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Stack #4546225
neuro 2 more
| Term | Definition |
|---|---|
| tactile function | |
| type of affereant response | |
| location | |
| afferant fibers and stumulis | |
| Neuroplasticity | a change in the nervous system over time |
| where does neuroplasticity occur | apoptosis, pruning,synpatic strenghth, geomic plasticity |
| Habituation is the | reduced response to a repeated, benign stimulus |
| Sensitization is the process by which a | repeated or intense stimulus leads to an increased response in the nervous system |
| Receptor desensitization | a change in postsynaptic response to a stimulus |
| Henry Molaison (long term changes) | Classic case study that demonstrated hippocampus role in declarative memories |
| Long-term potentiation (LTP) is a | permanent increase in the strength of a synapse in response to a pattern of stimulation |
| Long-term depression (LTD) is a | decrease in the strength of a synapse in the absence of stimulation |
| Silent Synapses | Fail to evoke a detectable post synaptic signal • Become functional with AMPA |
| Duplication in MeCP2 gene causes | autism and autism-like disorders |
| Autism Spectrum Disorder (ASD) | developmental disability caused by differences in the brain |
| Excitatory synaptic changes rely on | AMPA and NMDA receptor activation, |
| Injuries to your peripheral nervous system include | sensory, motor, and autonomic |
| injuries to central nervous system include | truamatic brain injury, stroke, and spinal cord |
| examples of a primary injury | hemmorage, neruonal and axonal injury, BBB injury |
| examples of secondary injury | inflammation, demyleination, endema, oxidative stress |
| exampels of neurological defects | loss of function, congnitive decline,chronic dissability |
| Excitotoxicity Cascade | Excess glutamate overstimulates NMDA/AMPA receptors → excessive Ca²⁺ influx |
| Wallarian degeneration in axons | myelin degeneration Debris removal Soma reorganization Dendrite retraction |
| CNS does not regenerate | Myelin-Associated inhibitors |
| When neuron loses some or all synaptic INPUT | Post-synaptic plasticity, existing receptors become more responsive |
| PNS vs CNS injuries: | Peripheral nerves can regenerate, while central nervous system injuries (TBI, stroke, SCI) show limited repair. |
| Primary vs secondary injury | Primary injury is immediate trauma; secondary injury involves ischemia, edema, and ionic imbalance |
| Adaptive plasticity: | Neurons adjust through denervation hypersensitivity |
| developmental stages | fertilization (blastua and gasturlation) 2 weeks Nuerlation and Nueral tube - 2-4 weeks vesticle development 4-8 weeks ventricular system 4-8 spinal 4-8 somite 4-8 |
| nencephaly is the absence of | brain, skull, or scalp when rostral neural tube fails to close |
| Spina bifida occurs when | caudal end fails to close |
| Timothy Syndrome (rare) | Mutation in CACNA1C gene – L-type voltage gated calcium channels • QT-prolongation • Syndactyly • Autism spectrum disorders |
| Somatosensory system integrates | tactile and proprioception |
| Dorsal column/medial lemniscus DC/ML | discriminative touch, vibration, proprioception • Mechanoreceptor dependent |
| rapidly adapting | phasic |
| slowly adapting | tonic |
| Receptive field | area of sensory field that can activate sensory receptor |
| Dermatome | area of body innervated be each spinal nerve |
| receptive fields for discriminative touch are | small and non-overlapping. |
| Dysfunction of DC/ML | Causes of proprioception impairment • Aging • Injury (peripheral or CNS) |
| All plastic changes to the nervous system involve alterations in responses to | sensory stimuli |
| One neurological disorder where habituation is a standard treatment is | tactile defensiveness |
| The cellular level mechanism that results in habituation is | receptor desensitation |
| LTP is a | permanent increase in the strength of an excitatory synapse |
| When axon damage occurs, the neuron goes through a sequence of changes known as | Wallerian degeneration |
| ssuming a neuron survives damage and recovers from Wallerian degeneration, it may try to regrow its damaged axon or try to compensate for its loss in a process involving extension of processes seen in | sprouting |
| PNS neurons transplanted to the CNS cannot regenerate axons, whereas | CNS neurons placed in the PNS can regenerate axons |
| Thus, regenerative sprouting, or the regrowth of damaged axons | occurs in the PNS but is largely inhibited in the CNS |
| CNS trauma results first in mechanical injury to the neurons due to mechanical forces from the trauma itself. This is the | primary injury |
| However, the initial damage can be further exacerbated by the response to injury in a process called | secondary injury |
| Edema can compress axons, which can prevent | action potential propagation |
| enervation hypersensitivity, works | exactly opposite to the ways neurons decrease signaling either by receptor downregulation or desensitization |
| he presynaptic neuron that has lost some of its axonal branches may also display compensatory changes to maintain the same amount of neurotransmitter released to the postsynaptic cell as before the injury. This is called | synaptic hypereffecivenesss |
| When there is a much higher than normal release of glutamate, there is a large influx of | calcium into the postsynaptic cells. |
| Free radicals can cause | DNA mutation and damage to cellular membranes and protein |
| totipotent, | being capable of generating all the types of cells found in the human body given the appropriate chemical signals |
| gastrula is formed around the | 14th day of development |
| endoderm forms the | internal organs |
| the mesoderm forms the | tissues, skeletal muscles, bone and blood |
| the ecoderm forms the | lining of organs, nervous system, |
| The vast majority of development of nervous system structures occurs in the | embryonic system |
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ecoesfeldd