Selective lesions of the nucleus basalis magnocellularis impair cognitive flexibility.

Cabrera, Sara; Chavez, Candice M.; Corley, Sean Ryan; Kitto, Michael Ryan; Butt, Allen E.

doi:10.1037/0735-7044.120.2.298

Cited by 40 publications

(20 citation statements)

References 51 publications

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“…Learning deficits in the Morris water maze, a classic hippocampal-dependent task, were also found immediately after adolescent ethanol exposure, and this effect persisted into adulthood [11]. Other studies reported deficits during reversal learning (but not acquisition) in the Morris water maze[14] and Barnes maze [13] – two tasks thought to be hippocampally-dependent, although other brain regions, like the OFC [46] and basal forebrain [47], are thought to contribute to reversal learning per se. The results of this study contribute to the mounting evidence that adolescent ethanol exposure may lead to long-lasting deficits in cognition, particularly affecting tasks that are relatively hippocampal-dependent.…”

Section: Discussionmentioning

confidence: 99%

Consequences of ethanol exposure on cued and contextual fear conditioning and extinction differ depending on timing of exposure during adolescence or adulthood

Broadwater

Spear

2013

Behavioural Brain Research

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Some evidence suggests that adolescents are more sensitive than adults to ethanol-induced cognitive deficits and that these effects may be long-lasting. The purpose of Exp 1 was to determine if early-mid adolescent [Postnatal day (P) 28-48] intermittent ethanol exposure would affect later learning and memory in a Pavlovian fear conditioning paradigm differently than comparable exposures in adulthood (P70-90). In Exp 2 animals were exposed to ethanol during mid-late adolescence (P35-55) to assess whether age of initiation within the adolescent period would influence learning and memory differentially. Male Sprague-Dawley rats were given 4 g/kg i.g. ethanol (25%) or water every 48 hours for a total of 11 exposures. After a 22 day non-ethanol period, animals were fear conditioned to a context (relatively hippocampal-dependent task) or tone (amygdala-dependent task), followed by retention tests and extinction (mPFC-dependent) of this conditioning. Despite similar acquisition, a deficit in context fear retention was evident in animals exposed to ethanol in early adolescence, an effect not observed after a comparable ethanol exposure in mid-late adolescence or adulthood. In contrast, animals that were exposed to ethanol in mid-late adolescence or adulthood showed enhanced resistance to context extinction. Together these findings suggest that repeated ethanol imparts long-lasting consequences on learning and memory, with outcomes that differ depending on age of exposure. These results may reflect differential influence of ethanol on the brain as it changes throughout ontogeny and may have implications for alcohol use not only throughout the developmental period of adolescence, but also in adulthood.

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Section: Discussionmentioning

confidence: 99%

Consequences of ethanol exposure on cued and contextual fear conditioning and extinction differ depending on timing of exposure during adolescence or adulthood

Broadwater

Spear

2013

Behavioural Brain Research

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“…Lesion studies of the basal forebrain demonstrate its involvement in behavioral flexibility (Cabrera et al, 2006; Tait and Brown, 2008). Non-selective ibotenic acid lesions in the basal forebrain impair reversal learning but leaves set shifting intact (Tait and Brown, 2008).…”

Section: Discussionmentioning

confidence: 99%

Muscarinic receptor/G-protein coupling is reduced in the dorsomedial striatum of cognitively impaired aged rats

Nieves-Martinez

Haynes

Childers

et al. 2012

Behavioural Brain Research

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Behavioral flexibility, the ability to modify responses due to changing task demands, is detrimentally affected by aging with a shift towards increased cognitive rigidity. The neurobiological basis of this cognitive deficit is not clear although striatal cholinergic neurotransmission has been implicated. To investigate the possible association between striatal acetylcholine signaling with age-related changes in behavioral flexibility, young, middle-aged, and aged F344 X Brown Norway F1 rats were assessed using an attentional set-shifting task that includes two tests of behavioral flexibility: reversal learning and an extra-dimensional shift. Rats were also assessed in the Morris water maze to compare potential fronto-striatal-dependent deficits with hippocampal-dependent deficits. Behaviorally characterized rats were then assessed for acetylcholine muscarinic signaling within the striatum using oxotremorine-M-stimulated [35S]GTPγS binding and [3H]AFDX-384 receptor binding autoradiography. The results showed that by old age, cognitive deficits were pronounced across cognitive domains, suggesting deterioration of both hippocampal and fronto-striatal regions. A significant decline in oxotremorine-M-stimulated [35S]GTPγS binding was limited to the dorsomedial striatum of aged rats when compared to young and middle-aged rats. There was no effect of age on striatal [3H]AFDX-384 receptor binding. These results suggest that a decrease in M2/M4 muscarinic receptor coupling is involved in the age-associated decline in behavioral flexibility.

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“…These capacities are acquired during development as a result of synaptic maturation in the sensory circuit and can be improved by training in adulthood (Sanes and Woolley, 2011). Lesions of cortical cholinergic fibers can result in decreased detection, identification, and localization of stimuli and impaired learning, storage, and flexible retrieval of sensory associations (Berger-Sweeney et al, 2000; Butt et al, 2002; Cabrera et al, 2006; Leach et al, 2013; Vale-Martinez et al, 2002). …”

Section: Improving Perception By Manipulating Neuromodulationmentioning

confidence: 99%

Cortical Plasticity, Excitatory–Inhibitory Balance, and Sensory Perception

Carcea

Froemke

2013

Progress in Brain Research

110

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Experience shapes the central nervous system throughout life. Structural and functional plasticity confers a remarkable ability on the brain, allowing neural circuits to adequately adapt to dynamic environments. This process can require selective adjustment of many excitatory and inhibitory synapses in an organized manner, in such a way as to enhance representations of behaviorally important sensory stimuli while preserving overall network excitability. The rules and mechanisms that orchestrated these changes across different synapses and throughout neuronal ensembles are beginning to be understood. Here, we review the evidence connecting synaptic plasticity to functional plasticity and perceptual learning, focusing on the roles of various neuromodulatory systems in enabling plasticity of adult neural circuits. However, the challenge remains to appropriately leverage these systems and forms of plasticity to persistently improve perceptual abilities and behavioral performance.

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Selective lesions of the nucleus basalis magnocellularis impair cognitive flexibility.

Cited by 40 publications

References 51 publications

Consequences of ethanol exposure on cued and contextual fear conditioning and extinction differ depending on timing of exposure during adolescence or adulthood

Consequences of ethanol exposure on cued and contextual fear conditioning and extinction differ depending on timing of exposure during adolescence or adulthood

Muscarinic receptor/G-protein coupling is reduced in the dorsomedial striatum of cognitively impaired aged rats

Cortical Plasticity, Excitatory–Inhibitory Balance, and Sensory Perception

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