Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
196 Cards in this Set
- Front
- Back
|
Describe the Allocortex
|
3 layers
pyramidal cells present pyramidal layer & polymorphic layer |
|
|
Where can Allocortex be found?
|
Palecortex: olfactory cortex
Archiocortex: Hippocampus |
|
|
Describe the Neocortex
|
6 layers
unique to mammals majority of principle projection neurons in layers 2,3,5 (pyramidal cells) |
|
|
Describe the Mesocortex
|
transitional cortex found between the allo- and neocortex
|
|
|
Where is Mesocortex found?
|
Limbic areas
Parahippocampal gyrus, cingulate gyrus, insula |
|
|
How are the neurons of the cortex grouped?
|
Grouped according to function
|
|
|
what are the different groupings of neurons found in the cortex?
|
1. Pyramidal cells: excitatory principle neurons that project to other cortical areas, basal ganglia, thalamus, brainstem, and spinal cord
2. Stellate cells: excitatory interneurons in layer 4 receive input from thalamus 3. Inhibitory interneurons: GABAnergic cells with axons that project within columns or over short distances between columns |
|
|
What are the layers of the NEOCORTEX?
|
I. Molecular
II. Small Pyramidal III. Medium Pyramidal IV. Granular V. Large Pyramidal VI. Multiform (polymorphic) |
|
|
Describe the Molecular Layer of the Neocortex
|
Layer I
layer closest to pia surface with interneurons and apical dendrites of pyramidal cells diffuse modulatory NT system have heaviest projections to Layer I Association & commissural afferents |
|
|
what is found in Layer II of the neocortex
|
small pyramidal layer
Small pyramidal cells and inhibitory interneurons |
|
|
what is found in layer III of the neocortex?
|
Medium pyramidal cell layer
medium pyramidal cells and intercortical association and commissural fibers |
|
|
Describe the Granular layer of the Neocortex
|
Layer IV
Stellate cells: excitatory interneurons Primary targets of thalamocortical projections dense bands of myelinated fibers is prominent in sensory areas (Stria of Genari BA 17) |
|
|
What layer is the large pyramidal layer?
|
Layer V of Neocortex
|
|
|
Describe Layer V of Neocortex
|
Large pyramidal layer
Medium to large pyramidal cells Primary source of subcortical efferents from cortex to brainstem and spinal cord |
|
|
What type of cells are found in Layer VI of the Neocortex?
|
Multiform (polymorphic) layer
Fusiform, pyramidal, and stellate cells Both afferent and efferent fibers |
|
|
what layer of the cortex is the diffuse modulatory input the greatest?
|
Layer I (molecular layer)
|
|
|
what layer of the cortex receives the greatest projection from the thalamus?
|
Layer IV of the neocortex
|
|
|
where do the main efferents of Layer IV project to?
|
Thalamus
|
|
|
Where do the main efferents of Layer V project to?
|
Subcortical structures such as brainstem, spinal cord, striatum, superior colliculus, etc.
|
|
|
Layer III has an ________ projection.
|
Layer III has intercortical projections to the other hemisphere & cortical areas as association cortices
|
|
|
what two layers have interneurons present in them that project to other cortical areas?
|
Layer I and II
|
|
|
Commisural fibers connect corresponding areas of each hemisphere. What are the exceptions?
|
hand motor areas & striate cortex are exceptions
this allows for fine independent motor control dextarity of the hands |
|
|
What are excitatory connections between columns of the cortex the basis for?
|
Excitatory connections between columns are the basis for:
1. psychophysical phenomena . completion of images 2. experience dependent reorganization 3. Recovery of function after brain damage |
|
|
what is the Brodmann area classification based on?
|
Variation fo cytoarchitecture
|
|
|
Describe the Homotypica cortex
|
6 distinct layers
comparable in thickness of each layer Association areas |
|
|
Describe the heterotypical cortex
|
6 less distinct layers with layers varying in thickness according to function
|
|
|
What are some characteristics of the Granular (Koniocortex) Heterotypical cortex? where can it be found?
|
Primary sensory areas (primary somatosensory cortex, visual cortex, auditory cortex)
THICK LAYER 4 many stellate cells receiving thalamic input |
|
|
what are some characteristics of the Agranular Cortex? Where can it be found?
