Gangliosides fail to enhance behavioral recovery after bilateral ablation of the visual cortex

Abstract

Postsurgical injections of GM1 gangliosides (30 mg/kg IP) reduced neither behavioral deficits in rats following bilateral ablation of the visual cortex nor the extent of retrograde degeneration of neurons in the dorsolateral geniculate nucleus that typically accompanies large lesions of the visual cortex. Our findings are in contrast to previous research, in which ganglioside treatments have been shown to enhance the rate of functional recovery after lesions in other parts of the central nervous system. The negative findings in the present experiment may be due to the disruption of normal circadian rhythms caused by occipital cortex injury.

Exercise-induced improvement in cognitive performance after fimbria-fornix transection depends on the timing of exercise administration

“…This may be due to methodological differences -the use of a particular strain of rats (Johnson and Mitchell, 2003) and amount of time with access to the running wheels -both per day and in total. We used Wistar rats and 6 hours/day access to the running wheels for 1 week based on results showing elevation in plasticity-related proteins after the first week of voluntary running (Butler et al, 1987;Griesbach et al, 2004aGriesbach et al, , 2004bGriesbach et al, , 2008Griesbach et al, , 2009. Interestingly, in a study comparing different intensities of forced running, Shen et al (2013) reported that low intensity exercise led to a significant improvement in spatial memory after controlled cortical impact.…”

“…The timing of a behavioural treatment is of crucial importance for successful outcome, but the number of preclinical studies investigating the topic is so far sparse. Whether to start early or later after injury appears to depend on severity of lesion, the nature of behavioural rehabilitative intervention, and the function to be recovered (Barbay et al, 2006;Biernaskie et al, 2004;Butler et al, 1987;Griesbach et al, 2004aGriesbach et al, , 2004bGriesbach et al, , 2007Malá et al, 2012;Shen et al, 2013).…”

“…Voluntary exercise, both acute and chronic, increases levels of hippocampal activity (Holschneider et al, 2003(Holschneider et al, , 2007 and induces hippocampal neurogenesis, cell proliferation and survival in the injured and aging brain (Ehninger and Kempermann, 2003;Speisman et al, 2013;van Praag et al, 1999). Data from both human and animal studies suggest a beneficial link between exercise and cognitive functioning (Hillman et al, 2008;Wogensen et al, 2015), which is (at least partly) mediated by upregulation of neurotrophic and growth factors, such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and fibroblast growth factor (FGF) (Berchtold et al, 2010;Butler et al, 1987;Farmer et al, 2004;Gomez-Pinilla et al, 1997;Griesbach et al, 2004aGriesbach et al, , 2004bGriesbach et al, , 2009Kleim et al, 2003;Neeper et al, 1996;Vaynman et al, 2003Vaynman et al, , 2004.…”