Long-lasting transneuronal dendritic changes of GABAergic neurons in the monkey dentate gyrus following entorhinal cortex lesion

This study analyses dendritic changes of GABAergic neurons in the dentate gyrus of the African green monkey Cercopithecus aethiops upon lesioning of their main afferents, i.e., fibers originating form the entorhinal cortex (EC). Monkeys received a unilateral EC lesion (ECL) under visual control. Fou...

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Veröffentlicht in:Neuroscience letters 1994-02, Vol.168 (1), p.115-118
Hauptverfasser: Miehe, Uta, Leranth, Csaba, Ohm, Thomas G., Nitsch, Robert
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Sprache:eng
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Zusammenfassung:This study analyses dendritic changes of GABAergic neurons in the dentate gyrus of the African green monkey Cercopithecus aethiops upon lesioning of their main afferents, i.e., fibers originating form the entorhinal cortex (EC). Monkeys received a unilateral EC lesion (ECL) under visual control. Four, 10 and 365 days after surgery, GABAergic dentate neurons were immunostained for parvalbumin (PV). In comparison to the contralateral side. immunolabeled dendrites ipsilateral to the lesion appeared to be retracted from the outer portions of the molecular layer at all survival times. Dendritic changes were further analysed using an interactive neuron-tracing system. Whereas immunoreactive cell bodies were not reduced in number, the relative extension of dendrites throughout the dentate molecular layer was reduced by 40% 10 days postlesion (dpl) and recovered only up to 80% 365 dpl when compared with the control side. This was reflected by a decrease of the mean segment length, which included proximal dendrites and was apparent even after 365 dpl. The spread of the dendritic field was initially diminished by 50% and seemed to exhibit a long-lasting reduction. The findings are in line with previous results obtained in the rat, thus, indicating that similar transneuronal changes after ECL occur in the primate dentate gyrus. This may be of importance, since the EC appears to be a very early target area of affection in human neurodegenerative disorders, such as Alzheimer's disease.
ISSN:0304-3940
1872-7972
DOI:10.1016/0304-3940(94)90429-4