|
Prmary motor (4) & Premotor (6) cortex
Motor areas with prominent Layer V (output) and narrow layer IV Pyramidal cells (projections/output) numerous Layer III & V Narrow Layer IV reflecting the less thalamic input |
|
|
What occurs in Disconnection syndrome?
|
lesion in white matter affects communication between areas
can get information in but cannot get it to the proper place |
|
|
What are some features seen with damage to association cortices?
|
changes in personality
cognitive deficits Agnosia Anasognosia Aphasia Apraxia |
|
|
Agnosia
|
loss of ability to recognize familiar objects
may affect a single sense |
|
|
Prosopagnosia
|
inability to recognize faces
|
|
|
Anasognosia
|
lack of awareness of functional deficits
patient will deny anything wrong with them |
|
|
Aphasia
|
disorder of speech
may have varying degrees |
|
|
Anomia
|
naming
|
|
|
Alexia
|
problems with reading
|
|
|
agraphia
|
problems with writing
|
|
|
dysarthria
|
motor problem with speech
|
|
|
Apraxia
|
loss of ability to correctly perform motor response in the absence of damage to language, primary motor, cerebellar pathways
|
|
|
Rasmussen's syndrome
|
encephalitis, progressive neurodegenerative autoimmune disorder affecting the L hemisphere of the brain
|
|
|
what hemisphere is mainly dominant hemisphere in humans?
|
Left
|
|
|
which hemisphere is language found in?
|
Dominant
so mostly the left |
|
|
what hemisphere is responsible for attention and spatial awareness
|
Right
NON-dominant |
|
|
At what age does lateralization develop
|
Age 3
|
|
|
Is there a physical asymmetry seen because of dominance?
|
YES
Platnum temporale is larger on the left, language Parietal lobe is larger on the Right |
|
|
what is the function of the asymmetry of the brain?
|
90% of people are right handed
Gross motor skills are controlled by contralateral hemisphere for both hands Complex motor task primarily controlled by the Dominant hemisphere which is usually the L hemisphere |
|
|
How can hemisphere dominance be demonstrated in preparation for neurosurgery?
|
Wada's procedure
sodium amytal injection into internal carotid on oen side produces complete loss of sensation and paralysis on opposite side of body NO SPEECH if anesthetized hemisphere is dominant examiner determines which hemisphere is dominant by asking questions |
|
|
What are the functional specializations of the L hemisphere?
|
analysis of R visual field
Gross motor control of R side of body Complex motor task for BOTH hands language, including reading and writing Music production Analytical skills: arithmetic |
|
|
What are the functional specialization fo the R hemisphere?
|
analysis of L visual field
Gross motor control of the L side of the body Complex visual spatial skills Emotional expression of language and rudimentary speech music appreciation spatial attention: body image and coordination of body in space |
|
|
What is the pericallosal artery a branch of? what does it supply?
|
branch of ACA
found above corpus callosum supplies medial surface of cerebral hemisphere (cingulate gyrus) and corpus callosum |
|
|
what is the callosomarginal artery a branch of? what does it supply?
|
branch of ACA
lies in cingulate sulcus and marginal artery supplies medial surface of cerebral hemisphere |
|
|
what does the superior division of MCA supply
|
lateral frontal cortex
|
|
|
what does the inferior division of MCA supply
|
lateral temporal and part of parietal cortex
|
|
|
what does PCA supply?
|
inferior and medial temporal cortex
occipital cortex |
|
|
what does anterior choridal artery supply ?
|
branch of Internal carotid
supplies globus pallidus, putamen, thalamus, inferior portions of PLIC |
|
|
what does the Recurrent artery of Huebner supply?
|
Medial striate artery branch of ACA
supplies head of caudate, anterior putamen, GP, inferior portions of ALIC |
|
|
what are the important penetrating arteries that supply large portions of basal ganglia and internal capsule?
|
Lenticulostriate arteries branch of MCA
|
|
|
what branch of PCA supplies much of the thalamus and posterior portions of PLIC
|
Thalamogeniculate and Thalamoperforater arteries
|
|
|
What part of the brain is considered to the prefrontal cortex?
