title: Aging and cholinergic deafferentation alter GluR1 expression in rat frontal cortex.
abstract: Previously, we demonstrated that plasticity of frontal cortex is altered in aging rats: lesions of the nucleus basalis magnocellularis (NBM) produce larger declines in dendritic morphology in frontal cortex of aged rats compared to young adults. Cholinergic afferents from the NBM modulate glutamatergic transmission in neocortex, and glutamate is known to be involved in dendritic plasticity. To begin to identify possible mechanisms underlying age-related differences in plasticity after NBM lesion, we assessed the effect of cholinergic deafferentation on expression of the AMPA receptor subunit GluR1 in frontal cortex of young adult and aging rats. Young adult, middle-aged, and aged rats received sham or 192 IgG-saporin lesions of the NBM, and an unbiased stereological technique was used to estimate the total number of intensely GluR1-immunopositive neurons in layer II-III of frontal cortex. While the number of GluR1-positive neurons was increased in both middle-aged and aged rats, lesions markedly increased the number of intensely GluR1-immunopositive neurons in frontal cortex of young adult rats only. This age-related difference in lesion-induced expression of AMPA receptor subunit protein could underlie the age-related differences in dendritic plasticity after NBM lesions.
authors.affiliation: Department of Psychology, Indiana University, Bloomington, IN 47405, USA.
authors.forename: Irene
authors.initials: I
authors.lastname: Kim
authors.forename: Randall E
authors.initials: RE
authors.lastname: Wilson
authors.forename: Cara L
authors.initials: CL
authors.lastname: Wellman
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000367:Age Factors; D000375:Aging / Q000502:physiology*; D000704:Analysis of Variance; D000818:Animals; D000911:Antibodies, Monoclonal / Q000633:toxicity; D020532:Basal Nucleus of Meynert / Q000187:drug effects; D002452:Cell Count / Q000379:methods; D018678:Cholinergic Agents / Q000633:toxicity; D002799:Cholinergic Fibers / Q000187:drug effects / Q000378:metabolism*; D005625:Frontal Lobe / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000187:drug effects; D007150:Immunohistochemistry / Q000379:methods; D000922:Immunotoxins / Q000633:toxicity; D008297:Male; D009699:N-Glycosyl Hydrolases; D009474:Neurons / Q000378:metabolism; D051381:Rats; D011916:Rats, Inbred F344; D018091:Receptors, AMPA / Q000378:metabolism*; D054789:Ribosome Inactivating Proteins, Type 1; D000076985:Saporins; D013238:Stereotaxic Techniques
chemical_list: D000110:Acetylcholinesterase; D000911:Antibodies, Monoclonal; D018678:Cholinergic Agents; D000922:Immunotoxins; D009699:N-Glycosyl Hydrolases; D018091:Receptors, AMPA; D054789:Ribosome Inactivating Proteins, Type 1; D000076985:Saporins; C085696:192 IgG-saporin