgetiness. death about 15 years after first symptoms

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

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

10% of population over 65, 35% over 85. progressive, terminal. neurofibrillary tangles and amyloid plaques and neuron loss

partial and generalized

automatisms

parkinson's

nigrostriatal dopamine pathway

huntington's

early onset familal forms of the disorder

multiple sclerosis

alzheimers

neurofibrillary tangles and amyloid plaques

• learning: how experience changes the brain
• memory: how these changes are stored and ractivated

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

transfer of short term memories to long term storage

• explicit: conscious memories
• implicit: memories taht are expressed by improved test performance without conscious awareness

menemonic deficits like HM, with preserved intellectual functioning, and evidence of medial temporal lobe damage

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

• 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

an interruption of blood supply to the brain

medial temporal

implicit

explicit memories

ischemic

medial diencephalon

retrograde amnesia

mediodorsal

acetylcholine

electro-convulsive

consolidation

reverberating

engrams

seventh month of prenatal developement

1) synaptogenesis 2) myelination 3) dendritic arborization

• isocortex: 6 layers, more complex connections. no reptilian homologues
• allocortex: primitive 3 layered, homologues in reptiles (more ancient)

• stage two markers
• spindles: mini seizure
• k complexes: spike in activity
• marks for cognitive condiiosn like dementia

low/high

• initial: rapid/retained muscle tone/no REM
• emergent: expands each cycle/lack of muscle tone/REM

• general : zeitgeiber (exposure to light)
• specific: neurotransmitters

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)

anterior hypothalamus

retinal ganglion cells w/ melanopsin photopigmen excited by light--- excite suprachiasmatic nucleus in hypothalaus-- inhibitory on pineal gland which releases little melatonin

• "seat of the soul"
• releases melatonin

peribrachial area of pons

magnocellular nucleus becomes active in REM sleep

• also orexin
• stimulates basal forebrain and RAS
• promotes wakefulness

• 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

kinase

up regulation

more, glutamate

nitric oxide

frontal and superior temporal lobes

acetylcholine neurons become dysfunctional

• 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

beta-amyloid plaques

tau/microtubules

substantia nigra

J DOPA

caudate and putamen

there are retrieval problems but consolidation is ok

• ca1= no retrograde amnesia
• hippocampal=10 yr. retrograde amnesia
• hippocampal and temporal lobe=10-30 yr retrograde amnesia

• anterograde
• retrograde