|
PFC is the region of the frontal lobe anterior to motor, premotor, and limbic areas
|
|
|
What is the heteromodal association cortex?
|
reciprocal connections with unimodal association cortices (both motor and sensory) as well as hetermodal cortex of parietal, temporal, and occipital lobes
|
|
|
TQ
What connects the PFC with the amygdala and the temporal lobes as well as the hippocampus? |
Prefrontal cortex connection to the amygdala and temporal lobes via the uncinate fasiculus and hippocampal formation via the cingulate gyrus
|
|
|
what is the primary thalamic input to the PFC?
|
Mediodorsal nucleus of thalamus
contributions from pulvinar and intralaminar nuclei |
|
|
What part of the basal ganglia does PFC project to?
|
head of caudate
From parietal and pre-motor cortex Executive and cognitive functions |
|
|
What are the subcortical projection of PFC?
|
hypothalamus
septal nuclei cerebellum midbrain |
|
|
True or False
The PFC receives projections from the diffuse modulatory system |
True
|
|
|
What are the functionally distinct areas of the PFC?
|
Dorsolateral PFC
Orbitomedial PFC |
|
|
What is the function of the Dorsolateral PFC?
|
planning
strategy formation organize motor response |
|
|
what is the function of the orbitomedial PFC?
|
involved in emotional aspects of behaviors
|
|
|
What are the functions of the PFC?
|
enable to interact in a socially appropriate and effective way with others and our environments
1. Goal oriented behaviors 2. Working memory 3. Social emotional decision making 4. Restraint 5. Personality 6. Abstract reasoning |
|
|
describe how working memory occurs in the PFC.
|
Everything concsiously aware of at a given moment
external sensory recall of memories relevant to task mediated by on-going activity in networks with motor and sensory association areas and parietal temproal heteromodal cortex |
|
|
what is involved in social emotional decision making?
|
processing, evaluating, and filtering social and emotional information
|
|
|
what is involved in restraint?
|
judgement, delayed gratification, inhibition of inappropriate responses
|
|
|
Descrive the characteristics associated with Dorsolateral Prefrontal Cortex syndromes?
|
Abulic: lack of initiative/will
unable to make decisions independently 1. diminished sponteneity 2. Diminshed verbal output (mutism) 3. Diminished motor behavior (akinesia) 4. Lack of ability to plan/sequence 5. Working memory deficits |
|
|
describe the characteristics of PFC Orbitomedial syndromes
|
Disinhibited
1. impulsivity 2. stimulus driven behavior 3. diminished social insight 4. inappropriate humor 5. confabulation 6. emotional lability |
|
|
what are some symptoms associated with PFC damage?
|
perservation or impersistance
Incontinence w/ a lack of concern impaired attentional capacity ansomia: lack of functioning olfaction |
|
|
How do you assess frontal lobe damage?
|
1. behavioral
2. Mental status exam 3. Perservation and set shifting ability 4. Suppression of inappropriate responses 5. Judgement |
|
|
Describe how behavior is assessed in frontal lobe function
|
1. frontal release signs
2. motor impersistence 3. confabulation |
|
|
When examining a patient for mental status what are you checking is intact?
|
oriented to person, time, and place
|
|
|
What are some test that you would have your patient do in order to assess Perservation and set shifting ability?
|
1. Luria sequencing tasks
2. Wisonsin card sorting task: ability to modify what you are looking for: must figure out correct pattern |
|
|
How do you test for suppression of inappropriate response?
|
Stroop Test
What colors are the written words? |
|
|
How do you assess a patient for judgement?
|
Damasios Gambling Test
-If PFC damage will choose from riskier deck continuously |
|
|
What can cause frontal lobe disorders?
|
Trauma
Tumors Vascular |
|
|
Describe the signs seen with a L ACA infarct?
|
Right leg weakness of UMN
Right leg sensory loss of corttical type R grasp reflex, frontal lobe behavior abnormalities Large left infarct > Right hemiplegia Transcortical aphasia |
|
|
describe the signs seen with a R ACA infarct?
