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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cajal described both the morphology and plasticity of neurons. He summarized the structure of neurons as composed of membrane, protoplasm, Golgi apparatus, nucleus, spongioplasm and neurofibrils (cytoskeleton). He initially considered the cytoskeleton as absorbing excitation energy and forming a "conductive pathway in the protoplasm" within the neuron. Later, he viewed the neurofibrillary threads as independent, living entities and called them neurobiones. Cajal recognized neuroplasticity in development, memory, sleep, injury and dementia, as well as after exposure to cold and starvation. He noted cytoskeletal changes during these events. However, he did not causatively connect the plastic changes in neurons with the changes in cytoskeleton. Finally, Cajal proposed a theory of chemoaffinity in 1892, and modified his neurotropic theory over the next 40 years. Today we accept that changes in the cytoskeleton produce changes in neuronal morphology. The properties of the cytoskeleton and neurobione as described by Cajal are similar to those of microtubules. These long intraneuronal neurofibrils are polymers of the protein tubulin and, whilst not being living entities, are highly dynamic, sensitive to environmental stimuli, and stabilized by microtubule associated proteins (MAPs). Furthermore, Cajal was very specific in his characterization of the neurotropic factor derived from Schwann cells. Initially, he thought the chemicals attracted the axonal fibers, but later he wrote that the factor was not attractant but rather was involved in assimilation, growth and ramifications. The neurotropic hypothesis described by Cajal in Degeneration and Regeneration in the Nervous System is more similar to a neurite extension factor (NEF) than to a neurotrophic growth factor or specific chemoaffinity (attractant) molecule. S-100 beta is the major NEF found in PNS Schwann cells and CNS astroglial cells. In summary, the views of Cajal on neuroplasticity, its frequency and function, agree with the modern hypothesis of neuronal instability. This concept states that MAPs regulate microtubule stability by a S-100 beta sensitive phosphorylation processes. Serotonin, by acting on the astroglial 5-HT1A receptor, releases S-100 beta and regulates neuronal morphology and apoptosis. This neuronal-glial connection provides a fresh view for linking neuroplasticity, mental illness, and memory with changes in the cytoskeleton.
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PMID:Cajal's hypotheses on neurobiones and neurotropic factor match properties of microtubules and S-100 beta. 1214 7

It has been indicated that the Golgi apparatus contributes to autophagy, but how it is involved in autophagosome formation and maturation is not well understood. Here we show that amino acid starvation causes trans-Golgi derived membrane fragments to colocalize with autophagosomes. Depletion of the Golgi stacking protein GORASP2/GRASP55, but not GORASP1/GRASP65, increases both MAP1LC3 (LC3)-II and SQSTM1/p62 levels. We demonstrate that GORASP2 facilitates autophagosome-lysosome fusion by physically linking autophagosomes and lysosomes through the interactions with LC3 on autophagosomes and LAMP2 on late endosomes/lysosomes. Furthermore, we provide evidence that GORASP2 interacts with BECN1 to facilitate the assembly and membrane association of the phosphatidylinositol 3-kinase (PtdIns3K) UVRAG complex. These findings indicate that GORASP2 plays an important role in autophagosome maturation during amino acid starvation. Abbreviations: ATG14: autophagy related 14; BafA1: bafilomycin A1; BSA: bovine serum albumin; CQ: chloroquine; EBSS: earle's balanced salt solution; EM: electron microscopy; EEA1: early endosome antigen 1; GFP: green fluorescent protein; GORASP1/GRASP65: golgi reassembly stacking protein 1; GORASP2/GRASP55: golgi reassembly stacking protein 2; LAMP1: lysosomal-associated membrane protein 1; LAMP2: lysosomal-associated membrane protein 2; MAP1LC3: microtubule associated protein 1 light chain 3; MTOR: mechanistic target of rapamycin kinase; PBS: phosphate-buffered saline; PtdIns3K: phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol 3-phosphate; PK: protease K; PNS: post-nuclear supernatant; RFP: red fluorescent protein; SD: standard deviation; TGN: trans-Golgi network; UVRAG: UV radiation resistance associated.
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PMID:GORASP2/GRASP55 collaborates with the PtdIns3K UVRAG complex to facilitate autophagosome-lysosome fusion. 3089 53