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Molecular, Systems, and Developmental Neuroscience Week 2 Notes

by: SierraMonroe

Molecular, Systems, and Developmental Neuroscience Week 2 Notes NEUR 335

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These notes cover chapter 22 in the textbook - neural circuits, development of the neural system, etc.
Molecular and Developmental Neuroscience
Vita Vock
Class Notes
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This 7 page Class Notes was uploaded by SierraMonroe on Monday February 8, 2016. The Class Notes belongs to NEUR 335 at George Mason University taught by Vita Vock in Winter 2016. Since its upload, it has received 43 views. For similar materials see Molecular and Developmental Neuroscience in Neuroscience at George Mason University.

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Date Created: 02/08/16
 MDS Neuroscience – Exam One Material Cont.  Connections form after neurons migrate o Neurons are generated first, then migrate  Neurons generate processes called “neurtites” o These become dendrites and axons  Some will extend over long distances (PNS)  Dendrite development o A process still under investigation  Current thought: complex array of intracellular and extracellulcar cues  Transcription factors o CUT, Abrupt, Spineless  Inducing molecules and receptors o BMPs, Wnts o Signaling is thought to control both dendrite length and arborization (complexity  of the dendrite structure)  A growth cone is generated at the tip of a developing axon o Is highly motile o Develops a:   “lamellipodium”  Sheet­like expansion at the tip  “fiolpodia”  Occur inside lemellipodium  Processes that extend from it  Like fingers that sense the environment o All are transient structures  How does the growth cone extend? o Rapid and controlled rearrangement of special cytoskeletal molecules  ATP­dependent process  Actin and Tubulin are components of these structures o Actin   Primary component of lamellipodia and filopodia  Regulates changes in axon shape  Found as small spikes of actin  o Tubulin   Primary component of the axon shaft  Allows for axon elongation  Microtubules rearrange/continue to stack in order to allow the axon to extend  Molecular composition of these change in an extending axon o Change from monomers (actin and tubulin) to polymers (filaments and  microtubules)  Microtubules  o Cylindrical form  Actin o 3D folded glob shape  This changing occurs via dynamic polymerization and depolymerization o Actin dynamics help orient the growth cone toward or away from a regional  substrate  Sets direction of movement o Tubulin/microtubule dynamics stabilize the axon shaft to allow movement of the  growth cone in a specified direction  Actin­ and Tubilin­ Binding proteins o Regulate assembly/disassembly of polymer units  Catalyze posttranslational modifications  Recruit enzymes  Molecular cues guide extending axons o Molecules encountered by a growth cone help it move in a specific direction at a  specific time  Use receptors and transduction mechanisms  Families of ligands and their receptors  These are extracellular pathways  Extracellular Matrix (ECM) Molecules o Are between cells o Create a structure of connections between cells o Work to chemically attract/repulse the growth cone o Laminins, collagens, fibronectin  Form polymers to create a durable surface  Bind to integrin receptors  Transductions of signals  axon growth and elongation  “Basal Lamina”  o Sheet of ECM molecules o In the PNS  Supportive substrate for growing axons  Harder to study in CNS o Helps guide axons to grow on a specific plane/direction  Cell Adhesion Molecule (CAM) and Cadherins are CAMs o Membrane­bound, both inside and outside of cells o Can function as ligands OR receptors  Hemophilic binding  bind to one another o Work through signal transduction o Some function in fasciculation   Bundling of axons as they extend  Fasciculation = the separation of smaller bundles from a larger  bundle o Cadherins help indicate a growing axons final target  Netrins o Well­characterized chemoattractants  Mutation in C. elegans (worm) Unc (uncoordinated) gene leads to  misrouted axons o Work cooperatively with Slit proteins  Netrin binds DCC receptors  Other proteins must bind with netrin in order for signal  transduction to occur o Helps guide axons that cross at the midline  Mutation in netrin­1 gene disrupts axon pathways that cross the midline  In spinal cord: ventral commissure  In cortex: corpus collosum, hippocampal commissure  Slit and Robo o Work with netrin to prevent re­crossing  Netrin attracts an axon across the midline  Slit/Robo prevent recrossing  Slit: secreted factor found just off the midline  Binds to robo receptors o System is silent BEFORE the axon crosses the midline o Terminates growth cone’s sensitivity to netrins once the  axon has crossed the midline  Semaphorins o Bound to the surface of RCM o Largest family of chemorepellents  Prevent extension of nearby axons o Receptors are plexin and neuropilin  On the growth cone 2+  Signaling leads to changes in Ca  concentration  microtubule  depolymerization  Growth cone collapses  Axon extension stops  Trophic support o Similar to chemoattraction  promotes survival of the cell o Reinforce interactions between a cell and its environment  “Topographic Maps” o Form during axon extension  Arrangement of neuronal connections such that neighboring points in the  periphery are represented at similarly adjacent locations in CNS  Found in somatosensory, visual, motor, auditory, and olfactory systems  (all of the sensory