|
L leg weakness of UMN type
L leg cortical sensory loss L grasp reflex Frontal lobe behavioral abnormalities L hemineglect large infarct may cause L hemiplegia |
|
|
What is a degenerative disorder that affects the PFC?
|
Huntington's disease
involves all channels of basal ganglia Prefrontal channel: deteroriation of cognitive and executive functions Limbic channel: impaired impulse control & socially inappropriate behavior |
|
|
What causes psychiatric disorders?
|
imbalance of diffuse modulatory NT
|
|
|
What is the imbalance causing Schizophrenia.
|
imbalance of DA transmission in mesocortical pathway
DA antagonist are used to treat schizophrenia |
|
|
what part of the PFC is affected in depression?
|
Dorsolateral portions of PFC
|
|
|
describe what depression does to the PFC.
|
affects the dorsolateral PFC
inablility to handle stress > weakens PFC functions over activation of LIMBIC circuits |
|
|
how do you treat depression ?
|
restore balance with drugs acting in serotonergic and NE systems
|
|
|
what is occurring in the PFC in patients who have ADHD?
|
non-optimal level of activity of PFC
|
|
|
who does ADHD affect?
|
3-5% of school aged children
5X more common in males > suggest X linkage |
|
|
describe characteristics of ADHD
|
hyperactivity, impaired attention, and impulsivity
|
|
|
where is the reduced activity in the PFC in association with ADHD?
|
Reduced activity in prefrontal cortex and basal ganglia
anterior cingulate dorsolateral PFC |
|
|
what does the genetic linkage associated with ADHD suggest?
|
abnormality in DA receptors/transporters/enzymes
|
|
|
what may occur in utero that can cause your child to increase the incidence of ADHD?
|
exposed to alcohol or tobacco
|
|
|
How do you treat a child with ADHD?
|
treat with stimulants @ low doses that increase DA and NE levels in PFC
this increases the input from VTA to PFC |
|
|
what do genetic mutations cause in stage development?
|
Genetic mutations affect specific proteins involved in contolling brain development
|
|
|
what are some extrinsic factors in utero that affect brain development?
|
Extrinsic factors:
Maternal nutrition Alcohol: fetal alcohol syndrome tobacco Drugs/toxicity/heavy metal exposure |
|
|
what in the postnatal environment affects stage development of the brain?
|
Drugs/toxicity/heavy metal exposure
sensory stimulation and social interaction critical for normal brain development |
|
|
True or False
It is possible to genetically determine the trillions of specific synaptic connection. |
FALSE
it is NOT possible to genetically determine the trillions of specific synaptic connections |
|
|
How many synapses are added per second as the brain develops?
|
1.8 million synapses added per second
The Cerebral cortex triples in thickness in 1st year of life |
|
|
What are the final stages of brain development dependent on?
|
Experience dependent
Sensory stimulation and social interaction are necessary for development |
|
|
What are the stages of Neuronal development?
|
1. Cell proliferation
2. Migration 3. Differentiation 4. Development of Axonal connections 5. Synapse formation 6. Restriction of synaptic connections 7. Synaptic rearrangement |
|
|
Where does cell proliferation occur in cerebral cortex development?
|
occurs in the ventricular zone of developing brain
|
|
|
What can a stem cell produce in the cerebral cortex?
|
common stem cells can produce both neurons and glia
|
|
|
What is cell fate determined by in the development of the cortex?
|
Cell fate specified by environment, which changes as gestation proceeds
|
|
|
What can result in microcephaly or macrocephaly?
|
Due to genetic dysfunction
Disregulation of neuronal cell proliferation can result in microcephaly vera or macrocephaly |
|
|
when are neurons in the Neocortex born?
|
Neurons in human neocortex are born from the 5th week to the 5th month of gestation
|
|
|
where are neurons generated in adult life?
|
some neurons are developed in adult life
hippocampus is on place for generation of new neurons |
|
|
what is important for guidance of other neurons?
|
Cajal-retcius neurons
|
|
|
What does proper neuronal migration in the cerebral cortex result in?
|
proper migration results in laminar organization of cortex
|
|
|
What provides scaffolding in the cortex?
|
Radial glial cells provide scaffolding of the cerebral cortex
|
|
|
What is in the molecular cell layer controlling migration?
|
Reelin in the molecular layer is one signaling controlling migration
|
|
|
How do neurons migrate throughout the cortex?
|
Neuroblast (immature neurons) migrate along fibers that extend from the ventricular zone to pial surface.
