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Lectures 7 and 8: Developmental biology

by: Rachael Couch

Lectures 7 and 8: Developmental biology NSC 3361

Marketplace > University of Texas at Dallas > Neuroscience > NSC 3361 > Lectures 7 and 8 Developmental biology
Rachael Couch
GPA 3.9

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About this Document

Organized notes in word format including information from the lectures slides and class
Behavioral Neuroscience
Van S Miller
Class Notes
behavioral neuro; neuro; behavioral neuroscience; miller; van miller; utd; nsc 3361; 3361
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This 6 page Class Notes was uploaded by Rachael Couch on Thursday February 4, 2016. The Class Notes belongs to NSC 3361 at University of Texas at Dallas taught by Van S Miller in Summer 2015. Since its upload, it has received 18 views. For similar materials see Behavioral Neuroscience in Neuroscience at University of Texas at Dallas.

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Date Created: 02/04/16
Lectures 7 and 8: Brain development Brain weight as a function of age  Brain grows quickly in the first year of life then slows down some  Growth dramatically slows down after 4/5 years old   Brain reaches maximum weight at about 20   Men have bigger brains than women because they have bigger body sizes Human brain development  3 parts of brain: forebrain, midbrain, hindbrain   Forebrain  o Becomes the largest part of the brain (90%) o Two cerebral hemispheres   Outer cerebral hemisphere = cortex  Wrinkled for increased surface area  o Ridge = gyrus (plural – gyri) o Groove = sulcus = space between gyri; CSF/water only o Smooth globe in fetus becomes wrinkled at birth to compress and increase SA  3 layers: endoderm, mesoderm, and ectoderm o Brain and the skin have the same origin  Can diagnose brain problems from a skin disorder if they have a common  origin/genetic basis o Ectoderm becomes brain plate   Starts with flat plate, rolled into sphere, crumbled to form wrinkles o In the mesoderm  Starts with notochord which becomes neural groove – long open “half­ tunnel”   Closes to form neural tube which becomes the spinal cord  Segmentation occurs  spinal segments 6 stages of development of the nervous system Neurogenesis   Mitosis of ependymal cells produces neurons and glial cells in the area next to the central  canal  Precursor (stem) cells divide to form the ventricular zone  o This process ends by about birth o A handful of stem cells survive that can still make neurons slowly   Problem – not making enough neurons (not enough materials) o Failure of neurogenesis  severe microcephaly  o Skull growth is determined by brain growth  o Zika virus  destroys neurogenesis  Different effects depending on age of acquisition of virus Cell migration   Cells move to final location (transport materials to site of new house)  Older cells leave the ventricular zone/layer forming the marginal zone o Some move back to ventricular zone to make more neurons   Movement o Radial cells are attached to the outer surface, cells climb along the radial cells  toward the surface, radial cells then release from the inner surface   Radial “glial” (precursor) cells acts as guides for cells to migrate along  This process requires kinesin  o Axons are guided by chemicals released by target cells  Growth cones are sensory­motile organelles at the tip of growing axons  and dendrites  Filopodia and lamellipodia are outgrowths of growth cones  Adhere to the local environment and pull the cone one direction  Chemoattractants are chemicals that attract certain growth cones  Chemorepellants repel growth cones  Attractants and repellants act at close or long range  Long range – attraction to a general area   Close range – physical contact attraction; trial and error  Chemoaffinity hypothesis­ each cell has a genetic chemical identity that  guides its development  Problem – Some cells don’t make it all the way  o Cells stop at wherever they make it to; once planted can’t be moved o Disorders are likely to cause brain malformations o Can cause double cortex syndrome = double band cortex  Second cortex forms where some of the cells were incorrectly dropped off o Can cause pachygria/lissencephaly  Thick gyrus – cells are too spread out, didn’t travel far enough  Microtubule malfunctioned so the cells couldn’t travel properly  o Drug that blocks kinesin function would impair migration  Differentiation   Cells become distinctive neurons (sensory or motoneurons) or glial cells  Cells in the notochord release a protein (Sonic hedgehog) that directs some cells in the  spinal cord to become motoneurons o Notochord – only there temporarily – induce cells then disappears o Induction­ the influence of one set of cells on the fate of nearby cells o Cells far from the notochord become sensory neurons  Problem – astrocytoma  Synaptogenesis   Establishment of synaptic connections  Synapses form on dendrites and spines  o Synapses form rapidly from 0 – 16 days postnatally  o At about 28 days no more synapses made   After no more synapses are being made, the neurons enlarge  o Spines proliferate after birth and connections are affected by experience o The nerve cell body increases in volume to support the dendritic tree o 11 months postnatal = about the same volume as an adult  Neuronal cell death   Selective death of some nerve cells (apoptosis); synaptic pruning  Decrease in number of synapses in the auditory, visual, and prefrontal cortexes  During synaptogenesis, couldn’t tell which synapses were good so made all possible  connections and then narrowed it down to good connections only   