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CBNS 121 Exam with complete solutions latest version.pdf, Exams of Neuroscience stages in targeting - ANSWER-defasciculation (axons gathering together)
- branching
- topographic mapping (creates boarder)
- connect to targets innervation caused by balance of attracting / repulsive cues - ANSWERshifting the concentration of attraction and repulsion cues can enhance the desired state of innervation sympathetic innervation of neutrophins - ANSWERNT3 can cause cell innervation, without NT3 theres no innervation of sympathetic cells neurotrophins - ANSWERpromotes cell growth and survival semaphorins - ANSWERsuch as sema3A is a repulsion cue that keeps targets out of the target region (found in the ventral cord)
sema3A knockout in the SP - ANSWERallows sensory neurons to enter the dorsal cord target selection is achieved by what factors - ANSWER-attractive (NT3) and repulsive (sema3Z) cues
- branching and defasciculation topographic mapping - ANSWERordered representation of the world inside the NS, it creates neuroanatomy Frog experiment - ANSWERinverting the eye disrupted the visual mapping of the world inside the frogs NS purpose of complimentary gradients in topographic mapping - ANSWERthese opposing gradients guide the axons and show them where to reside chemo affinity and repulsion - ANSWERwithin the A-P axis these cues are what the axons recognize inside the gradients mentioned earlier (flipping the frogs eye, flipped these gradients and therefore flipped his visual representation) in A-P topographic mapping - ANSWERits created by contact mediated repulsion, ephrin molecules stops neurons from passing their target location via ephrin A ephrins in A-P mapping - ANSWERhigher concentrations increase the POSTERIOR region of the superior colliculus, without ephrins axons would go past their target region
how target cells play a role in survival - ANSWERwhen there are more target cells in a growing embryo, cell death decreases, (due to a survival factor existing in target regions) what happens when you reduce the amount of target cells - ANSWERcell death increases neurotrophic hypothesis - ANSWER-neurons must require target-derived trophic factor
- this factor is limited in the target neurotrophic predictions that determined to be required - ANSWER-it prevents death
- present in the target
- effective on the axons dendritic tips (retrogradely) neuron growth factor (NGF) - ANSWER-sufficient and required for sympathetic growth (SG) survival
- can enhance growth and survival rates NGF's effects on nerve terminals (retrograde behavior) - ANSWERNGF applied at the dendrites increased survival compared to neurons w/o it which resulted in cell death when is NGF's survival signal activated - ANSWERwhen it bind to its receptor, TrkA
neurotrophins and their receptors - ANSWEReach neurotrophin binds to a specific receptor with high affinity, eliminating the receptors increase the death rate in their designated region list of neurotrophins and their receptors - ANSWERNGF---> TrkA NT3--->TrkC BDNF---> TrkB p75NTR - ANSWERthis receptor has low affinity binding (to proNGF) & can bind to many protein types, because of this it can promote survival or death p75NRT binding that results in survival or death - ANSWERif it bind to NGF= promotes survival it it binds to proNGF= promotes PCD extrinsic apoptotic pathway - ANSWERuses ligand & receptor bind to initiate a signal cascade for apoptosis intrinsic apoptotic pathway - ANSWERcytochrome-c is released from the mitochondria to activate caspace 9 for protein cleavage microglia's role in apoptotic process - ANSWER-they clean up the apoptotic body residues
- derive from the mesoderm
- they use phagocytosis to clean up dying neurons
- they eat & digest the dying nerve cells
adhesion and increase in transmission - ANSWERthe longer the muscle and GC are in contact with each other, stronger currents result from ACh clustering AChR clustering - ANSWERinduced by contact with the spinal neurites how are AChRs clustered - ANSWERmotor axons release signal into the matrix, this clusters the receptors to one region under the basal lamina basal lamina components - ANSWERcutting / destroying the axons leaving only the basal lamina (w its matrix molecules) were able to grow new myofibers were AChR clustering took place under the lamina agrin - ANSWERAChR clustering signal released by the motor axons Agrin, MuSK, Rapsyn ---> AChR clustering - ANSWERagrin binds to a receptor complex (complex has Lrp4 & MuSK), Dok-7 required for agrin-musck activation causes phosphorylation of AChR and then AChR clustering regulation of AChR density in the NMJ - ANSWERmotor activity affects the clustering of receptors, during active transmission the receptors are tightly clusterd, during inactivity (no NT release/ no transmission) the receptors disperse how are receptors clustering during active state transmission - ANSWERCa++ influx during transmission activates CamKII and this suppresses them receptors to one spot, myogenin is the +P transcription factor that blocks synaptic transcription
how are receptors clustering during inactive state transmission - ANSWERno transmission = no Ca++ so CamKII isn't activated to inhibit synaptic transmission on the nuclei which allows the AChR to move around competing pathways for clustering - ANSWERAggregation Signal
- agrin-musk increases e-AChR subunit and mediates aggregation Dispersion Signal
- Cdk5 activation (by Ca++) leads to aggregation musk pathway inhibits - ANSWERdispersal signal AChR activity inhibits - ANSWERtranscription purpose of the scaffold protein - ANSWERbinds to the receptor to cluster onto the postsynaptic side postsynaptic scaffold clustering in the inhibitory synapses - ANSWERGABAergnic synapses
- NRXN binding to NLNN2 can influence GABA aggregation GABARs with a2-subunit - ANSWERinteracts with gephyrin GABARs with y2-subunit - ANSWERcan cluster with gephyrin by unknown proteins
