Cholinergic deafferentation after focal cerebral infarct in rats.

Kataoka, Keisuke; Hayakawa, T; Kuroda, R.; Yuguchi, Takamichi; Yamada, Kazuo

doi:10.1161/01.str.22.10.1291

Cited by 74 publications

(23 citation statements)

References 25 publications

(15 reference statements)

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“…Previous studies have shown that the levels of ACh in rat brain are markedly decreased following MCA occlusion [24], and the numbers of muscarinic receptors and AChE-positive fibers are markedly decreased in the chronic phase after MCA occlusion in rats [25,26]. These reports suggested that LCBF decrease in our study is triggered by a deficiency of cholinergic systems.…”

Section: Discussionsupporting

confidence: 58%

Nefiracetam Improves the Impairment of Local Cerebral Blood Flow and Glucose Utilization after Chronic Focal Cerebral Ischemia in Rats

Jin

Watabe²,

Yamamoto³

2002

Pharmacology

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In this study we investigated the effects of nefiracetam (DM-9384) on local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCMR_glc) in the chronic phase after middle cerebral artery (MCA) occlusion in rats. Nefiracetam (10 mg/kg) was administered orally once a day for 2 weeks from day 15 after MCA occlusion. On day 28 after MCA occlusion, LCBF and LCMR_glc were measured by an autoradiographic image-processing method. In MCA-occluded rats, LCBF and LCMR_glc in the ischemic side of seven regions including the frontal cortex were significant decreased compared with those of the nonischemic side. Nefiracetam significantly improved the impairment of LCBF in the frontal cortex, parietal cortex, caudate putamen, ventral thalamus, amygdaloid nucleus and hippocampus. It also improved the decrease of LCMR_glc in the frontal cortex, ventral thalamus and hippocampus. These results suggested that nefiracetam has ameliorating effects on chronic disorders of LCBF and LCMR_glc induced by MCA occlusion.

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Section: Discussionsupporting

confidence: 58%

Nefiracetam Improves the Impairment of Local Cerebral Blood Flow and Glucose Utilization after Chronic Focal Cerebral Ischemia in Rats

Jin

Watabe²,

Yamamoto³

2002

Pharmacology

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“…In the MCA occlusion model, the cholinergic basal forebrain complex is not involved in the infarcted area, but the cholinergic fibers from the basal nucleus to the cortex are injured. 29 It was reported that the acetylcholinesterase-positive fiber density was significantly reduced in the cortex on the occluded side and the acetylcholine levels in the infarcted cortex were significantly decreased. 29 " 31 Based on the results cited above, the memory disturbance observed in this study is ascribed to the impairment of cerebral neocortex.…”

Section: Discussionmentioning

confidence: 98%

Disturbance of retention of memory after focal cerebral ischemia in rats.

Hirakawa

Tamura

Nagashima

et al. 1994

Stroke

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Background and Purpose The purpose of this study was to investigate the behavioral changes, in particular retention of memory, after focal cerebral ischemia in rats.Methods Ischemia was produced by permanent occlusion of the left middle cerebral artery (MCA). For quantitative behavioral analysis, one-trial passive avoidance response and active avoidance response with the discrete lever-press avoidance procedure were observed. One group of animals was trained once to learn the passive avoidance task 1 day before surgery. The response latency was examined 4 and 14 days after surgery. The second group was trained to learn the active avoidance task for 2 weeks before surgery. The avoidance rate was examined 3 and 14 days after surgery.

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“…The blood supply to the hippocampus, recognized for its key role in spatial memory, is not derived from the MCA (Scremin, 1995). Spatial memory deficits after MCAO reported using the watermaze may be explained by denervation of the hippocampus due to damaged projections from infarcted cortex, thalamic atrophy, or denervated basal nucleus cholinergic fibers to the cortex (Fujie et al, 1990;Kataoka et al, 1991). Alternatively, neocortical sites, some of which lie within the MCA territory, are known to be involved in spatial learning and memory (Frankland and Bontempi, 2005).…”

Section: Introductionmentioning

confidence: 99%

Watermaze Performance after Middle Cerebral Artery Occlusion in the Rat: The Role of Sensorimotor versus Memory Impairments

Bingham

Martin

Macrae

et al. 2012

J Cereb Blood Flow Metab

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In rodent stroke models, investigation of deficits in spatial memory using the Morris watermaze may be confounded by coexisting sensory or motor impairments. To target memory specifically, we devised a watermaze protocol to minimize the impact of sensory and motor impairments in female Lister-hooded rats exposed to proximal electrocoagulation of the middle cerebral artery (MCAO). Rats were trained in a reference-memory task comprising 4 trials/day; trial 1 being a probe trial (platform absent for the first 60 seconds). Training ended once animals reached a strict criterion based on the probe-trial performance. Memory retention was tested 1, 7, and 28 days later. The MCAO did not affect the number of days to reach criterion during acquisition or the time spent in target quadrant during retention testing, compared with sham or unoperated rats. However, MCAO rats showed slightly poorer accuracy in crossing the platform location and increased thigmotactic swimming compared with controls. Our results show that spatial memory deficits are minimal in this rodent stroke model, and suggest that previously published watermaze impairments are attributable to sensory and motor deficits but not memory deficits. We recommend using probe trials and training to a predetermined performance criterion in future studies assessing watermaze memory deficits in rodent stroke models.

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Cholinergic deafferentation after focal cerebral infarct in rats.

Cited by 74 publications

References 25 publications

Nefiracetam Improves the Impairment of Local Cerebral Blood Flow and Glucose Utilization after Chronic Focal Cerebral Ischemia in Rats

Nefiracetam Improves the Impairment of Local Cerebral Blood Flow and Glucose Utilization after Chronic Focal Cerebral Ischemia in Rats

Disturbance of retention of memory after focal cerebral ischemia in rats.

Watermaze Performance after Middle Cerebral Artery Occlusion in the Rat: The Role of Sensorimotor versus Memory Impairments

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