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Adams, M.M. et al.

Attenuated lesion-induced N-methyl-D-aspartate receptor ( NMDAR) plasticity in the dentate gyrus of aged rats following perforant path lesions.

Young animals demonstrate a significant upregulation of N-methyl-d-aspartate receptor 1 (NMDAR1) in the outer molecular layer (OML) of the dentate gyrus following a total unilateral ablation of the perforant path, and this response presumably facilitates a degree of functional recovery. Aged animals have attenuated responses to lesion-induced synaptic plasticity as compared with young subjects, and in fact display decreased synaptogenesis and sprouting following a unilateral perforant path lesion. To investigate the response of NMDAR1 in the dentate gyrus of aged animals to perforant path ablation, 24-month-old Sprague-Dawley male rats received a unilateral knife cut of the angular bundle. Our results demonstrated that aged animals displayed a blunted response to lesion-induced NMDA receptor-mediated plasticity, suggesting that aged animals have an impaired ability to respond to deafferentation through an increase in NMDA receptor levels in the deafferented zone.[1]

References

Attenuated lesion-induced N-methyl-D-aspartate receptor (NMDAR) plasticity in the dentate gyrus of aged rats following perforant path lesions. Adams, M.M., Gazzaley, A.H., Morrison, J.H. Exp. Neurol. (2001) [Pubmed]

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