Neuroscience letters
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Neuroscience letters · Jul 2008
Region-specific modulation of PER2 expression in the limbic forebrain and hypothalamus by nighttime restricted feeding in rats.
Feeding schedules that restrict food access to a predictable daytime meal induce in rodents food-anticipatory behaviors, changes in physiological rhythms and shifts in the rhythm of clock gene expression in the brain and periphery. However, little is known about the effects of nighttime restricted feeding. Previously, we showed that daytime restricted access to a highly palatable complete meal replacement, Ensure Plus (Ensure), shifts the rhythm of expression of the clock protein PER2 in limbic forebrain areas including the oval nucleus of the bed nucleus of the stria terminalis (BNSTov), central nucleus of the amygdala (CEA), basolateral amygdala (BLA) and dentate gyrus (DG), and induces a rhythm in the dorsomedial hypothalamic nucleus (DMH) in food deprived (restricted feeding), but not free-fed rats (restricted treat). ⋯ In contrast to previous work with daytime restricted feeding, nighttime restricted feeding had no effect on PER2 rhythms in the BLA and DG. Finally, nighttime restricted treats, as was the case for daytime restricted treats, had no effect on PER2 expression in any of the brain areas studied. The present results together with our previous findings show that the effect of restricted feeding on PER2 rhythms in the limbic forebrain and hypothalamus depend on a negative energy balance and vary as a function of time of day in a brain region-specific manner.
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Neuroscience letters · Jul 2008
Activation of spinal microglia in a murine model of peripheral inflammation-induced, long-lasting contralateral allodynia.
Increased sensitivity contralateral to an injury has been described in humans and in various models of neuropathic pain in rats. The mechanism underlying contralateral hypersensitivity is as yet unclear, although previous studies have implicated involvement of both spinal neurons and glia. ⋯ The delayed development of contralateral allodynia correlated with an increase in OX-42, but not GFAP immunoreactivity in the contralateral dorsal horn. Furthermore, intrathecal treatment with minocycline inhibited the development of contralateral allodynia, suggesting that microglial activation plays a key role in contralateralization, and may be a potential target for clinical intervention after injury or inflammation has occurred, to eliminate the subsequent development of extraterritorial pain.
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Neuroscience letters · Jul 2008
Tx3-4 a toxin from the venom of spider Phoneutria nigriventer blocks calcium channels associated with exocytosis.
The purpose of the present work was to investigate the pharmacological action of a calcium channel-blocking toxin from the venom of the spider Phonetic nigriventer, Tx3-4 on calcium channels coupled to exocytosis of synaptic vesicles. Tx3-4 blocked KCl-induced exocytosis of synaptic vesicles with an IC50 of 1.1 nM. ⋯ The results indicate that the main population of voltage-sensitive calcium channels altered by Tx3-4 is P/Q calcium channels. In conclusion, Tx3-4 is a potent inhibitor of calcium channels involved in the KCl-induced exocytosis of synaptic vesicles in brain cortical synaptosomes.
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Neuroscience letters · Jul 2008
Activation of p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK) and c-jun N-terminal kinase (JNK) during hypoxia in cerebral cortical nuclei of guinea pig fetus at term: role of nitric oxide.
Previously we have shown that cerebral tissue hypoxia results in generation of nitric oxide (NO) free radicals as well as increased expression of mitogen-activated protein kinase like extracellular signal-regulated kinase (ERK) and c-jun N-terminal kinase (JNK). The present study tested the hypothesis that administration of l-nitro-l-arginine methyl ester (L-NAME), a NOS inhibitor, prior to hypoxia prevents the hypoxia-induced activation of p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK) and c-jun N-terminal kinase (JNK) and in the cerebral cortex of the term guinea pig fetus. To test this hypothesis normoxic (Nx, n=6), hypoxic (Hx, n=7) and hypoxic pretreated with l-NAME (Hx+L-NAME, n=6) guinea pig fetuses at 60 days gestation were studied to determine the phosphorylated p38, ERK and JNK. ⋯ The data show that administration of l-NAME prior to hypoxia decreased the relative level of phosphorylated p38, ERK and JNK at term gestation. Since a NOS inhibitor prevented the hypoxia-induced phosphorylation of p38, ERK and JNK, we conclude that the hypoxia-induced activation of p38, ERK and JNK in the cerebral cortical nuclei of guinea pig fetus at term is NO-mediated. We speculate that NO-mediated modification of cysteine residue leading to inhibition of MAP kinase phosphatases results in increased activation of p38, ERK and JNK in the guinea pig fetus at term.
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Neuroscience letters · Jul 2008
Virtual needle pain stimuli activates cortical representation of emotions in normal volunteers.
Psychological factors are known to play an extremely important role in the maintenance and development of chronic pain conditions. However, it is unclear how such factors relate to the central neural processing of nociceptive transmission in healthy individuals. To investigate this issue, the activation of the brain was studied in 30 healthy volunteers responding to virtual pain stimuli by fMRI. ⋯ On the other hand, right parietal operculum (S2: BA40), premotor area, parietal association cortex, left inferior frontal gyrus and bilateral temporal association cortex were activated in the non-preconditioned group. In addition, activation of anterior insula, inferior frontal gyrus, precentral gyrus and cerebellum significantly increased in the preconditioned group compared with the non-preconditioned group. These results suggest that the virtual needle puncture task caused memory retrieval of unpleasant experiences which is possibly related to empathy for pain, resulting in the activation of specific brain areas.