Persistent spatial working memory deficits in rats with bilateral cortical microgyria

Fitch, R. Holly; Breslawski, Heather; Rosen, Glenn D.; Chrobak, James J.

doi:10.1186/1744-9081-4-45

Cited by 10 publications

(18 citation statements)

References 62 publications

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“…Concomitant evidence from animal models suggests that rapid auditory processing deficits (as seen in cortically disrupted animals) are aggravated when difficulty and complexity of the task are increased (Peiffer et al ., 2004a; Fitch et al ., 2008). Data from these studies suggest evidence of higher order learning and memory deficits in cortically disrupted animals, prompting questions about a possible relationship between cortical dysgenesis and other cognitive deficits associated with developmental dyslexia (i.e.…”

Section: Discussionmentioning

confidence: 99%

“…working memory; Smith-Spark and Fisk, 2007). In fact, deficits in working memory have been reliably replicated in the same animal models that showed difficulties in rapid auditory processing (Boehm et al ., 1996, Waters et al ., 1997, Hoplight et al ., 2001, Threlkeld et al ., 2007; Fitch et al ., 2008). The fact that deficits in both rapid auditory processing (RAP), and also learning and memory, can be reliably elicited from rodent models employing different forms of cortical disruption (e.g., microgyria, ectopia, hypoxic-ischemic injury) suggests that cortical disruption during vulnerable periods early in development appears to cause robust long-term impairments across an array of processing modalities (Threlkeld et al ., 2007; Fitch et al ., 2008).…”

Section: Discussionmentioning

confidence: 99%

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Persistent spatial working memory deficits in rats following in utero RNAi of Dyx1c1

Szalkowski

Hinman

Threlkeld

et al. 2010

Genes, Brain and Behavior

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Disruptions in the development of the neocortex are associated with cognitive deficits in humans and other mammals. Several genes contribute to neocortical development, and research into the behavioral phenotype associated with specific gene manipulations is advancing rapidly. Findings include evidence that variants in the human gene DYX1C1 may be associated with an increased risk of developmental dyslexia. Concurrent research has shown that the rat homolog for this gene modulates critical parameters of early cortical development, including neuronal migration. Moreover, recent studies have shown auditory processing and spatial learning deficits in rats following in utero transfection of an RNA interference (RNAi) vector of the rat homolog Dyx1c1 gene. The current study examined the effects of in utero RNAi of Dyx1c1 on working memory performance in Sprague-Dawley rats. This task was chosen based on the evidence of short-term memory deficits in dyslexic populations, as well as more recent evidence of an association between memory deficits and DYX1C1 anomalies in humans. Working memory performance was assessed using a novel match-to-place radial water maze task that allows the evaluation of memory for a single brief (∼4-10 seconds) swim to a new goal location each day. A 10-min retention interval was used, followed by a test trial. Histology revealed migrational abnormalities and laminar disruption in Dyx1c1 RNAi-treated rats. Dyx1c1 RNAi-treated rats exhibited a subtle, but significant and persistent impairment in working memory as compared to Shams. These results provide further support for the role of Dyx1c1 in neuronal migration and working memory.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Persistent spatial working memory deficits in rats following in utero RNAi of Dyx1c1

Szalkowski

Hinman

Threlkeld

et al. 2010

Genes, Brain and Behavior

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“…Each trial ended when the animal located the platform, or when 90 sec had elapsed. Although, a 15 min ITI was used in the present working memory paradigm, other studies have used shorter and longer ITIs in rodents, some reaching several hours in length (Means, 1993; Means et al, 1996; Kline et al, 2002; Fitch et al, 2008; Schulteis et al, 2008). …”

Section: Methodsmentioning

confidence: 99%

COG1410 Improves Cognitive Performance and Reduces Cortical Neuronal Loss in the Traumatically Injured Brain

Hoane

Kaufman

Vitek

et al. 2009

Journal of Neurotrauma

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We have previously shown that a single dose of COG1410, a small molecule ApoE-mimetic peptide derived from the apolipoprotein E (ApoE) receptor binding region, improves sensorimotor and motor outcome following cortical contusion injury (CCI). The present study evaluated a regimen of COG1410 following frontal CCI in order to examine its preclinical efficacy on cognitive recovery. Animals were prepared with a bilateral CCI of the frontal cortex. A regimen of COG1410 (0.8 mg/kg intravenously [IV]) was administered twice, at 30 min and again at 24 h post-CCI. Starting on day 11, the animals were tested for their acquisition of a reference memory task in the Morris water maze (MWM), followed by a working memory task in the MWM on day 15. Following CCI, the animals were also tested on the bilateral tactile adhesive removal test to measure sensorimotor dysfunction. On all of the behavioral tests the COG1410 group was no different from the uninjured sham group. Administration of the regimen of COG1410 significantly improved recovery on the reference and working memory tests, as well as on the sensorimotor test. Lesion analysis revealed that COG1410 significantly reduced the size of the injury cavity. Administration of COG1410 also reduced the number of degenerating neurons, as measured by Fluoro-Jade C staining, in the frontal cortex at 48 h post-CCI. These results suggest that a regimen of COG1410 appeared to block the development of significant behavioral deficits and reduced tissue loss. These combined findings suggest that COG1410 appears to have strong preclinical efficacy when administered following traumatic brain injury (TBI).

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“…Mice with neocortical ectopias are impaired in spatial and non-spatial working memory (Balogh SA et al, 1998; Boehm GW et al, 1996; Denenberg VH et al, 2001; Hoplight BJ et al, 2001; Hyde LA et al, 2002), and in processing rapid auditory stimuli (Clark MG et al, 2000; Frenkel M et al, 2000; Peiffer AM et al, 2001). Similarly, male rats with induced-microgyria in parietal cortex, a disruption in cortical lamination with similarities to and often associated with ectopias, display rapid auditory processing deficits (Clark MG et al, 2000; Fitch RH, SW Threlkeld et al, 2008; Herman AE et al, 1997) and working memory deficits (Fitch RH, H Breslawski et al, 2008). In all, the animal studies indicate importantly that even relatively small malformations in neocortical structure can have very specific effects on sensory and learning tasks without having large scale effects on general learning ability.…”

Section: Neuroanatomy Of Rdmentioning

confidence: 99%

Progress towards a cellular neurobiology of reading disability

Gabel

Gibson

Gruen

et al. 2010

Neurobiology of Disease

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Reading Disability (RD) is a significant impairment in reading accuracy, speed and/or comprehension despite adequate intelligence and educational opportunity. RD affects 5-12% of readers, has a wellestablished genetic risk, and is of unknown neurobiological cause or causes. In this review we discuss recent findings that revealed neuroanatomic anomalies in RD, studies that identified 3 candidate genes (KIAA0319, DYX1C1, and DCDC2), and compelling evidence that potentially link the function of candidate genes to the neuroanatomic anomalies. A hypothesis has emerged in which impaired neuronal migration is a cellular neurobiological antecedent to RD. We critically evaluate the evidence for this hypothesis, highlight missing evidence, and outline future research efforts that will be required to develop a more complete cellular neurobiology of RD.

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Persistent spatial working memory deficits in rats with bilateral cortical microgyria

Cited by 10 publications

References 62 publications

Persistent spatial working memory deficits in rats following in utero RNAi of Dyx1c1

Persistent spatial working memory deficits in rats following in utero RNAi of Dyx1c1

COG1410 Improves Cognitive Performance and Reduces Cortical Neuronal Loss in the Traumatically Injured Brain

Progress towards a cellular neurobiology of reading disability

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