Reelin in molecular layer is one signal controlling migration |
|
|
What layers are developed first in the cortex?
|
Inside out: first migration is to layer VI, then V, etc.
|
|
|
What is implicated in lissencephaly?
|
Genetic defects are implicated in lissencephaly affects migration
> smooth brain |
|
|
what do mutations in microtubule related proteins cause?
|
mutations in LISI gene on chromosome 17 affect cell movement
|
|
|
What results in neurons not knowing they have reached the appropriated layer in the cortex during migration ?
|
Mutation in proteins such as Reelin
|
|
|
When does differentiation occur in neurons in the cortex?
|
Differentiation occurs as soon as neurons reach "place" in the cortex
Neurons in layer VI are differentiated before the neurons in upper layers have migrated |
|
|
How is a neuron differentiated?
|
Neurites sprout and develop as dendrites or axons
|
|
|
What is the morphology of a cell in specific layers dependent upon?
|
Morphology of cells is dependent on stage of development, growth factors, and cell-cell interactions
|
|
|
What type of cells are found in Layer V of the neocortex?
|
Pyramidal cells
|
|
|
what type of cells are found in Layer IV of the neocortex?
|
stellate cells
|
|
|
describe the development of axonal connections
|
Tip of axon forms growth cone
Navigates by interaction with extracellular matrix and diffusible guidance molecules |
|
|
Give an example development of axonal connections.
|
Path of ALS commissural axons is dependent on both attractant and repellant factors secreted from midline of developing spinal cord, while non-commisural axons are repelled
|
|
|
Fasiculation (relevant to neuronal cell migration)
|
one neuron making path that other neurons will join
|
|
|
Retinotopy:
Describe the mechanism involved in specification of connections from the retina to the LGN and from LGN to striate cortex. |
1. Gradient of cell surface markers on retinal ganglion cells that changes from nasal to temporal retina
2. Attactant and repellant mechanisms in extension of the axon and guidance to correct area of LGN: Temporal retina axons are repelled at the optic chiasm by radial glial cells expressing ephrin while nasal axons cross because they do NOT express ephrin receptors and are attacted to CD44+ neurons at the chiasm |
|
|
what keeps the temporal retinal axons from crossing at the optic chaism?
|
chemorepellant signal keeps them from crossing
|
|
|
What would occur if CD44+ was blocked at the optic chiasm?
|
there will be no crossing of fibers
|
|
|
During pathway selection what keeps neighboring axons together in their migration via interaction with cell-adhesion molecules?
|
Fasciculation
|
|
|
How is innervation of a structure determined?
|
Innervation of structure is determined by chemo affinity, as well as, diffusible factors
Once appropriate layer is reached, inhibitory factors stop axon growth |
|
|
what occurs to the growth cone once a cell has reached its destination?
|
once target has been reached, the growth cone collapses and pre-synaptic terminal begins to develop
|
|
|
how do the receptors and proteins get into the post synaptic density & presynaptic terminal?
|
Receptors and other proteins essential for synaptic transmission cluster in post synaptic density and in pre-synaptic terminal
|
|
|
What are Neurexins and Neuroligins examples of ?
|
Synaptic cell adhesion molecules
|
|
|
what is the function of Neurexins and Neuroligins?
|
Synaptic cell adhesion molecules that connect pre- and post-synaptic specializations and regulate synaptic function
|
|
|
What may be disrupted in autism & schizophrenia?
|
Synaptic cell adhesion molecules that connect pre- and post-synaptic specializations and regulates function may be disrupted in autism and schizophrenia
|
|
|
what is a disorder of synapse formation and stabilization?
|
Autism
Schizophrenia |
|
|
What restricts a synaptic connection?
|
1. Cell death
2. Synapse Elimination |
|
|
describe how cell death restricts synaptic connections
|
cell death: neurons that DO NOT successfully compete for trophic factors undergo apoptosis
|
|
|
How many neurons are estimated to die that originally generate?
