Septo-hippocampal cholinergic and neurotrophin markers in age-induced cognitive decline

Sugaya, Kimio; Greene, R.; Personett, David; Robbins, Michael E.; Kent, Caroline; Bryan, David R.; Skiba, Elżbieta; Gallagher, Michela; McKinney, Michael

doi:10.1016/s0197-4580(98)00072-4

Cited by 68 publications

(35 citation statements)

References 66 publications

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“…Even if age-related cognitive deficits could be the consequence of multiple alterations rather than that of dysfunctions in (or of) a particular anatomically and/or neurochemically defined network or system, it is noteworthy that aged rats show a consistent reduction of cholinergic markers, especially in the basal forebrain. Interestingly, the extend of these cholinergic alterations correlate with the severity of some cognitive deficits (Aubert et al 1995;Baskerville et al 2006;Herzog et al 2003;Stemmelin et al 2000;Sugaya et al 1998). In a recent study, we found that aged rats exposed to lifelong enrichment had more cholinergic neurons in the basal forebrain and striatum as compared with their standard counterparts.…”

Section: Introductionmentioning

confidence: 55%

“…Alteration of the cholinergic system originating in the MS/vDBB has been implicated in the age-related spatial memory impairments (Aubert et al 1995;Baskerville et al 2006;Sugaya et al 1998). This view was challenged as selective cholinergic lesions of the septal region did not affect water maze performance or produced only modest alterations (e.g., Baxter et al 1995).…”

Section: Spatial Cognition and Forebrain Cholinergic Neuronsmentioning

confidence: 99%

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Lifelong environmental enrichment in rats: impact on emotional behavior, spatial memory vividness, and cholinergic neurons over the lifespan

Harati

Barbelivien

Herbeaux

et al. 2012

AGE

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We assessed lifelong environmental enrichment effects on possible age-related modifications in emotional behaviors, spatial memory acquisition, retrieval of recent and remote spatial memory, and cholinergic forebrain systems. At the age of 1 month, Long-Evans female rats were placed in standard or enriched rearing conditions and tested after 3 (young), 12 (middle-aged), or 24 (aged)months. Environmental enrichment decreased the reactivity to stressful situations regardless of age. In the water maze test, it delayed the onset of learning deficits and prevented age-dependent spatial learning and recent memory retrieval alterations. Remote memory retrieval, which was altered independently of age under standard rearing conditions, was rescued by enrichment in young and middle-aged, but unfortunately not aged rats. A protected basal forebrain cholinergic system, which could well be one out of several neuronal manifestations of lifelong environmental enrichment, might have contributed to the behavioral benefits of this enrichment.

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Section: Introductionmentioning

confidence: 55%

Section: Spatial Cognition and Forebrain Cholinergic Neuronsmentioning

confidence: 99%

Lifelong environmental enrichment in rats: impact on emotional behavior, spatial memory vividness, and cholinergic neurons over the lifespan

Harati

Barbelivien

Herbeaux

et al. 2012

AGE

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“…The data are expressed as the fold change (mean ± SEM) relative to the control value (6-month-old animals). Asterisk indicates p < 0.05 vs 6-month-old rats of mainly Sprague-Dawley rats and which mostly employed ELISA (Lapchak et al 1993;Croll et al 1998;Sugaya et al 1998;Silhol et al 2007Silhol et al , 2008Del Arco et al 2011). Our key finding is that the agerelated accumulation of proBDNF in the hippocampus is not transcriptionally driven.…”

Section: Discussionmentioning

confidence: 99%

BDNF transcripts, proBDNF and proNGF, in the cortex and hippocampus throughout the life span of the rat

Perović

Tešić

Djordjevic

et al. 2012

AGE

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Neurotrophins are established molecular mediators of neuronal plasticity in the adult brain. We analyzed the impact of aging on brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) protein isoforms, their receptors, and on the expression patterns of multiple 5′ exon-specific BDNF transcripts in the rat cortex and hippocampus throughout the life span of the rat (6, 12, 18, and 24 months of age). ProNGF was increased during aging in both structures. Mature NGF gradually decreased in the cortex, and, in 24-month-old animals, it was 30 % lower than that in adult 6-month-old rats. The BDNF expression did not change during aging, while proBDNF accumulated in the hippocampus of aged rats. Hippocampal total BDNF mRNA was lower in 12-month-old animals, mostly as a result of a decrease of BDNF transcripts 1 and 2. In contrast to the regionspecific regulation of specific exon-containing BDNF mRNAs in adult animals, the same BDNF RNA isoforms (containing exons III, IV, or VI) were present in both brain structures of aged animals. Deficits in neurotrophin signaling were supported by the observed decrease in Trk receptor expression which was accompanied by lower levels of the two main downstream effector kinases, pAkt and protein kinase C. The proteolytic processing of p75NTR observed in 12-monthold rats points to an additional regulatory mechanism in early aging. The changes described herein could contribute to reduced brain plasticity underlying the age-dependent decline in cognitive function.

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“…The degree of modulation of the hippocampus mediated by ACh is attenuated in aged individuals, and the extent of this loss correlates with the degree of memory impairment [39][40][41]. The decrease in ACh-mediated modulation is reflected in reductions in the levels of ACh-processing enzymes in the medial septum, which provides the major cholinergic innervation to all three subregions of the hippocampus (see Figure 1 for modulation details) [42][43][44][45][46].…”

Section: Reduced Modulation By the Cholinergic Systemmentioning

confidence: 99%

Neurocognitive aging: prior memories hinder new hippocampal encoding

Wilson

Gallagher

Eichenbaum

et al. 2006

Trends in Neurosciences

304

327

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Normal aging is often accompanied by impairments in forming new memories, and studies of aging rodents have revealed structural and functional changes to the hippocampus that might point to the mechanisms behind such memory loss. In this article, we synthesize recent neurobiological and neurophysiological findings into a model of the information-processing circuit of the aging hippocampus. The key point of the model is that small concurrent changes during aging strengthen the auto-associative network of the CA3 subregion at the cost of processing new information coming in from the entorhinal cortex. As a result of such reorganization in aged memory-impaired individuals, information that is already stored would become the dominant pattern of the hippocampus to the detriment of the ability to encode new information.

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Septo-hippocampal cholinergic and neurotrophin markers in age-induced cognitive decline

Cited by 68 publications

References 66 publications

Lifelong environmental enrichment in rats: impact on emotional behavior, spatial memory vividness, and cholinergic neurons over the lifespan

Lifelong environmental enrichment in rats: impact on emotional behavior, spatial memory vividness, and cholinergic neurons over the lifespan

BDNF transcripts, proBDNF and proNGF, in the cortex and hippocampus throughout the life span of the rat

Neurocognitive aging: prior memories hinder new hippocampal encoding

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