Neuroscience
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Chronic neuropathic pain is a frequent comorbidity following spinal cord injury (SCI) and often fails to respond to conventional pain management strategies. Preventive administration of docosahexaenoic acid (DHA) or the consumption of a diet rich in omega-3 polyunsaturated fatty acids (O3PUFAs) confers potent prophylaxis against SCI and improves functional recovery. The present study examines whether this novel dietary strategy provides significant antinociceptive benefits in rats experiencing SCI-induced pain. ⋯ The spinal cord levels of inositols were positively correlated with thermal hyperalgesia, supporting their role as biomarkers of chronic neuropathic pain. Notably, the O3PUFA-rich dietary intervention reduced the levels of these metabolites. Collectively, these results demonstrate the prophylactic value of dietary O3PUFA against SCI-mediated chronic pain.
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To our knowledge, the present data are the first to demonstrate that activation of membrane estrogen receptors (mERs) abolishes opioid receptor-like 1 (ORL1) receptor-mediated analgesia via extracellular signal-regulated kinase (ERK)-dependent non-genomic mechanisms. Estrogen was shown previously to both attenuate ORL1-mediated antinociception and down-regulate the ORL1 gene expression. The present study investigated whether non-genomic mechanisms contribute to estrogen-induced attenuation of ORL1-mediated antinociception by the mERs GPR30, Gq-coupled mER, ERα, and ERβ. ⋯ Activation of GPR30, Gq-mER, ERα, but not ERβ abolished ORL1-mediated antinociception in males and OVX females. E2BSA produced a parallel and significant increase in the phosphorylation of ERK 2 only in OVX females, and pre-treatment with MEK/ERK 1/2 inhibitor, U0126 (10 μg), blocked the mER-mediated abolition of ORL1-mediated antinociception in OVX females. Taken together, the data are consistent with the interpretations that mER activation attenuates ORL1-mediated antinociception through a non-genomic, ERK 2-dependent mechanism in females.
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Food hoarding, especially scatter hoarding and retrieving food caches, requires spatial learning and memory and is an adaptive behavior important for an animal's survival and reproductive success. In the present study, we examined the effects of hoarding behavior on cell proliferation and survival in the hippocampus of male and female Siberian chipmunks (Tamias sibiricus). ⋯ In addition, the display of hoarding behavior was associated with increased cell proliferation in the hippocampus and this increase occurred in a brain region-specific manner. These data provide further evidence to support the notion that new cells in the adult hippocampus are affected by learning and memory tasks and may play an important role in adaptive behavior.
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The quality of motion perception depends on visual input during early development. Even 1month of binocular deprivation (BD) from birth impairs motion coherence thresholds when tested in kittens; conversely BD with a 1-month delayed onset does not impair it (Mitchell et al., 2009). We showed that 6months of BD applied from birth induces a selective impairment in a Global Motion Detection task, but not in global form perception, when tested in adulthood (Burnat et al., 2002, 2005). ⋯ Motion coherence thresholds, when tested at the end of a long motion training were not affected by BD and did not differ from those obtained for the normal group. Impaired extraction of low contrast-defined motion signal was found in cats deprived solely in months 3-4 of life. Surprisingly, binocular pattern deprivation during the first 2months of life did not weaken motion sensitivity, revealing the occurrence of a critical period for motion perception later in development than previously suggested.
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Cholinergic interneurons, which provide the main source of acetylcholine (ACh) in the striatum, control the striatal local circuits and deeply involve in the pathogenesis of neurodegenerative diseases. Glycogen synthase kinase-3 (GSK-3) is a crucial kinase with diverse fundamental functions and accepted that deregulation of GSK-3 activity also plays important roles in diverse neurodegenerative diseases. However, up to now, there is no direct proof indicating whether GSK-3 activation is responsible for cholinergic dysfunction. ⋯ Furthermore, we proved that cellular ChAT distribution was dependent on low phosphorylation level of NFs. Nevertheless, the cholinergic dysfunction in the striatum failed to induce significant neuronal number reduction. In summary, our data demonstrates the link between GSK-3 activation and cholinergic dysfunction in the striatum and provided beneficial evidence for the pathogenesis study of relevant neurodegenerative diseases.