Med Neuro Lect2 Neuronal Mechanisms Part 1
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| show | surrounds the nueron, contains:
1.fibers.
2.Dendrites.
3.Lots of BV.
**Doesn't show up well on a Nissl Stain.
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| show | YES
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| show | 1.Axon.
2.Dendrites.
**Nissl stain stains ER purple.
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| show | Guide proteins once they are properly folded and translated.
**Very important in neurons due to the high level of protein folding, trafficking, and packaging occuring.
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| What happens to protein aggregates that are mis-folded or start to build up within the cell? | show 🗑
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| show | 1.Demyelination (Charcot-Marie-Tooth Syndrome: most common, hereditary, affects PNS).
2.Degeneration (Alzheimer's: build up of non-fnc protein in CNS neurons).
**Build up due to lack of processing of proteins. These lead to cell death.
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| show | Found in growing tips and dendritic spines. Involved in movement.
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| Where will you find Micortubules? what are they involved in? | show 🗑
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| Are Microtubules involved in the spindle apparatus in neurons? | show 🗑
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| show | Found mainly in axons
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| show | 1.Tubulins.
2.MAPs (create hooks on microtubules allowing them to interact).
3.MMPs (Kinesin & Dynein which are motor proteins mediating transport).
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| 2 directions of Axonal transport? what MMP is used for each | show 🗑
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| show | If they are picked up from the periphery extracellular fluid during vesicular endocytosis, they can be transported to the soma via RETROGRADE transport.
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| show | Used to transport structural proteins.
**ANTEROGRADE ONLY
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| Fast Axonal transport | show 🗑
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| Causes of Plaques and Tangles seen with Alzheimer's? what do they do? | show 🗑
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| What occurs in a cytoskeletal disease | show 🗑
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| 3 main components of Neuronal Metabolism | show 🗑
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| 3 main areas of high concentrations of mitochondria & metabolism within the neuron | show 🗑
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| Mitochondria's role in Ca buffering | show 🗑
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| show | Excitotoxicity can occur which leads to OXIDATIVE STRESS: productions of large amounts of free radicals which dissolves the cell internally cuases Apoptosis.
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| Mitochondrial Permeability Transition (MPT) Pores | show 🗑
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| show | 1.Alzheimer's (CNS).
2.ALS (PNS)
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| show | 1.Olfactory Bulb.
2.Hippocampal Formation.
**Difficult to re-grow due to complicated shape. This is the reason why there are NOT a lot of primary neuronal tumors.
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| show | synaptic connections
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| What determines the way a neuronal cell works? | show 🗑
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| Dendritic domains: Purkinje cell | show 🗑
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| Dendritic domains: Pyramidal (cortical) cell | show 🗑
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| Are all axons covered in something? | show 🗑
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| Are axons tapering or non-tapering? | show 🗑
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| 2 types of axonal distribution | show 🗑
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| Is size of the axon related to it's conduction velocity? | show 🗑
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| show | Seen in dendrites b/c they are tapering. it is the degradation of a signal b/c it is not self propagating.
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| show | Cluster of like minded neurons in the brain that project their axons to another nucleus elsewhere
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| show | Mapping of neurons from one nucleus to another.
**This can be used to locate lesions causes specific sensation loss.
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| 3 main locations of synapses | show 🗑
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| show | NO, NON-peptide neurotransmitters are produced in the terminal itself.
**Vesicle and Peptide come from the soma
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| What is responsible for opening V-gated Ca+ channels in the axon terminal and thus vesicular movement? | show 🗑
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| show | 1.Docking (moving vesicle to pre-syp mem).
2.Priming (Adding ATP).
3.Fusion/Exocytosis (Ca influx hydrolyzes ATP).
4.Endocytosis (brings in some extracellular fluid which could contain viruses).
5.Recycling.
**SNARE proteins involved in 1 & 2.
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| Where is Endocytosis of the vesicle particularly problematic? | show 🗑
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| show | 1.Ionotrophic (nicotinc): Ion channels that are very fast response but short lasting.
2.Metabotrophic (Muscarinic): associated w/ secondary messangers, much slower but last longer
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| Which post-synaptic receptor has the more powerful effect? | show 🗑
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| show | 1.D1: Inc cAMP causing Satiety.
2.D2: Dec cAMP causing Craving.
**Reinforces behavior and leads to addiction. Cocaine blocker re-uptake of dopamine which leads to prolonged satiety, also causes strong craving.
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| show | YES. They uptake glutamate at glutaminergic synapses.
**defective glial cells may impair neurotransmitter re-uptake which would cause overstimulation.
**ALS could be treated with INC glial cell activity.
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