Buse JE, Kim I, Wilson RE, Wellman CL (2005) Contributions of NMDA receptors to cortical plasticity after cholinergic deafferentation. Neuroscience 2005 Abstracts 214.21. Society for Neuroscience, Washington, DC.
Summary: Plasticity of frontal cortex is altered in aging rats: lesions of the nucleus basalis magnocellularis (NBM) increase both expression of the AMPA receptor subunit GluR1 and dendritic spines in frontal cortex of young adult but not aging rats. Others have shown that NMDA receptors are reduced in aged cortex. Given the role of NMDA receptors in synaptic plasticity, altered transmission at NMDA receptors may be responsible for the differential cortical plasticity in aging rats. To begin to test this hypothesis, we assessed the effect of NMDA receptor blockade on GluR1 subunit expression and dendritic spine density on pyramidal cells in layer II-III of frontal cortex after either sham or 192 IgG saporin lesions of the NBM. Young adult rats received unilateral sham or 192 IgG saporin lesions of the NBM, along with subscapular implants of osmotic minipumps delivering either MK801 (6 mg/ml; 0.5 μl/h) or phosphate-buffered saline. Two weeks after surgery, rats were euthanized and brains were processed for either immunohistochemical labeling of GluR1 subunit protein or Golgi-Cox histology. To quantify GluR1 expression, an unbiased stereological technique was used to estimate the number of intensely labeled neurons. To quantify spine density, second- and third-order basilar dendrites of Golgi-stained pyramidal cells were drawn and spines were counted. NBM lesions significantly increased both GluR1 expression and spine density, by 83% and 28% respectively. While NMDA blockade alone had no effect, it prevented the lesion-induced increases in GluR1 expression and spine density. Thus, transmission at NMDA receptors may be necessary for synaptic plasticity after cholinergic deafferentation, and age-related changes in NMDA receptors may contribute to altered plasticity of frontal cortex of aging rats.
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