|
estimate that half of neurons originally generated die
|
|
|
How are synapses eliminated?
|
synaptic capacity high during early development and declines in maturation
-50% loss of synapses in cerebral cortex at puberty |
|
|
What is the estimate of loss of synapses during puberty?
|
Cerebral cortex: estimate of 50% loss of synapses at puberty
|
|
|
What is the term for activity dependent fine tuning of connections?
|
Synaptic rearrangement
|
|
|
What is the critical period?
|
Critical period: normal development of neuronal circuitry that underlies certain behaviors requires exposure to appropriate environment stimuli within a specific time window
(language is one example) |
|
|
How is ocular dominance developed?
|
1. initially inputs from both eyes onto common targets
2. Activity dependent process: correlated activation of inputs from one eye that are out of phase with inputs from opposite eyes Critical period is early in development and relatively brief |
|
|
What is the Hebbian synaptic modification?
|
synapses that are active at same time as post synaptic target neurons are strengthened while others are eliminated
|
|
|
what occurs with monocular deprivation during critical periods?
|
monocular deprivation during critical period (1st six weeks postnatal to macaques) results in reduced representation of deprived eye in primary visual cortex that CANNOT be restored
This is why cataracts in infants must be treated early |
|
|
How is binocular vision developed?
|
-dependent on visual experience during infancy and early childhood
-produced by correlated pattern of activity in inputs from two eyes converging on "binocular neurons" outside layer IV of striate cortex |
|
|
where do binocular cells develop?
|
binocular cells develop in upper regions of BA 17
|
|
|
When does the greatest plasticity for development of stereopsis occur?
|
greatest plasticity in development in steropsis from 4-6 months
|
|
|
Stereopsis
|
depth perception
|
|
|
Even though the greatest plasticity for development of stereopsis is 4-6 months, what period might strabismus be treated and corrected?
|
Greatest plasticity in development of stereopsis from 4-6 months but with some possibility for effective intervention to treat strabsimus at up to 24 months
|
|
|
why is there a prolonged critical period of fine tuning in vision?
|
continued growth of head and eyes ending at age 10
|
|
|
Stabismus
|
eyes not properly aligned to each other
|
|
|
when is the most critical phase for development of connections in visual cortex?
|
1st 6months of life are very important for development of connections in visual cortex
|
|
|
Amblyopia:
|
poor vision caused by abnormal experience dependent development of visual system
|
|
|
what does cataracts during infancy cause?
|
Cataracts during infancy results in monocular deprivation, reduced cortical representation for deprived eye that CANNOT be restored with surgery after critical period
|
|
|
when is the ideal time to treat cataracts in an infant?
|
catarcts in infants must be treated early, ideally within 6 weeks
|
|
|
Stabismus
|
misalignment due to abnormality in eye muscles or their control
-occurs in 5% of children -results in failure to develop binocular vision and Lazy eye |
|
|
what does strabismus result in if not corrected?
|
failure to develop binocular vision and lazy eye
|
|
|
when should strabismus be corrected for the best outcome?
|
Should be corrected before 10 months of age
|
|
|
where does activity dependent changes in synaptic strength during development occur at ?
|
activity dependent changes in synaptic strength during development occurs at glutamate synapses
|
|
|
describe the activity dependent changes in synaptic strength during development at the glutamate synapses
|
Glutamate receptors have 2 major types of receptors: AMPA & NMDA
AMPA receptors provide major excitatory signal NMDA receptors detect coincident pre- and post synpatic activity because it is both ligand and voltage fated |
|
|
Describe the molecular basis of Hebbian modification
|
1. NMDA channel is blocked by magnesium ions at membrane potentials near resting value but block is relieved by membrane depolarizing
2. membrane depolarization provided by release of glutamate (pre-synaptic activity) opening AMPA receptors 3. this relief of Mg++ block by depolarization and the presence of glutamate activates NMDA receptors producing CALCIUM influx 4. intracellular effects of increasing CALCIUM lead to the changes in synaptic efficiency |
|
|
what is the most important 2nd messenger in the body?
|
Calcium
|
|
|
What relieves the block of NMDA receptor?
|
depolarization provided by glutamte opening AMPA receptors
|
|
|
what does the relief of Mg from NMDA receptors cause?
