Neuronal compartment

Like Glu, Asp plays an important role in general cell metabolism and in the synthesis of proteins. Thus, it can be difficult to identify the transmitter pool of Asp and Glu in the brain. By immunocytochemical methods it is possible to visualize the Asp and Glu content separately in different neuronal compartments. One would expect that a substance that has a transmitter role in the brain is localized in nerve endings, which is the site of transmitter release, rather than in neuronal cell bodies and dendrites. 

Transfection of cultures is required if SPT is performed on an exogenous protein or when one wants fluorescent markers of neuronal compartments such as synaptic scaffolding proteins to be expressed. 

The proposal that NO or its reactant products mediate toxicity in the brain remains controversial in part because of the use of non-selective agents such as those listed above that block NO formation in neuronal, glial, and vascular compartments. Nevertheless, a major area of research has been into the potential role of NO in neuronal excitotoxicity. Functional deficits following cerebral ischaemia are consistently reduced by blockers of NOS and in mutant mice deficient in NOS activity, infarct volumes were significantly smaller one to three days after cerebral artery occlusion, and the neurological deficits were less than those in normal mice. Changes in blood flow or vascular anatomy did not account for these differences. By contrast, infarct size in the mutant became larger... 

Upon activation, neurons begin trafficking TRPVl to the membrane where the receptors become activated, desensitized and then recycled to the intracellular compartments. Translocation of TRPVl to the cell membrane occurs via SNARE (snapin and synaptotagmin IX)-mediated exocytosis [37]. Broadly speaking, activation involves phosphorylation by protein kinases (most notably, protein kinase A [PKA] and C [PKC]) and desensitization involves de-phosphorylation by phosphatases (e.g. calcineurin) [38]. Among PKC isozymes, PKCp seems to be of particular importance [39]. 

Pow, D.V., and Morris, J.F. (1991) Membrane routing during exocytosis and endocytosis in neuroendocrine neurons and endocrine cells Use of colloidal gold particles and immunocytochemical discrimination of membrane compartments. Cell Tissue Res. 264, 299-316. 

Hayashi, H., Campenot, R. B., Vance, D. E. and Vance, J. E. Glial lipoproteins stimulate axon growth of central nervous system neurons in compartmented cultures. J. Biol. Chem. 279 14009-14015,2004. 

MTs serve multiple roles in neurons. Besides acting as the substrate for the transport of membrane-bounded organelles, MTs are necessary for the extension of neurites during development they provide the structural basis for maintaining neurites after extension and they also help maintain the definition and integrity of intracellular compartments. The diversity of these functions is reflected in differences in the biochemistry and metabolic stability of different MTs. 

Eukaryotic cells have evolved a complex, intracellular membrane organization. This organization is partially achieved by compartmentalization of cellular processes within specialized membrane-bounded organelles. Each organelle has a unique protein and lipid composition. This internal membrane system allows cells to perform two essential functions to sort and deliver fully processed membrane proteins, lipids and carbohydrates to specific intracellular compartments, the plasma membrane and the cell exterior, and to uptake macromolecules from the cell exterior (reviewed in [1,2]). Both processes are highly developed in cells of the nervous system, playing critical roles in the function and even survival of neurons and glia. 

In non-neuronal cells, electron microscopy studies reveal very complex endosomal compartments composed of a highly dynamic array of heterogeneous tubulovesicular-membrane structure extending from close vicinity to the plasma membrane to the cell interior, reaching the boundaries of the Golgi apparatus. Presynaptic terminals have similar endosomal systems, albeit less extensive [73, 74]. 

Ligand-receptor complexes that do not dissociate in the EEs have different fates. In some cells, they may be returned to the same plasma membrane compartment from which they originated, whereas in polarized cells such as endothelial cells or astrocytes they can be moved to a different plasma membrane domain, resulting in transcytosis. In other cases, the complexes go to LEs and lysosomes for degradation. In neurons, these vesicles may serve as signaling organelles that are transported from the EEs back to the cell body where they influence gene expression [71]. 

Details of the mechanisms by which endocytosed material moves from the early to the late and lysosomal compartment are still poorly understood. However, portions of the EEs tubulovesicular structures may be actively transported along microtubules towards the perinuclear region of the cell in both neurons and non-neuronal cells. These endosomes on the move may enclose invaginated membranes and also internally bud off vesicles. For that reason, these complex structures are called multivesicular bodies (MVBs) [76]. Material returning by retrograde axonal transport to the neuronal cell body includes many MVBs [67]. The eventual fate of these structures may vary. Some MVBs may fuse with LEs or they may fuse with each... 

Choline is supplied to the neuron either from plasma or by metabolism of choline-containing compounds 193 A slow release of acetylcholine from neurons at rest probably occurs at all cholinergic synapses 194 The relationship between acetylcholine content in a vesicle and the quanta of acetylcholine released can only be estimated 194 Depolarization of the nerve terminal by an action potential increases the number of quanta released per unit time 194 All the acetylcholine contained within the cholinergic neuron does not behave as if in a single compartment 194... 

All the acetylcholine contained within the cholinergic neuron does not behave as if in a single compartment. 

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