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Med Neuro Lect2
Med Neuro Lect2 Neuronal Mechanisms Part 1
| Question | Answer |
|---|---|
| Neuropil | surrounds the nueron, contains: 1.fibers. 2.Dendrites. 3.Lots of BV. **Doesn't show up well on a Nissl Stain. |
| Does a neuronal soma contain all the organelles seen in a typical mammalian cell? | YES |
| What structures are stained jet black by the Golgi stain | 1.Axon. 2.Dendrites. **Nissl stain stains ER purple. |
| Chaperone Proteins | 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. |
| What happens to protein aggregates that are mis-folded or start to build up within the cell? | Ubiquitin is added to them and they are escorted to a proteosome to be degraded. **Problems with this or protein build up in general can cause Deposition Diseases |
| 2 main types of Deposition diseases? (give example of each) | 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. |
| Where will you find Micorfilaments? what are they involved in? | Found in growing tips and dendritic spines. Involved in movement. |
| Where will you find Micortubules? what are they involved in? | Found in axons, dendrites, and the soma. Involved in transporting and organizing. |
| Are Microtubules involved in the spindle apparatus in neurons? | NOOO, they don't divide and therefore do not form spindle apparatuses. |
| Where will you find Intermediate filaments? | Found mainly in axons |
| 3 main types of Microtubules | 1.Tubulins. 2.MAPs (create hooks on microtubules allowing them to interact). 3.MMPs (Kinesin & Dynein which are motor proteins mediating transport). |
| 2 directions of Axonal transport? what MMP is used for each | 1.Retrograde: Uses DYNEIN to move from the synaptic terminal to the cell body. 2.Anterograde: Uses Kinesin to move from the cell body to the synaptic terminal. |
| How can viruses infiltrate neurons? | If they are picked up from the periphery extracellular fluid during vesicular endocytosis, they can be transported to the soma via RETROGRADE transport. |
| Slow Axonal transport | Used to transport structural proteins. **ANTEROGRADE ONLY |
| Fast Axonal transport | Used to transport synaptic related proteins. **Can be antero or retrograde. |
| Causes of Plaques and Tangles seen with Alzheimer's? what do they do? | 1.Plaques: Build up of amyloid protein. 2.Tangles: Build up of Tau proteins. **1&2 cause cell death and brain atrophy bc they tie up cytoskeleton of the cell. |
| What occurs in a cytoskeletal disease | Proteins are abnormally phosphorylated which ties the cytoskeleton together. |
| 3 main components of Neuronal Metabolism | 1.Oxidative Phosphorylation. 2.Decomposition of glucose to CO2 & H2O. 3.Energy is used to form NADH & ATP. |
| 3 main areas of high concentrations of mitochondria & metabolism within the neuron | 1.Soma. 2.Dendrites. 3.Axon terminal (Synaptic endings). |
| Mitochondria's role in Ca buffering | During high cellular [Ca+] levels, Mitochondria can absorb excess Ca to prevent extreme excitation (Excitotoxicity) within the neuron. |
| What happens if the Mitochondria is unable to effectively buffer high Ca levels? | Excitotoxicity can occur which leads to OXIDATIVE STRESS: productions of large amounts of free radicals which dissolves the cell internally cuases Apoptosis. |
| Mitochondrial Permeability Transition (MPT) Pores | Serve as a Ca+ sink from the mitochondria. Normally they are transiently opened during cell signaling. **High [Ca] will cuase permanent opening leading to apoptosis from hypertonic swelling. |
| What diseases would you see permanent openings of MPT pores? | 1.Alzheimer's (CNS). 2.ALS (PNS) |
| What are the only 2 locations of Adult neurogenesis in the CNS? | 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. |
| What occurs at dendritic spines? | synaptic connections |
| What determines the way a neuronal cell works? | Shape of the Neuronal Dendritic Domain. |
| Dendritic domains: Purkinje cell | Found in the cerebellar cortex: Elaborate dendritic tree with a flat domain. |
| Dendritic domains: Pyramidal (cortical) cell | Found in the Cerebral cortex. Has a spine studed apical dendrite & lots of basal dendrites. **Apical dendrite can extend across multiple layers which can then integrate all that info. |
| Are all axons covered in something? | YES. Myelinated or non-myelinated, they are still wrapped in something. **Myelin covers K+ channels which leads to a stronger depolarization at the nodes of Rhanvier |
| Are axons tapering or non-tapering? | NON. **Dendrites are tapering b/c the signal dissapates as it moves along. |
| 2 types of axonal distribution | 1.Type I (Projection neurons): travel a longer distance to somewhere other than the brain. 2.Type II (local, circuit, interneurons): stay within the brain and CNS. |
| Is size of the axon related to it's conduction velocity? | YES. The larger the axon, the more myelin wrapping (thicker) and thus the faster the conduction velocity. |
| Electrotonic Spread | Seen in dendrites b/c they are tapering. it is the degradation of a signal b/c it is not self propagating. |
| In terms of neurons and axons, what does a "Nucleus" refer to? | Cluster of like minded neurons in the brain that project their axons to another nucleus elsewhere |
| Topography | Mapping of neurons from one nucleus to another. **This can be used to locate lesions causes specific sensation loss. |
| 3 main locations of synapses | 1.Axosomatic (synapsing onto a neuronal soma). 2.Axodendritic Shaft synapse. 3.Axodendritic Spine synapse. |
| Are all neurotransmitters produced in the soma and moved to the axon terminal via anterograde movement? | NO, NON-peptide neurotransmitters are produced in the terminal itself. **Vesicle and Peptide come from the soma |
| What is responsible for opening V-gated Ca+ channels in the axon terminal and thus vesicular movement? | ELECTROTONIC spread. **Not and AP |
| 5 stages involved in vesicular release and recovery | 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. |
| Where is Endocytosis of the vesicle particularly problematic? | Neuromuscular junctions. That extracellular fluid is exposed to body fluid so viral uptake is more likely. **Polio |
| 2 main types of post-synaptic receptors | 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 |
| Which post-synaptic receptor has the more powerful effect? | Metabotrophic. **Can affect metabolism & muscarinic receptors. |
| Specific Dopamine receptors and their effects? | 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. |
| Are Glial cells involved in the re-uptake of neurotransmitter? | 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. |
Created by:
WeeG
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