|
activates the NMDA receptor producing calcium > intracellular effects of increasing calcium concentration lead to changes in synaptic efficiency
|
|
|
what is synaptic strength proportional to?
|
Synaptic strength is proportional to AMPA receptors
|
|
|
what do changes in synaptic strength involve?
|
altered synaptic proteins
|
|
|
what does LTP cause?
|
LTP, increased synaptic strength, mediated by insertion of AMPA receptors
> increases level of response |
|
|
what does LTD cause?
|
LTD, decreases synaptic strength mediated by removal of AMPA receptors
|
|
|
how is an NMDA receptor silent?
|
there are NO AMPA receptors
|
|
|
what is the purpose of having silent NMDA receptors?
|
can be modified
RECOVERY OF FUNCTION |
|
|
Why do critical periods end?
|
1. Capacity for outgrowth of axons is lost
2. Reduced synaptic excitatory synapses 3. mechanism that dampen cortical activation |
|
|
Describe how the capacity for outgrowth of axons is lost.
|
reduced trophic signaling, alterations in extracellular matrix, and myelination
-once axons are myelinated >limites the response |
|
|
how many of our synapses are lost at puberty?
|
50% of synapses lost at puberty
|
|
|
what occurs in the maturation of excitatory synapses?
|
1. altered properties of glutamate receptors
2. stabilization of synaptic proteins 3. altered intracellular response to receptor activation |
|
|
what are some mechanisms that dampen cortical activation?
|
1. development of inhibitory circuitry can limit/control effects of excitatory input on NMDA receptors
2. changes in modulatory NT or its effects |
|
|
True or FAlse
Genetic evidence links development and other disorders to defects in brain development |
TRUE
|
|
|
what is one of the most heritable neuropsychiatric disorders?
|
Autism spectrum of disorders
|
|
|
do males or females have a higher incidence of Autism?
|
males have 4X higher incidence suggesting some variants may have X-link
|
|
|
what do family linkage studies about autism suggest?
|
family linkage studies implicate genes important for neural development (Neuroligins & neurexins)
|
|
|
what is evidence of abnormal structure/function related to Autism disorders?
|
-brain overgrowth early in development may interfere with development of connections between areas
-But possible growth arrest later because many autistic adults have reduced volume in specific cortical areas -Pyramidal cells reduces in size and dendritic branching |
|
|
what is associated with mental retardation?
|
pyramidal cells reduced in size and dendritic branching
|
|
|
What have genetic studies identified in dyslexia?
|
Family studies have identified polymorphisms in genes important for neuronal migration presumably affecting connections between visual and language centers
|
|
|
ROBO1
|
important for development of commissural connections
|
|
|
DCDC2
|
expressed at high levels in language areas
|
|
|
What do subtel abnormalities in dyslexics inidicate?
|
expression levels or pattern of expression affected but mutation is NOT complete
|
|
|
anything you know about Schizophrenia.
|
incidence 1%
believed to be polygenic, neural development disorder with late onset 30% incidence in people with deletion in chromosome 22 Mutations in DISC J which controls axon guidance and outgrowth Mutations in Neuregulin, a member of EGF family of proteins important at several stages in brain development |
|
|
what mutations are present in schizophrenia?
|
1. DISC J: disrupted in schizophrenia which controls axon guidance and outgrowth
2. Neuregulin: member of EGF family of proteins important at several stages in brain development |
|
|
what single genes are associated with mental retardation
|
Several single gene mutations
Fragile X Rett Noonan syndrome |
|
|
what causes DOWN'S SYNDROME?
|
extra copy of chromosome 21 with over expression of DSCAM, cell adhesion molecule promoting neuronal differentiation and axonal outgrowth
|
|
|
what occurs in FRAGILE-X mental retardation
|
triplet repeat in an RNA binding protein FMR1 associated with immature dendritic morphology
-cannot have many synapses |
|
|
Rett Syndrome
|
X-linked dominant with developmental regression in early childhood
Mutations in MECP2 gene which encodes for transcriptional repressor that silences methylated genes |
|
|
Lissencephaly
|
one cause of loss of function of reelin which guides neuronal migration
|
