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585-3
Injury Response & Regeneration/ Memory & Learning
| Term | Definition |
|---|---|
| secondary damage | After the initial injury Will happen regardless of how you got the initial injury More profound in stroke, TBI, and SCI |
| secondary injury processing | Hemorrhagic necrosis Ischemia Excitotoxicity Progressive necrosis Transneuronal degeneration Cystic cavitation/ glial scar Demyelination |
| hemorrhagic necrosis | Blood crosses blood-brain barrier Leads to inflammatory response & edema since blood is toxic to CNS T-cells release toxic cytokines that breaks down tissue. T-cells aren't used to neural tissue and think its bad thing |
| ischemia vs. transneuronal degeneration | No longer getting blood supply to brain area Difficult to maintain metabolic process when area lacks O2 and nutrients vs. Spread of damage to connected neurons |
| excitotoxicity | Physical injury to neurons causes neurons to release a surge in AP Release a bunch of glutamate which astrocytes can't clean fast enough Many O2 free radicals also released, NS can't handle it |
| progressive necrosis | Macrophages & microglia invade to clean Many cytokine release happens which break down nearby tissue as well |
| cystic cavitation/ glial scar | Microglia digests dead cells and we get a void We create a barrier out of astrocytes to prevent spread The bigger the area, the more time is needed to create a scar of astrocytes |
| demyelination | Oligodendrocytes can branch to multiple axons for myelin supply If oligodendrocyte is in zone of death, those attached axons are demyelinated Healthy neurons can't get AP signals to other neurons |
| glial scar | Made to encase the injury to ensure it doesn't spread Astrocytes pack together tightly & form a glue of CSPG that helps hold it together Chemical inhibitors and the wall prevent neuronal growth into dead zone |
| chemical inhibitors | CSPG Semaphorin Ephrin |
| regeneration of PNS axons | Can regenerate & restore function, due to wear & tear Grow 1-4 mm/day Sensory is better than motor recovery due to motor end plate complexity Pain recovers 1st due to free nerve endings Crush & partial heal faster |
| PNS environment factors | Schwann cell tunnel stays to allow guidance Glial scar not formed Sheath has chemoattractants NGF, BDNF, NT3, NT4 released Not perfect, need motor relearning often |
| 1. NGF 2. BDNF 3. NT3, NT4 | 1. Big increase by tissue that lost innervation 2. Increases with anything that you do, growth promoter for everything 3. Upregulated in PNS |
| approaches to promote CNS regeneration | Breakdown glial scar Fill cavity w/ permissive env Neutralize oligodendrocyte myelin growth inhibitors Provide cues & sprouting Spared fibers Remyelination Prevent 2ndary damage |
| breakdown glial scar vs. fill cavity with permissive environment | Chondroitinase breaks down glue Leaves large gap behind vs. Fill w/ Schwann cells & olfactory ensheathing cells Neurons now have to cross large distances to get to target |
| neutralize oligodendrocyte myelin inhibitors vs. provide guidance | anti-NOGO is used to allow free growth of stuff Has promoted growth of tumors vs. Combine breaking down the scars & using promoting molecules Some success |
| take advantage of spared fibers vs. remyelination | Promote collateral sprouting of existing tissue using rehab techniques & GF Some non-functional movement restored vs. Very mild remyelination, not thick enough |
| preventing secondary damage | Inject chondroitinase into spinal cord immediately after injury Lack of scar means injury spreads Working on slowing secondary damage should be target |
| learning vs. memory | Acquiring new information vs. Storage & recall of learned information |
| declarative memory | Conscious recall Ability to recall information like facts & events Occurs in medial temporal lobe (hippocampus), diencephalon |
| non-declarative memory | Not conscious Procedural memory- muscle memory, skills & habits, occurs in striatum Conditioned memory- skeletal musculature (cerebellum), emotional response (amygdala) |
| procedural learning/ memory studies | Easy to train, measure, observe Can involve simple circuits, easier to pinpoint the mechanisms |
| non associative vs. associative | No association between event & behavior (habituation & sensitization) vs. Events are being associated with change in behavior (classical & operant conditioning) |
| habituation vs. sensitization | Response decreases w/ repeated exposure to stimulus vs. Stimulus that has increased responsiveness because of previous unrelated event |
