Journal of Neuroscience, Vol 14, 2476-2484, Copyright © 1994 by Society for Neuroscience
Multiple cholinergic markers are unexpectedly not altered in the rat dentate gyrus following entorhinal cortex lesions
I Aubert, J Poirier, S Gauthier and R Quirion
Department of Neurology, McGill University, Montreal, Quebec, Canada.
Since major cholinergic deficits are observed in Alzheimer's disease, the
development of models to study possible cholinergic plasticity has
generated great interest. In this regard, it has been shown that lesions of
the entorhinal cortex, which sends glutamatergic projections to the
hippocampus, promote the sprouting and plasticity of presumptive
cholinergic septohippocampal fibers in the dentate gyrus, as revealed by
AChE histochemistry. This sprouting was reported to be evident at 8 d and
up to 30 d postlesion (DPL) and is now widely used as a model of
cholinergic neuronal plasticity. In the present study, unilateral lesions
of the entorhinal cortex were made in adult rats, and the status of various
putative pre- and postsynaptic cholinergic markers was assessed after 2, 4,
8, 14, and 30 DPL. As expected, AChE was increased in the outer molecular
layer of the ipsilateral dentate gyrus from 8 to 30 DPL. In contrast, the
activity of ChAT, the enzyme responsible for the synthesis of ACh, and the
densities of specific binding sites for 3H-AH5 183/vesamicol (blocker of
the ACh vesicular transport sites), 3H-hemicholinium-3 (blocker of the
high-affinity choline uptake sites), muscarinic-M2 (3H-AF-DX 384 and
3H-ACh), muscarinic-M1 (3H-pirenzepine), and nicotinic (3H-N-
methylcarbamylcholine) cholinergic receptors were not increased on the
ipsilateral molecular layer of the dentate gyrus, as compared to their
contralateral controls. We conclude that the increase in AChE staining in
the molecular layer of the dentate gyrus following entorhinal cortex
lesions may be due to changes in noncholinergic neurons.
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