Neuroscience letters
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Neuroscience letters · Sep 2014
Docosahexaenoic acid intake ameliorates ketamine-induced impairment of spatial cognition and learning ability in ICR mice.
Several studies have reported the ketamine-induced cognitive impairment. Docosahexaenoic acid (DHA) supplementation improves cognitive function in human infants and protects against learning impairment in patients with Alzheimer's disease (AD). In this study, we investigated the effect of DHA on ketamine-induced impairment of spatial cognition and learning ability in Institute of Cancer Research (ICR) mice. ⋯ The results showed that intraperitoneal injection of ketamine (30mg/kg, twice per day) for 4 weeks led to the decline of spatial cognitive ability in mice, and 420mg/(kgd) DHA supplementation for 6 weeks improved ketamine-induced spatial cognitive impairment to a certain extent. The up-regulation of GABA levels in the hippocampus and prefrontal cortex was related to the improvement in spatial learning. Our results suggested that DHA supplementation would be a promising intervention to improve ketamine-induced spatial memory and cognitive dysfunction, and this effect of DHA might be correlated with the up-regulation of GABA levels.
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Neuroscience letters · Sep 2014
Disrupted MEK/ERK signaling in the medial orbital cortex and dorsal endopiriform nuclei of the prefrontal cortex in a chronic restraint stress mouse model of depression.
Depression is one of the most prevalent mental illnesses, and causes a constant feeling of sadness and lose of interest, which often leads to suicide. Evidence suggests that depression is associated with aberrant MEK/ERK signaling. However, studies on MEK/ERK signaling in depression have only been done in a few brain regions, such as the hippocampus and mesolimbic reward pathways. ⋯ This depressive behavior was ameliorated by imipramine. The behavioral changes well corresponded to a decrease in MEK/ERK immunoreactivity in the medial orbital (MO) cortex and dorsal endopiriform nuclei (DEn), which was averted by imipramine, but not in cingulate, prelimbic, infralimbic, and motor cortex. These results suggest that MEK/ERK signaling is disrupted in the DEn and MO subregions of the prefrontal cortex in the depressive phenotype, and that blocking a decrease in activated MEK/ERK is inherent to the antidepressant imipramine response.
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Neuroscience letters · Sep 2014
Blast-induced tinnitus and spontaneous activity changes in the rat inferior colliculus.
High-pressure blast shockwaves are known to cause tinnitus. Imaging studies have shown that blast-induced tinnitus may result from damage to the inner ear structures and/or direct brain impact that trigger a cascade of neuroplastic changes in both auditory and non-auditory centers. Nevertheless, information is still lacking on the neurophysiological mechanisms underlying blast-induced tinnitus. ⋯ Although the induced hyperactivity persisted throughout a three-month recording period, it was more robust in middle frequency loci at one month after blast exposure and in middle-to-high-frequency loci at three months after blast. Our results also showed increased bursting rate in the low and middle frequency regions at one day after blast, in the middle frequency region at one month after blast, and in all frequency regions at three months after blast. The findings suggest that neuroplasticity as reflected by shifted tonotopic representations of hyperactivity and bursting activity subserves blast-induced tinnitus and hearing impairment.
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Neuroscience letters · Sep 2014
Morphine and oxycodone, but not fentanyl, exhibit antinociceptive effects mediated by G-protein inwardly rectifying potassium (GIRK) channels in an oxaliplatin-induced neuropathy rat model.
It has begun to be understood that μ-opioid receptor (MOR) produces ligand-biased agonism, which contributes to differential physiological functions of MOR agonists. We previously demonstrated that in oxaliplatin-induced neuropathy in rats, morphine and oxycodone exhibited antinociceptive effects while antinociception of fentanyl was partial, and such different efficacies might result from the different level of Gi/o protein activation. Based on our background, to reveal further mechanism, we focused on the role of Gi/o protein-related downstream signaling, the G-protein inwardly rectifying K(+)1 (GIRK1) channel. ⋯ Partial antinocicpetion of fentanyl (0.017mg/kg, s.c.) was neither affected by i.c.v nor i.t. tertiapin-Q. These results demonstrated that GIRK1 channels differentially contribute to antinociceptive effects of MOR agonists, and that action site of GIRK1 channels is also different between morphine and oxycodone in oxaliplatin model. This study suggests the possibility that GIRK1 channels have a crucial role for antinociception of MOR agonists in oxaliplatin-induced neuropathy.
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Neuroscience letters · Sep 2014
Expression profile of vesicular nucleotide transporter (VNUT, SLC17A9) in subpopulations of rat dorsal root ganglion neurons.
ATP plays an important role in the signal transduction between sensory neurons and satellite cells in dorsal root ganglia (DRGs). In primary cultured DRG neurons, ATP is known to be stored in lysosomes via a vesicular nucleotide transporter (VNUT), and to be released into the intercellular space through exocytosis. ⋯ On immunohistochemical analysis, VNUT was found in DRG neurons, and was predominantly expressed by the small- and medium-sized DRG ones, as judged upon visual inspection, and this was compatible with the finding that the number of VNUT-positive DRG neurons in IB4-positive cells was greater than that in NF200-positive ones. These results suggest that VNUT play a role in ATP accumulation in DRG neurons, especially in small- and medium-sized ones, and might be involved in ATP-mediated nociceptive signaling in DRGs.