Creutzfeldt-Jakob infection increases adenylate cyclase activity in specific regions of guinea pig brain.
Creutzfeldt-Jakob disease is a slow, infectious, progressive neurological disorder which results in human dementia. Synaptic membranes from various brain regions of guinea pigs infected with Creutzfeldt-Jakob disease show increased guanyl nucleotide- or 5-hydroxytryptamine-mediated activation of adenylate cyclase. This increased enzyme activity appears due, primarily, to facilitated 'coupling' between the GTP-binding protein which stimulates adenylate cyclase (GNs) and the catalytic moiety of that enzyme rather than increased sensitivity to 5-hydroxytryptamine. It is possible that this phenomenon is due to direct effects of the Creutzfeldt-Jakob infectious agent, or a pathological product resulting from that agent, upon synaptic membrane adenylate cyclase.
Rasenick
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Valley
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Manuelidis
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Manuelidis
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D000262:Adenylyl Cyclases / Q000032:analysis*; D000818:Animals; D001921:Brain / Q000201:enzymology*; D007562:Creutzfeldt-Jakob Syndrome / Q000201:enzymology*; D019204:GTP-Binding Proteins / Q000032:analysis; D006165:Guanylyl Imidodiphosphate / Q000494:pharmacology; D006168:Guinea Pigs; D009856:Oncogene Proteins, Viral / Q000032:analysis; D012608:Scrapie / Q000201:enzymology; D012701:Serotonin / Q000494:pharmacology; D012969:Sodium Fluoride / Q000494:pharmacology
D009856:Oncogene Proteins, Viral; D012701:Serotonin; D006165:Guanylyl Imidodiphosphate; D012969:Sodium Fluoride; D019204:GTP-Binding Proteins; D000262:Adenylyl Cyclases