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Creutzfeldt‐Jakob infection increases adenylate cyclase activity in specific regions of guinea pig brain
Author(s) -
Rasenick Mark M.,
Valley Susan,
Manuelidis Elias E.,
Manuelidis Laura
Publication year - 1986
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(86)81205-4
Subject(s) - adenylate kinase , cyclase , gtp' , enzyme , biochemistry , chemistry , guinea pig , biology , endocrinology
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 (GN s ) 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.