systems)  There is an organization to what is occurring at that location  Chemoaffinity Hypothesis o Describes how axons respond to molecules in their target region  Growing axons respond to gradients of cell surface molecules  Is how axons grow to form a topographic map o Was tested by Roger Sperry (guy who tested Organizer region)  Pioneering work  Showed that Retinal Ganglion Cell (RGC) axon terminals form a  precise topographic map o Step 1: crushed optic nerve and let it regenerate  Axons grew to original locations o Step 2: rotated the eye 180 degrees and repeated step 1  Axons still grew to their original locations o Avian experiments found additional cues  Ephrins (ligand) were found  Chemo attractant  Bind to Eph receptors o Have complementary gradients  Anterior vs. posterior tectum  Similar levels of ligand and receptor in these  locations o Disruption of genes encoding for ephrins or eph receptors  lead to disorganized projections  After reaching targets, axons form connections o determine  which cells they will form synapses with  Sets of molecules control synapse function o Which cells and who with? o “relative promiscuity”   Neurons making synaptic connections have many options  Initial contact via local recognition of membrane bound molecules o Cell adhesion molecules (CAMs)  Same molecules that help axons find their way, help them make  connections  Cadherins  Protocadherins  After initial contact, other molecules activate synaptic machinery o Presynaptic terminal  Synaptic vesicles, docking proteins, fusion molecules o Postsynaptic density (PSD)  Neurotransmitter (NT) receptors, ion channels, signaling pathways  2 adhesion molecules are found in the immature synaptic machinery o Neurexin – in presynaptic membrane 2  Synaptic vesicles, docking proteins, fusion molecules, voltage­gated Ca   channels o Neuroligin – in postsynaptic membrane  NT receptors & ion channels  3 varieties of synapse o Axodendritic  axon­dendrite o Axosomatic  axon­cell body  modulates activity of cell body o Axoaxonic  axon­axon  Survival of an early synapse is supported by target o Trophic interactions occur  Life support of a neuron  Receive stimulation/molecular feedback from the tissue they are targeting  Cellular manners in which a neuron is strengthened o Receive molecular signals from the target cell  Motor neuron survival in chick embryo: an example of trophic support o Depends on signals from the limb bud  Remove bud  dramatic reduction in number of motor neurons going to  that site  Add extra bud  neurons that would normally be pruned (apoptosis) are  maintained  Apoptosis = programmed cell death (pruning) o Occurs in neurons that don’t share trophic signals with their targets  they do not  receive the molecules that maintain the relationship o Highly regulated  Trophic interactions also modulate synaptic connections after birth o Modify/eliminate certain synapses to create functional circuits o Ex: the neuromuscular junction in some muscles of autonomic nervous system  Initial innervation is polyneuronal o Before birth, each target muscle fiber is innervated by axons from multiple motor  neurons  more innervation than necessary for muscle use o After birth, inputs are lost (selection/competition) until 1 motor neuron innervates  1 fiber  What determines axon/synapse survival? o Patterns of activity in pre­ and postsynaptic elements mediate the competition  Apply curare (Ach receptor antagonist) or tetrodotoxin (TTX)   polyneuronal innervation maintained  There is no withdrawal of axon – no pruning  Dying synapses undergo certain changes o Axons from these motor neurons go into a downward spiral of synaptic efficacy  NT receptors are lost  Ion channels and signaling proteins are lost  Presynaptic terminal withdraws  axon retracts back into its parent  terminal  Trophic factors regulate shape of the axon terminal as well as dendritic branches o Certain trophic factors lead to elaboration and growth of dendrites o Creates intricate branched patterns of dendrites  “arborization” o Neurotrophins: molecules that regulate differentiation, survival, and growth of  neurons  Nerve Growth Factor (NGF) = first neurotrophin discovered o Found in 1950’s o Causes massive outgrowth of neurites o mRNA isn’t seen in target tissues – gene product is not activated/present – until  they are innervated by neurons  NT must be released in order for the synapse to be considered functional o Other neurotrophins:  Brain­derived neurotrophic factor (BDNF)  Neurotrophin­3 (NT­3)  Neurotrophin­4/5 (NT­4/5)  Other molecules with neurotrophin­like functions  Ciliary neurotrophic factor  Lekumia inhibitory factor  Glial­derived growth factor  o Provide trophic support to muscles  Neurotrophins and Neurogenesis o Vast majority of neurons in the mammalian brain are generated prenatally o Certain regions can continue to establish new neurons through adulthood  Rare  Very strong neurotrophic signaling in these areas  Occurs in:  Hippocampus  Olfactory bulb   Neurotrophic signaling does not ALWAYS result in survival of the neuron  2 classes of Neurotrophin receptor: o Tyrosine receptor kinase (Trk)  TrkA binds NGF  TrkB binds BDNF, NT­4/5  TrkC binds NT­3  Neurite outgrowth  Cell survival o P75   Bind unprocessed forms of all 4 receptors  Cell cycle arrest  Cell death  Clinical implications of axon guidance disruption o Disruption results in anatomical and behavioral consequences  Can be mild to severe o Axon Guidance Disorders  Gene mutations  Can affect growth cone pathfinding and axon extension 


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