Locomotor hyperactivity and hippocampal CA1 injury after transient forebrain ischemia of gerbils

Kuroiwa, Toshihiko; Bonnekoh, Petra; Hossmann, Konstantin‐Alexander

doi:10.1016/0304-3940(91)90842-h

Cited by 72 publications

(43 citation statements)

References 12 publications

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“…A previous study in adult gerbils has shown increased locomotor activity after global brain ischemia. 29 These results and those of the present study may be related to the cortical and hippocampal damage. It has been proposed that the increased locomotion reflects a deficit in habituation or spatial mapping rather than primarily a defect in sensorimotor function.…”

Section: Behavioral Evaluationsupporting

confidence: 77%

Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A _2A Knockout Mice

Ådén

Halldner²,

Lagercrantz³

et al. 2003

Stroke

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Section: Behavioral Evaluationsupporting

confidence: 77%

Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A _2A Knockout Mice

Ådén

Halldner²,

Lagercrantz³

et al. 2003

Stroke

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“…One of the classic signs following global ischemia in the gerbil is an acute increase in locomotion that persists for at least 1 day following a 5 min occlusion (Kuroiwa et al, 1991;Colbourne et al, 1998). Our results show that ischemic animals from both suppliers exhibited an increase in locomotion following ischemia, however only the HO ischemic group displayed a sustained increase at 24 hr.…”

Section: Discussionmentioning

confidence: 54%

Increased Behavioral and Histological Variability Arising From Changes in Cerebrovascular Anatomy of the Mongolian Gerbil

Laidley¹,

Colbourne²,

Corbett

2005

CNR

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Abstract:The Mongolian gerbil (Meriones unguiculatus) has been used extensively as a model of forebrain ischemia. Its unique susceptibility to ischemia was suggested to be due to an incomplete circle of Willis. The relative ease to which ischemia can be induced combined with highly reproducible delayed CA1 cell death following a 5-min occlusion made the model popular in neuroprotection studies. Presently, this assumption was tested that complete forebrain ischemia occurs in all gerbils because increased variability was noticed in neuronal injury and behavioral outcome using this model in the last several years. Here it is reported that gerbils obtained from Charles River, the largest supplier in North America, show a high incidence (22.7 % with bilateral and 38.6% with unilateral anastomoses) of posterior communicating arteries compared to another supplier of gerbils (High Oak Farms, 2.6% with bilateral and 13.2% with unilateral anastomoses, P<0.0001). This increased incidence of complete or partial circle of Willis led to less severe CA1 cell loss in Charles River gerbils (P<0.0001) compared to High Oak gerbils, with an unacceptably high level of inter-animal variability. Similarly, behavioral indices of CA1 ischemic injury (increased locomotion, habituation deficits) were also significantly attenuated in the Charles River animals. High Oak gerbils also displayed increased histological and behavioral variability relative to the pattern obtained several years ago. Thus, the gerbil model of forebrain ischemia, at least using Charles River animals, no longer produces consistent injury and behavioral alterations. Investigators are urged to consider adopting other models in future neuroprotection studies or ensure that their gerbil population lacks communicating arteries.

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“…Following ischemic brain injury a locomotor hyperactivity has been noted for 7 days (Kuroiwa et al, 1991;Karasawa et al, 1994). Hyperactivity was directly connected with neuronal alterations in the ischemic hippocampus (Kuroiwa et al, 1991;Kiryk et al, 2011). Longer ischemia and longer locomotor hyperactivity is significantly associated with increased hippocampal neurons changes (Block 1999).…”

Section: Disabilities After Ischemiamentioning

confidence: 99%

“…Some spontaneous recovery of sensorimotor function has been demonstrated after brain ischemia . Following ischemic brain injury a locomotor hyperactivity has been noted for 7 days (Kuroiwa et al, 1991;Karasawa et al, 1994). Hyperactivity was directly connected with neuronal alterations in the ischemic hippocampus (Kuroiwa et al, 1991;Kiryk et al, 2011).…”

Section: Disabilities After Ischemiamentioning

confidence: 99%

Alzheimer's Factors in Ischemic Brain Injury

Pluta¹,

Jabłoński²

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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Locomotor hyperactivity and hippocampal CA1 injury after transient forebrain ischemia of gerbils

Cited by 72 publications

References 12 publications

Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A _2A Knockout Mice

Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A _2A Knockout Mice

Increased Behavioral and Histological Variability Arising From Changes in Cerebrovascular Anatomy of the Mongolian Gerbil

Alzheimer's Factors in Ischemic Brain Injury

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Locomotor hyperactivity and hippocampal CA1 injury after transient forebrain ischemia of gerbils

Cited by 72 publications

References 12 publications

Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A 2A Knockout Mice

Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A 2A Knockout Mice

Increased Behavioral and Histological Variability Arising From Changes in Cerebrovascular Anatomy of the Mongolian Gerbil

Alzheimer's Factors in Ischemic Brain Injury

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Product

Resources

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Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A _2A Knockout Mice

Aggravated Brain Damage After Hypoxic Ischemia in Immature Adenosine A _2A Knockout Mice