In the present study, we demonstrate a direct role for d-aspartate in regulating hippocampal synaptic plasticity. These evidences were obtained using two different experimental strategies which enabled a non-physiological increase of endogenous d-aspartate levels in the mouse hippocampus: a genetic approach based on the targeted deletion of d-aspartate oxidase gene and another based on the oral administration of d-aspartate. Overall, our results indicate that increased d-aspartate content does not affect basal properties of synaptic transmission but enhances long-term potentiation in hippocampal slices from both genetic and pharmacological animal models. Besides electrophysiological data, behavioral analysis suggests that altered levels of d-aspartate in the hippocampus do not perturb basal spatial learning and memory abilities, but may selectively interfere with the dynamic NMDAR-dependent processes underlying cognitive flexibility.

Increased levels of d-aspartate in the hippocampus enhance LTP but do not facilitate cognitive flexibility / Errico, Fernando; Nistico', ROBERT GIOVANNI; G., Palma; M., Federici; A., Affuso; E., Brilli; E., Topo; D., Centonze; G., Bernardi; Y., Bozzi; A., D'Aniello; R. D., Lauro; N. B., Mercuri; A., Usiello. - In: MOLECULAR AND CELLULAR NEUROSCIENCES. - ISSN 1044-7431. - 37(2008), pp. 236-246. [10.1016/j.mcn.2007.09.012]

Increased levels of d-aspartate in the hippocampus enhance LTP but do not facilitate cognitive flexibility.

ERRICO, FERNANDO;NISTICO', ROBERT GIOVANNI;
2008

Abstract

In the present study, we demonstrate a direct role for d-aspartate in regulating hippocampal synaptic plasticity. These evidences were obtained using two different experimental strategies which enabled a non-physiological increase of endogenous d-aspartate levels in the mouse hippocampus: a genetic approach based on the targeted deletion of d-aspartate oxidase gene and another based on the oral administration of d-aspartate. Overall, our results indicate that increased d-aspartate content does not affect basal properties of synaptic transmission but enhances long-term potentiation in hippocampal slices from both genetic and pharmacological animal models. Besides electrophysiological data, behavioral analysis suggests that altered levels of d-aspartate in the hippocampus do not perturb basal spatial learning and memory abilities, but may selectively interfere with the dynamic NMDAR-dependent processes underlying cognitive flexibility.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11573/514119
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