Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Beta amyloid (Abeta) plays a central role in the pathogenesis of Alzheimer's disease. Abeta is the major constituent of senile plaques, but there is a significant presence of Abeta in the brain in soluble forms. The results of functional studies indicate that soluble Abeta interacts with the alpha7 nicotinic acetylcholine receptor (nAChR) complex with apparent high affinity. However, conflicting data exist as to the nature of the Abeta-alpha7 nAChR interaction, and whether it is the result of specific binding. Moreover, both agonist-like and antagonist-like effects have been reported. In particular, agonist-like effects have been observed for presynaptic nAChRs. Here, we demonstrate Abeta(1-42)-evoked stimulatory changes in presynaptic Ca(2+) level via exogenous alpha7 nAChRs expressed in the axonal varicosities of differentiated hybrid neuroblastoma NG108-15 cells as a model, presynaptic system. The Abeta(1-42)-evoked responses were concentration-dependent and were sensitive to the highly selective alpha7 nAChR antagonist alpha-bungarotoxin. Voltage-gated Ca(2+) channels and internal Ca(2+) stores were both involved in Abeta(1-42)-evoked increases in presynaptic Ca(2+) following activation of alpha7 nAChRs. In addition, disruption of lipid rafts by cholesterol depletion led to substantially attenuated responses to Abeta(1-42), whereas responses to nicotine were largely intact. These results directly implicate the nicotinic receptor complex as a target for the agonist-like action of pico- to nanomolar concentrations of soluble Abeta(1-42) on the presynaptic nerve terminal, including the possible involvement of receptor-associated lipid rafts. This interaction probably plays an important neuromodulatory role in synaptic dynamics.
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PMID:beta-Amyloid activates presynaptic alpha7 nicotinic acetylcholine receptors reconstituted into a model nerve cell system: involvement of lipid rafts. 2037 80

Recently, a large number of physiological studies on stress and hibernation had described an unusual morphological phenomenon of the rapid disappearance and reapperance of apical dendrites of pyramidal neurons of the hippocampus, prefrontal cortex and other parts of the brain. In this article an attempt is maid to explain this phenomenon on the basis of morphological analysis of natural elastic properties of neuroplasm and structural kinetics of partially preserved processes of the living isolated neurons. The neuroplasm displacement with its bidirectional flow was identified in the processes. A new physiological phenomenon is described--the isometric retraction of nerve cell processes, during which the neuroplasm fluxes were directed to the opposite sides, leading to abrupt thinning of middle parts of the processes and to a thickening of both ends. It is suggested that the extremely attenuated processes can reach the submicroscopic sizes, becoming invisible in the light microscope. The repeated reversible "disappearance" and "appearance" of the processes was demonstrated supravitally in the culture of neurons and of C-1300 neuroblastoma cells. Reduction of the diameter of the processes to a limit of their visibility was demonstrated by the example of their natural stretching. The same effect was observed in the areas between the reversible varicosities of the processes. These areas became extremely thin, and then invisible. Becoming thinner, the processes were capable of sharp extension. A review of the available literature and our own data allow to conclude that the phenomenon of the disappearance of the apical dendrites was due to their isometric retraction, which lead to the emergence of "invisible processes".
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PMID:[ISOMETRIC RETRACTION AND THE INVISIBLE PROCESSES OF NERVE CELLS]. 2714 78


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