Late behavioural and neuropathological effects of local brain irradiation in the rat

Hodges, Helen; Katzung, Nicole; Sowiński, P.; Hopewell, J. W.; Wilkinson, John; Bywaters, T.; Rezvani, M.

doi:10.1016/s0166-4328(97)00108-3

Cited by 96 publications

(73 citation statements)

References 54 publications

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“…* P Ͻ .05, ** P Ͻ .01, compared with their corresponding sham. jury that mimics the clinical manifestation to a large extent by testing different irradiation dosages (10,20, and 40 Gy) with a linear accelerator.…”

Section: Figmentioning

confidence: 99%

“…To our knowledge, only a few reports have established cognitive dysfunction in rats exposed to irradiation but have mainly focused on late-onset RE. 19 Hodges et al 20 reported radiation-induced deficits in a T-maze forced choice alteration and a subsequent dose-dependent water maze deficit during a period of 44 weeks. They indicated that local cranial irradiation with a low dose (20 Gy) of x-rays could produce a cognitive deficit in adult rats without evidence of pathologic changes.…”

Section: Figmentioning

confidence: 99%

See 1 more Smart Citation

An Experimental Study of Acute Radiation-Induced Cognitive Dysfunction in a Young Rat Model

Liu¹,

Xiao²,

Liu³

et al. 2009

AJNR Am J Neuroradiol

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Section: Figmentioning

confidence: 99%

Section: Figmentioning

confidence: 99%

An Experimental Study of Acute Radiation-Induced Cognitive Dysfunction in a Young Rat Model

Liu¹,

Xiao²,

Liu³

et al. 2009

AJNR Am J Neuroradiol

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“…Postnatal neurogenesis probably plays an important role in normal hippocampal function, [15][16][17] and IR has been demonstrated to decrease neuronal proliferation 18,19 and contribute to memory dysfunction in rodents. 20,21 Malignant cells are generally highly sensitive to IR because of their loss of growth regulation and genomic stability. However, as part of the perturbed growth regulation, most tumor cells have lost their ability to undergo apoptosis, which means that they will die through mitotic catastrophe or senescence-like permanent growth arrest upon RT.…”

Section: Introductionmentioning

confidence: 99%

Irradiation-induced progenitor cell death in the developing brain is resistant to erythropoietin treatment and caspase inhibition

et al. 2004

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One hemisphere of postnatal day 8 (P8) rats or P10 mice was irradiated with a single dose of 4-12 Gy, and animals were killed from 2 h to 8 weeks after irradiation (IR). In the subventricular zone (SVZ) and the granular cell layer (GCL) of the dentate gyrus, harboring neural and other progenitor cells, nitrosylation and p53 peaked 2-12 h after IR, followed by markers for active caspase-3, apoptosis-inducing factor and TUNEL (6-24 h). Ki67-positive (proliferating) cells had disappeared by 12 h and partly reappeared by 7 days post-IR. The SVZ and GCL areas decreased approximately 50% 7 days after IR. The development of white matter was hampered, resulting in 50-70% less myelin basic protein staining. Pretreatment with erythropoietin did not confer protection against IR. Caspase inhibition by overexpression of XIAP prevented caspase-9 and caspase-3 activation but not cell death, presumably because of increased caspase-independent cell death.

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“…The high toxicity of low doses of 56 Fe particles leads to shortened latency for age-like cognitive deficits, in contrast to chronic cognitive impairments induced by clinical brain irradiation schemes (19,20). At 1 month after 1.5 Gy whole-body 56 Fe irradiation, analysis of the Morris water maze behavioral tests in rats revealed deterioration of spatial learning and memory (3).…”

Section: Discussionmentioning

confidence: 99%

Neuroimaging assessment of memory‐related brain structures in a rat model of acute space‐like radiation

Huang¹,

Smith²,

Cummings³

et al. 2009

Magnetic Resonance Imaging

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Purpose: To investigate the acute effects on the central nervous system (CNS) of 56 Fe radiation, a component of high-energy charged particles (HZE) in space radiation, using quantitative magnetic resonance imaging (MRI) noninvasively. Materials and Methods:Sprague-Dawley rats were exposed to whole-brain 56 Fe (0, 1, 2, and 4 Gy). At 1 week postirradiation, MRI scans were made using T2-weighted (T2WI), diffusion-weighted (DWI), and contrast enhanced T1-(CET1) imaging. T2 relaxation time and apparent diffusion coefficient (ADC) values were obtained from memoryrelated brain regions of interest (ROIs). Histopathology was correlated using ex vivo tissues. Results:No overt abnormalities were visualized using T2WI and DWI at 1 week postradiation. CET1 values did not differ significantly between the irradiated and control animals. Compared to 0 Gy, there were significant prolongations in T2 values and reductions in ADC after irradiation. In the absence of evident neuronal pathology, immunohistochemistry revealed astrocytic activation in 4 Gy animals. Conclusion:At 1 week after whole-brain 56 Fe exposure, T2 and ADC values can differentiate radiosensitivity in regions critical for hippocampal-related memory. MRI may provide noninvasive assessment of the initial molecular/cellular disturbances in vivo after HZE irradiation.

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Late behavioural and neuropathological effects of local brain irradiation in the rat

Cited by 96 publications

References 54 publications

An Experimental Study of Acute Radiation-Induced Cognitive Dysfunction in a Young Rat Model

An Experimental Study of Acute Radiation-Induced Cognitive Dysfunction in a Young Rat Model

Irradiation-induced progenitor cell death in the developing brain is resistant to erythropoietin treatment and caspase inhibition

Neuroimaging assessment of memory‐related brain structures in a rat model of acute space‐like radiation

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