| operant conditioning | Using rewards to reinforce behavior that you wish to see Very powerful behavior modification Can train very complex behaviors |
| gill withdrawal reflex | Touch to siphon will cause the gill to retract Protective reflex 2 neuron system, very simple |
| habituation & aplysia | Decreased gill withdrawal reflex W/ repeated stimulation to siphon, less Ca in presynaptic neuron has less flow due to high conc of Ca in cell Synaptic vesicles less activated which means less NT release (less glutamate) |
| sensitization & aplysia | Increased gill withdrawal reflex Sensitizing event is bonk to the head Neuron from head synapses onto sensory neuron Sensitizing neuron releases 5HT which binds to G-protein coupled receptor Activates kinase A, which deactivates K channels |
| deactivated K channels means | Ca channels stay open longer More Ca into cell More synaptic vesicles More NT Bigger response |
| long term nonassociative learning- habituation | Drop in synapses being formed Presynaptic neuron wants collateral sprouting while post synaptic neuron inhibits sprouting |
| long term nonassociative learning- sensitization | Increase in synapses being formed Both pre- and post-synaptic neurons want sprouting to occur |
| classical conditioning & aplysia | Pairing unconditioned & conditioned stimulus together We see a much larger response Ca amps up cAMP which shuts down K channels Ca channels stay open longer, more Ca into cell, more vesicels, more NT cAMP is more effective than kinase A |
| take home messages from aplysia | Learning & memory can result from modifications of synaptic transmission Synaptic modifications can be triggered by conversion of neural activity into intracellular messengers Memory can result from alt in existing synaptic proteins |
| cerebellum as a model | Well studied for motor learning Involved in adjusting movements based on detected errors (large sensory & motor inputs into cerebellum) Unique anatomy |
| Purkinje fibers vs. climbing fibers | Main output cell of cerebellum, gaba-ergic (uses NT GABA) vs. 1:1 relationship with purkinje cells, makes 100s of synapses onto that single Purkinje cell. Input of somatosensory feedback of periphery |
| parallel fiber | Makes single synapse onto a single purkinje cell Input from mossy fibers, what we intend to do with movement |
| how we detect errors | Proprioceptors indicate movement that occurred, mossy fibers indicate movement that was expected Plasticity of parallel & Purkinje synapse adjusts motor coordination to adjust for errors |
| long term depression | Suppressed amplitude of EPSP for at least 1 hour |
| climbing fiber process vs. parallel fiber | Glutamate binds to Na channel on Purkinje cell, causes EPSP Activates voltage gated Ca channels vs. Release glutamate which binds to AMPA (EPSP cause). Also activates G protein coupled receptor that activates PKC |
| long term depression process for Purkinje cell | Both cells fire together PKC will now be influenced by presence of Ca PKCs job is to block AMPA receptors on parallel- Purkinje side Every EPSP from parallel will now be blocked |
| learning vs. memory in cerebellum | Occurs when climbing fiber & parallel fiber active simultaneously vs. Occurs when AMPA receptors are removed. |
| why does LTD occur in cerebellum | If both climbing fiber and parallel fiber fire together, then Purkinje cell will be unlikely to fire from subsequent parallel inputs. We did the movement correctly, and don't need to get extra thinking for the movement now. |
| 1. entorhinal cortex 2. dentate gyrus 3. CA3 cells | 1. Provides input via perforant path to dentate gyrus 2. Give rise to mossy fibers that synapse on cells in CA3 3. Provide Schaffer collaterals that synapse onto CA1 neurons |
| LTP in hippocampus | Glutamate binds to AMPA receptor, depolarize CA1 Glutamate also binds to NMDA receptor (Ca channel) NMDA will only open if neuron is depolarized to certain level (ligand & voltage gated) Ca will enter & activate kinases |
| Kinase role in hippocampus | Increase conductance of AMPA (more Na in) Insert new AMPA receptors into membrane |
| LTD in hippocampus | Same process as LTP But there are lower levels of Ca, which causes activation of protein phosphate Phosphatase will decrease amount of AMPA |
| injecting swimming rats with NMDA receptor blocker | Prevents rats from learning the task |
Created by:
craftycats_
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