Lectures 7 and 8: Developmental biology
Lectures 7 and 8: Developmental biology NSC 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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