+ Site Statistics
+ Search Articles
+ PDF Full Text Service
How our service works
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ Translate
+ Recently Requested

Bilateral changes in glutamate uptake muscarinic receptor binding and acetylcholinesterase level in the rat hippocampus after unilateral entorhinal cortex lesions



Bilateral changes in glutamate uptake muscarinic receptor binding and acetylcholinesterase level in the rat hippocampus after unilateral entorhinal cortex lesions



Neurochemistry International 9(2): 255-264



This report examines the effects of unilateral electrolytic and knife-cut lesions of entorhinal cortex on glutamate uptake, the muscarinic receptor [3H]QNB binding and acetylcholinesterase (AChE) activity in the dorsal and ventral parts of the ipsi- and contralateral hippocampus of the rat. We found that (1) in unoperated, control rats there are no pre-existing differences in the level of the investigated markers between the right and left hippocampus, (2) both electrolytic and knife-cut lesions of the entorhinal cortex evoke bilateral changes in the investigated markers and (3) the character of the response is dependent on the survival time and on the hippocampal part involved. Four days after operation a substantial reduction in glutamate uptake was found in both the dorsal and ventral parts of the ipsi- and contralateral hippocampus. At the same time there was a drop in muscarinic receptor binding, while AChE activity was not affected. The decrease in glutamate uptake persisted on the 21st postoperative day, whereas muscarinic receptor binding was enhanced, in comparison with the control level, in the ventral part of both the ipsi- and contralateral hippocampus. This overshoot was not so evident on the 30th postoperative day; glutamate uptake at that time reached or even surpassed the control level. Enhancement of AChE activity on the ipsi- and contralateral sides was noted on both the 21st and 30th day after operation. We suggest the following interpretation of these results: (1) glutamatergic projections from the entorhinal cortex to the hippocampus are bilateral, (2) some transneuronal changes probably contribute to the decline in glutamate uptake, particularly on the contralateral side, (3) neuronal depolarization does not seem to be the only mechanism responsible for the decrease in muscarinic receptor binding and (4) some compensatory mechanism occur in the hippocampus at a larger time after the lesion. Moreover, we believe that the use of the contralateral side as a control should be considered with caution in studies with unilaterally lesioned animals.

Please choose payment method:






(PDF emailed within 0-6 h: $19.90)

Accession: 004823469

Download citation: RISBibTeXText

PMID: 20493124

DOI: 10.1016/0197-0186(86)90061-6


Related references

Unilateral entorhinal cortex lesion causes bilateral muscarinic receptor changes in the rat hippocampus. Journal of Neurochemistry 44(SUPPL): S134, 1985

Muscarinic receptor binding following cholinergic nerve lesions of the cingulate cortex and hippocampus of the rat. Brain Research 209(2): 432-439, 1981

Muscarinic M4 receptor changes in the hippocampus and entorhinal cortex of adrenalectomized rats. FASEB Journal 18(4-5): Abst 833 12, 2004

Kainate receptors in the rat hippocampus: a distribution and time course of changes in response to unilateral lesions of the entorhinal cortex. Journal of Neuroscience 10(7): 2352-2362, 1990

Glutamate receptor expression changes in rat hippocampus after entorhinal cortex lesion. Society for Neuroscience Abstracts 18(1-2): 90, 1992

Effects of entorhinal lesions on trophic activities present in rat entorhinal cortex and hippocampus as studied using primary cultures of entorhinal and septal tissues. Journal of Neuroscience Research 18(2): 274-288, 1987

Changes in NOS protein expression and activity in the rat hippocampus, entorhinal and postrhinal cortices after unilateral electrolytic perirhinal cortex lesions. Hippocampus 13(5): 561-571, 2003

Infusion of glutamate receptor antagonists into the amygdala, hippocampus, and entorhinal cortex causes amnesia. Journal of the Neurological Sciences 150(SUPPL ): S334, 1997

Lesions-induced plasticity of central neurons Sprouting of single fibres in the rat hippocampus after unilateral entorhinal cortex lesion. Progress in Neurobiology 53(6): 687-727, 1997

Indirect excitotoxin lesion of layer III in rat entorhinal cortex produces glutamate receptor changes in hippocampus. Society for Neuroscience Abstracts 20(1-2): 492, 1994

Corticosterone differentially regulates the bilateral response of astrocyte mRNAs in the hippocampus to entorhinal cortex lesions in male rats. Brain Research. Molecular Brain Research 10(4): 291-297, 1991

Amnesia by post-training infusion of glutamate receptor antagonists into the amygdala, hippocampus, and entorhinal cortex. Behavioral and Neural Biology 58(1): 76-80, 1992

Persitent activity in entorhinal cortex neurons induced by muscarinic and metabotropic glutamate receptor activation and its dependence on trp channels. Society for Neuroscience Abstract Viewer & Itinerary Planner : Abstract No 377 5, 2003

Corticosterone differentially regulates the bilateral response of astrocyte messenger rnas in the hippocampus to entorhinal cortex lesions in male rats. Molecular Brain Research 10(4): 291-298, 1991

Ultrastructural localization of kainate class glutamate receptor subunits GLUR5/6/7 in monkey hippocampus and entorhinal cortex. Society for Neuroscience Abstracts 19(1-3): 473, 1993