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Basal and stimulated hippocampal adenylate cyclase activity in the experimentally lesioned rat entorhinal cortex

Early stage development of Alzheimer-related neurofibrillary tangles occurs primarily in neurons of entorhinal cortex layers pre-α and pre-β. These excitatory neurons project into the hippocampus. At this stage (‘entorhinal’ case), while neurofibrillary tangles are still absent from the hippocampus,...

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Main Authors: Ohm, Thomas Georg (Author) , Dewitz, Goswin von (Author) , Witte, Klaus (Author) , Nitsch, Robert (Author) , Lemmer, Björn (Author)
Format: Article (Journal)
Language:English
Published: September 1999
In: Acta neuropathologica
Year: 1999, Volume: 98, Issue: 4, Pages: 389-395
ISSN:1432-0533
DOI:10.1007/s004010051099
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1007/s004010051099
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Author Notes:T.G. Ohm, Goswin von Dewitz, Klaus Witte, Robert Nitsch, Björn Lemmer

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520 |a Early stage development of Alzheimer-related neurofibrillary tangles occurs primarily in neurons of entorhinal cortex layers pre-α and pre-β. These excitatory neurons project into the hippocampus. At this stage (‘entorhinal’ case), while neurofibrillary tangles are still absent from the hippocampus, a significant reduction in hippocampal adenylate cyclase activity has been detected. To test whether this reduction is a consequence of a deafferentation (and thus not a specifically disease-related alteration), we performed unilateral electrolytic lesions and sham-operations of the rat entorhinal cortex. The animals were killed 2, 12 and 55 days post lesion (dpl) and hippocampal adenylate cyclase activity was assayed. The major results were as follows: (1) both lesioned and unlesioned sides showed higher activity than a sham-operated control; (2) the adenylate cyclase activity of the lesioned side increased to a significantly lesser degree than that of the unlesioned side at 12 dpl; (3) this ‘decrease’ was attributed to changes in G protein-mediated activation of adenylate cyclase; (4) at no time point post lesion did the pattern of rat adenylate cyclase activity resemble that observed in Alzheimer’s disease. Our data suggests that the loss of entorhinal afferents alone cannot explain the reduction in cyclase-activity seen in ‘entorhinal’ cases. 
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