Hippocampal (CA1) activities in Wistar rats from different vendors

Is endothelial dysfunction of cerebral small vessel responsible for white matter lesions after chronic cerebral hypoperfusion in rats?

“…Chronic bilateral occlusion of the common carotid arteries of the rat reduces corpus callosum blood flow to 48.8% of normal levels at 2.5 h post-occlusion [24]. Seven days later, the reduction in flow has abated to 60-75% and it remains at this reduced level for at least several months [23]. In the present study, first we induced WMLs in a rat chronic cerebral hypoperfusion model by permanent occlusion of both common carotid arteries.…”

“…The cerebral blood flow (CBF) immediately falls and remains very low in the acute phase after the start of occlusion and lasts for a maximum of 2-3 days creating hypoxic-ischemic conditions [23]. Chronic bilateral occlusion of the common carotid arteries of the rat reduces corpus callosum blood flow to 48.8% of normal levels at 2.5 h post-occlusion [24].…”

Resveratrol treatment has neuroprotective effects and prevents cognitive impairment after chronic cerebral hypoperfusion

“…36 Although the temporal profiles of NGF in the hippocampal CA1 pyramidal cells after CCH remain poorly understood, several lines of evidence indicate that in noxious conditions astrocytes may be the site of NGF production. 37,38 Reactive astrogliosis is considered to be a late-emerging event in the hippocampus after CCH induction 3,39,40 and this may explain the high hippocampal NGF levels even under a significant pyramidal cell loss in the CA1 region.…”

Fundamental interstrain differences in cortical activity between Wistar and Sprague–Dawley rats during global ischemia

“…Many previous studies have revealed significant interstrain and intrastrain differences in rat collateral anastomoses (Oliff et al, 1997), the infarct volumes caused by focal cerebral ischemia (Oliff et al, 1995a,b), the responses evoked in the hippocampal CA1 subfield after 2VO (Marosi et al, 2006) and variable neuroprotective effects of MK-801 (Oliff et al, 1996), but the main reason for this variability is still unclear. Although there are considerable discrepancies in cerebral vascular anatomy (Brown, 1966), the collateral anastomoses display nearly equal luminal widths for all the strains/lines (Brown, 1966;Oliff et al, 1997).…”

“…As merely one example, there are six different variations in the anatomy of the arterial circle of rats (Brown, 1966). In consequence of such anatomical differences, it has been found that the specific features of the different rat and mouse strains (Ginsberg and Busto, 1989;Barone et al, 1992) supplied by the different vendors (Marosi et al, 2006) are the determining factors most strongly influencing the outcome of global or focal cerebral ischemia (Barone et al, 1993). To the best of our knowledge, there are no published comparative morphological and electrophysiological data dealing with the ischemic interstrain differences between Wistar and Sprague-Dawley rats.…”