Diss. (sammanfattning) Umeå : Umeå universitet, 2006. / Härtill 4 uppsatser.

Diss. (sammanfattning) Uppsala : Uppsala universitet, 2005. / Härtill 4 uppsatser.

Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2006. / Härtill 3 uppsatser.

Thesis (doctoral)--University of Copenhagen, 2007. / Thesis is based on seven published studies by the author. Includes bibliographical references.

Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2006. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2001. / Härtill 5 uppsatser.

Since caloric restriction (CR) can modify multiple pathways central to the ischemic cascade and enhance neuroplasticity mechanisms, we hypothesized that CR should exert protective effects following brain ischemia. Previous studies have suggested benefit when CR was administered prior to ischemia. This study investigated whether prolonged CR beginning after global ischemia would result in lasting protection as assessed by performance in the open field, as a measure of functional outcome, and hippocampal CA1 neuronal counts. Adult male Mongolian gerbils were subjected to five minute bilateral carotid artery occlusion (I) or sham surgery (S) with tympanic temperature maintained at 36.5 ± 0.2ºC during the intra-ischemic period. After screening out gerbils with incomplete ischemia, each of the two surgical groups were randomly assigned to control diet (CON) or 30% CR for the duration of the study (60d). Gerbils were tested in the open field on d3, 7, 10, 30 and 60. Ischemic animals on control diet showed a significantly higher level of activity in the open field (impaired habituation) compared to SCON gerbils on all test days (p<0.001). Open field activity was decreased 9% in the ICR group versus ICON gerbils on d7 (p=0.024), suggesting a transient neuroprotective effect. Open field activity of the SCR gerbils began increasing relative to that of SCON gerbils during the last 30 days of the study (p=0.055 on d60), raising the question of suitability of the open field test for long-term studies of CR and ischemia. Brain sections obtained at d60 were stained with hematoxylin & eosin. Hippocampal CA1 neuron counts were reduced 88% by ischemia (p<0.001), and there was no sparing effect of CR. These findings suggest that prolonged CR administered beginning after global ischemia cannot diminish brain injury or enhance long-term recovery.

Since caloric restriction (CR) can modify multiple pathways central to the ischemic cascade and enhance neuroplasticity mechanisms, we hypothesized that CR should exert protective effects following brain ischemia. Previous studies have suggested benefit when CR was administered prior to ischemia. This study investigated whether prolonged CR beginning after global ischemia would result in lasting protection as assessed by performance in the open field, as a measure of functional outcome, and hippocampal CA1 neuronal counts. Adult male Mongolian gerbils were subjected to five minute bilateral carotid artery occlusion (I) or sham surgery (S) with tympanic temperature maintained at 36.5 ± 0.2ºC during the intra-ischemic period. After screening out gerbils with incomplete ischemia, each of the two surgical groups were randomly assigned to control diet (CON) or 30% CR for the duration of the study (60d). Gerbils were tested in the open field on d3, 7, 10, 30 and 60. Ischemic animals on control diet showed a significantly higher level of activity in the open field (impaired habituation) compared to SCON gerbils on all test days (p<0.001). Open field activity was decreased 9% in the ICR group versus ICON gerbils on d7 (p=0.024), suggesting a transient neuroprotective effect. Open field activity of the SCR gerbils began increasing relative to that of SCON gerbils during the last 30 days of the study (p=0.055 on d60), raising the question of suitability of the open field test for long-term studies of CR and ischemia. Brain sections obtained at d60 were stained with hematoxylin & eosin. Hippocampal CA1 neuron counts were reduced 88% by ischemia (p<0.001), and there was no sparing effect of CR. These findings suggest that prolonged CR administered beginning after global ischemia cannot diminish brain injury or enhance long-term recovery.

Thesis (doctoral)--Lund University, 1996. / Added t.p. with thesis statement inserted.

Thesis (doctoral)--Lund University, 1996. / Added t.p. with thesis statement inserted.