Process o Apoptosis starts with Ca influx that causes mitochondria to release Diablo o Diablo binds to inhibitors of apoptosis proteins (IAPs), which normally inhibit  caspases  Caspases ­ proteases that cut up proteins and DNA o Without IAP inhibition, caspases dismantle the cell o Cells “commit suicide” – shrivel up and deteriorate o Microglial cells clean up the remains   Deciding which neurons to kill.. o About 50% are killed o Neurons compete for…  Neurotrophic factors ­ chemicals that target cells make  Nerve growth factor (NGF) and brain­derived neurotrophic factor  (BDNF) are produced by targets and taken up by axons of  incoming neurons  These factors keep neurons alive or help them regrow after injury  Synaptic connections  More contacts = more beneficial – less likely to be killed   Without enough of both, they die  Some mental retardation cases are caused by this   o Can also kill only one synapse of a neuron instead of killing the entire cell   Problem  o Fragile X syndrome and autism  Failures in synaptic pruning (apoptosis)  Slightly larger brain  Brain keeps good and bad contacts o Induction of excessive apoptosis postnatally  Chronic traumatic encephalopathy – head trauma causes cell  death/apoptosis   Case of Tre – too many brain cells died  Synapse rearrangement   Loss or growth of synapses; fine­tuning  Lifelong process of updating/renovating  Sensitive period of development ­ when experience makes permanent alterations o Only early visual deprivation can lead to blindness  o Amblyopia (lazy eye)– early impairment of vision in one eye causes vision loss  in that eye  Can be caused by misalignment of the eyes (caused by the eye muscle)  Misaligned eye doesn’t fire as much   Lack of firing during development causes apoptosis of those  neurons  Can be easily fixed but if done too late (after 1  month of life), the brain  has re­wired itself and vision can be permanently lost in that eye o In the development of visual cortex, axons from each eye compete for synaptic  targets o Working eye strengthens synapses  o Covered eye loses inputs because of bad firing   Becomes permanent – neurons do not come back  o Infants with cataracts removed after 6 months have poor facial recognition later  Problems – autism, and epilepsy o Maybe also ADD, dyslexia, and learning differences? Autism Rise in diagnosis  Prevalence more than doubled from 2000 to 2010  Epidemic of diagnosis not increased disorder prevalence  Mild cases that previously would not have been diagnosed are now being diagnosed  Possibility of over­diagnosis   Becomes important to distinguish between mild, moderate, and severe o Classification based on how much it interferes with daily function Features  Communication/language o Broad range, from no verbal communication to complex skill o Two common impairments:  Delayed language  Echolalia – talk but don’t communicate   Only repeat some word in the question but don’t answer it  Lack of social interaction o Impaired nonverbal behavior o Failure to share enjoyment with others or form human contacts   Unable to empathize – low activation of frontal cortex mirror neurons o Poor eye contact  Repetitive behaviors, obsessions and perseveration o Self­injurious behavior o Rocking back and forth, pacing, tapping leg   Odd movements o Abnormal posture and movements o Repeated gestures/mannerisms o Movement disorder can be detected early o Sensory integration disorder  Using movements to stimulate senses  Ex: spinning (left to get rid of bad thoughts, right to bring in good  thoughts)  Predictability o Change in routine is stressful (change in furniture arrangement, food, TV shows) o Sometimes overwhelmed by the environment  Intellectual functioning o Autism occurs in children from gifted to retarded o Most have mental retardation – 75% have IQ below 70 o Savant syndrome is very rare  Can memorize things that normal people can’t even if they can’t read  General theory  Multiple genes implicated and environmental exposure that cause the brain to be mis­ wired  Normalizing abnormal neurons in autism  An excess of mGlu receptors alters normal synaptic signal transmission, thus disrupting  development  Treating a mouse model of fragile X syndrome with arbaclofen reduces number of  neuronal projections to normal  Neuroligin­3 knockout mice had disrupted synaptic competition and perturbed  metabotropic glutamate receptor­dependent synaptic plasticity o This could be rescued by re­expression of neuroligin­3 in juvenile mice o Treatment would have to be delivered in fetus but cannot make a diagnosis in  utero Vaccines and autism  Dozens of studies conclusively show no relation  Possibly still talked about because o Autism becomes evident about the time vaccinations are given o Success in controlling measles, mumps, diphtheria, polio has made parents  complacent o Celebrity influence: Jenny McCarthy Case studies Case: Chris  Senior playing high school football  During a game, a collision snaps his head back and he falls  Chris says he can’t move or feel anything – spinal cord injury ­ paralyzed  Chris regained only partial use of his hands, and cannot sit or walk   Over the past five seasons in Texas alone, 14 athletes have been paralyzed in a spinal  cord injury playing for their high school team  Possible treatment: spinal cord transplant  o Could replace spinal cord but can’t force it to make new connections to work o Connections are not remade because chemical (nogo) is released when  oligodendroglia are damaged that tell them not to remake o Possibly block this chemical o Works slightly but not enough for full recovery 


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