Age-related impairment in complex maze learning in rats: Relationship to neophobia and cholinergic antagonism

Spangler, Edward L.; Chachich, Mark E.; Curtis, Nancy J.; Ingram, Donald K.

doi:10.1016/0197-4580(89)90022-5

Cited by 46 publications

(17 citation statements)

References 40 publications

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“…Thus, we sought to assess cognitive function in APP × PS1 mice using the Stone T-maze maze, which is a task of procedural learning and memory that is very well suited for use in mice as it does not require the animals to swim, and is not confounded by changes in motor impairment, feeding behavior, or nociception (Pistell and Ingram, 2010), (Pistell et al, 2010), (Pistell et al, 2010). This task, which is described in detail in Methods, was developed following the success of this maze in assessing age-related cognitive deficits in rats (Ingram, 1988), (Spangler et al, 1989), (Markowska et al, 1989). In addition to documenting age-related cognitive decline, this task has been successfully used in both rats and mice to document the detrimental effects of cholinergic antagonists (Spangler et al, 1989), (Bratt et al, 1994) , cerebral ischemia (Caldwell et al, 1997), and diabetes/obesity (Pistell et al, 2010), (Morrison et al, 2010), (Stranahan et al, 2008) on cognitive function.…”

Section: Resultsmentioning

confidence: 99%

“…This task, which is described in detail in Methods, was developed following the success of this maze in assessing age-related cognitive deficits in rats (Ingram, 1988), (Spangler et al, 1989), (Markowska et al, 1989). In addition to documenting age-related cognitive decline, this task has been successfully used in both rats and mice to document the detrimental effects of cholinergic antagonists (Spangler et al, 1989), (Bratt et al, 1994) , cerebral ischemia (Caldwell et al, 1997), and diabetes/obesity (Pistell et al, 2010), (Morrison et al, 2010), (Stranahan et al, 2008) on cognitive function. Furthermore, studies in rats in which both Stone maze and Morris water maze tasks were employed demonstrated that errors made during Stone maze training mirrored latency data obtained using the Morris water maze (Lee et al, 2006), (Markowska et al, 1989).…”

Section: Resultsmentioning

confidence: 99%

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Cognitive impairment in humanized APP×PS1 mice is linked to Aβ1–42 and NOX activation

Bruce‐Keller

Gupta

Knight

et al. 2011

Neurobiology of Disease

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Cognitive impairment in Alzheimer’s disease (AD) is strongly associated with both extensive deposition of amyloid β peptides and oxidative stress, but the exact role of these indices in the development of dementia is not clear. This study was designed to determine the relationship between cognitive impairment, activation of the free radical producing enzyme NADPH oxidase (NOX), and progressive changes in Aβ deposition and solubility in humanized APP × PS1 knock-in mice of increasing age. Data show that cognitive performance and expression of key synaptic proteins was progressively decreased in aging APP × PS1 mice. Likewise, NOX activity and expression of the specific NOX subunit NOX4 was significantly increased in APP × PS1 mice in an age-dependent manner, and NOX activity and cognitive impairment shared a significant linear relationship. Data further show that age-dependent increases in Aβ1-42 had a significant linear relationship with both NOX activity and cognitive performance in APP × PS1 knock-in mice. Collectively, these data show that NOX expression and activity are significantly upregulated with age in this humanized model of Aβ pathogenesis, and suggest that NOX-associated redox pathways are intimately linked to both the loss of cognitive function and the deposition of Aβ1-42.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Cognitive impairment in humanized APP×PS1 mice is linked to Aβ1–42 and NOX activation

Bruce‐Keller

Gupta

Knight

et al. 2011

Neurobiology of Disease

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“…Recording place cells in a new environment involves an inherent technical obstacle in that: (1) old rats tend to explore new environments with some hesitation; and (2) old rats fail to explore them sufficiently even when they are motivated by hunger and food is dispersed in the environment (Spangler et al, 1989). Yet free voluntary movement has been shown to be necessary for place-specific activity by CA1 pyramidal cells (Foster et al, 1989), and movement variables such as speed and direction further modify the firing rate of these place cells (Wiener et al, 1989).…”

Section: Abstract: Aging; Hippocampus; Place Field; Spatial Learningmentioning

confidence: 99%

Brain Aging: Impaired Coding of Novel Environmental Cues

et al. 1997

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Studies of the spatial memory capacities of aged animals usually focus on performance during the learning of new environments. By contrast, efforts to characterize age-related alterations in spatial firing information processing by hippocampal neurons typically use an environment that is highly familiar to the animals. In the present study we compared the firing properties of hippocampal neurons in young adult and aged rats as they acquired spatial information about new environmental cues. Hippocampal complex spike cells were recorded while rats performed a radial arm maze task in a familiar environment and then recorded again after many of the spatial cues were changed. After the change in the environment, in aged rats 35-42% of place fields retained their original shape and location with respect to the maze center, although they usually rotated to another arm. By contrast, all place fields in young animals either disappeared or appeared in a new location. Some of the new place fields appeared in the new environment during the first 5 min of exploration, whereas others needed more than 30 min to develop fully. In the familiar environment spatial selectivity of place cells was similar in young and aged rats. By contrast, when rats were placed into a new environment, spatial selectivity decreased considerably in aged memory-impaired rats compared with that of young rats and aged rats with intact memory performance.

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“…Previous studies conducted from our laboratory have demonstrated that blockade of NO formation by systemic or central administration of the nonspecific NOS inhibitor N ω -nitro-L-arginine produces a learning impairment in rats trained on the 14-unit T-maze task (Ingram et al 1998a,b), a complex learning paradigm used to model age-related cognitive decline in rodents (Spangler et al 1986(Spangler et al , 1988(Spangler et al , 1989. In addition, we have recently shown that systemic administration of the phosphodiesterase type 5 (PDE5) inhibitor sildenafil citrate has cognitive-enhancing effects in attenuating the complex maze learning impairment induced by blockade of muscarinic cholinergic receptors (Devan et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Phosphodiesterase inhibition by sildenafil citrate attenuates a maze learning impairment in rats induced by nitric oxide synthase inhibition

et al. 2005

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Age-related impairment in complex maze learning in rats: Relationship to neophobia and cholinergic antagonism

Cited by 46 publications

References 40 publications

Cognitive impairment in humanized APP×PS1 mice is linked to Aβ1–42 and NOX activation

Cognitive impairment in humanized APP×PS1 mice is linked to Aβ1–42 and NOX activation

Brain Aging: Impaired Coding of Novel Environmental Cues

Phosphodiesterase inhibition by sildenafil citrate attenuates a maze learning impairment in rats induced by nitric oxide synthase inhibition

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