@article{cc7fa7f9ff254592b704ec04059ea600,
title = "Age-related recurrence of basal forebrain lesion-induced cholinergic deficits",
abstract = "Lesions of basal forebrain cholinergic nuclei projecting to neocortex have recently been employed as an animal model for the cholinergic deficits in Alzheimer's desease. However, unlike Alzheimer's patients, whose deterioration appears to be progressive and irreversible, basalis lesioned rats usually recover both behaviorally and neurochemically within several months after the lesion. We now demonstrate that this recovery may be a function of the age of the rat and that cholinergic deficits re-occur in the aged rat. Choline acetyltransferase (ChAT) activity and [3H]hemicholinium-3 ([3H]HCh-3) binding are reduced in cortex ipsilateral to ibotenic acid lesions in the 12-month postlesion rat following an initial recovery to normal levels by about 3 months postlesion. The recurrence of decrease of cholinergic markers is not a consequence of a non-specific age-related decline since the activity of glutamic acid decarboxylase remains constant between 3 and 12 months postlesion.",
keywords = "Aged rat, Choline acetyltransferase, [H]Hemicholinium-3, Glutamic acid decarboxylase, Neocortex, Nucleus basalis magnocellularis (NBM) lesion",
author = "Hohmann, {Christine F.} and Wenk, {Gary L.} and Pedro Lowenstein and Brown, {Michael E.} and Coyle, {Joseph T.}",
note = "Funding Information: behaviorald eficitsrecur after 9-13 months postoperativelyIn. addition, Bartus et al. [1] have reportedt hat NBM lesions of 9-montho ld rats resulitn persistenct holi-nergic deficits in cortex when they werea ssesseda t 15 months oaf ge. Their findings are consistent with aang e-relatedp ersistenceo r recurrenceo f cholinergicd eficits analogousto the resultos f the presents tudy.A ccordingly,it is importantt o consider the ageo f the animal at the time of lesion and at the time of assessmente,s pecially with regard to a model for an age-relatedd isordersuch as Alzheimer's disease. Furthermoret,h e inability of NBM cholinergicn euronsto sustain a more extensive axonal arbor in the contexto f an earlylo ss of the NBM neurons suggeststh at a con-genitallyd eterminedre ductionin NBM cell number in Down's syndromem ay render thesei ndividualsm orev ulnerableto an earlyo nsetof Alzheimer'sd isease[5 ] This researchw as supported by PHS Grants NS-18414, NS-13584, and grants from the Scottish Rite and Mcknight Foundations. Wthea nk Alice Trawinski for her editoriala ssistance.",
year = "1987",
month = dec,
day = "4",
doi = "10.1016/0304-3940(87)90265-5",
language = "English (US)",
volume = "82",
pages = "253--259",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "3",
}