Neuroscience
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Motor feedback usually engages distinct sensory and cognitive processes based on different feedback conditions, e.g., the real and sham feedbacks. It was thought that these processes may rely on the functional connectivity among the brain networks. However, it remains unclear whether there is a difference in the network connectivity between the two feedback conditions. ⋯ Using independent component analysis and functional connectivity analysis, we found that as compared with the sham feedback, the real feedback recruited stronger negative connectivity between the executive network (EN) and the posterior default mode network (pDMN). More intriguingly, the left frontal parietal network (lFPN) exhibits positive connectivity with the pDMN in the real feedback while in the sham feedback, the lFPN shows connectivity with the EN. These results suggest that the connectivity among EN, pDMN, lFPN could differ depending on the real and sham feedbacks, and the lFPN may balance the competition between the pDMN and EN, thus supporting the sensory and cognitive processes of the motor feedback.
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Tastes and odors influence the perception of a meal. Especially food aromas can act as potent signals to modulate our eating behavior with strong dependency on the reward produced by food. In this investigation we aimed to study the electrophysiological response to food- and non-food-related odors in healthy volunteers. Analyses revealed specific scalp potential maps for the two conditions; in particular the source of the map in the "food" condition seemed to be associated with the processing of rewards; the specific map in the "non-food" condition reflects odor characteristics excluding the reward.
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Our understanding of the role of somatosensory feedback in regulating motility during chicken embryogenesis and fetal development in general has been hampered by the lack of an approach to selectively alter specific sensory modalities. In adult mammals, pyridoxine overdose has been shown to cause a peripheral sensory neuropathy characterized by a loss of both muscle and cutaneous afferents, but predominated by a loss of proprioception. We have begun to explore the sensitivity of the nervous system in chicken embryos to the application of pyridoxine on embryonic days 7 and 8, after sensory neurons in the lumbosacral region become post-mitotic. ⋯ Therefore, pyridoxine causes a peripheral sensory neuropathy in embryonic chickens largely consistent with its effects in adult mammals. However, the lesion may be more restricted to proprioception in the chicken embryo. Therefore, pyridoxine lesion induced during embryogenesis in the chicken embryo can be used to assess how the loss of sensation, largely proprioception, alters spontaneous embryonic motility and subsequent motor development.
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Nuclear hormone receptor coregulator-interacting factor 1 (NIF-1) is a zinc finger nuclear protein that was initially identified to enhance nuclear hormone receptor transcription via its interaction with nuclear hormone receptor coregulator (NRC). NIF-1 may regulate gene transcription either by modulating general transcriptional machinery or remodeling chromatin structure through interactions with specific protein partners. We previously reported that the cytoplasmic/nuclear localization of NIF-1 is regulated by the neuronal Cdk5 activator p35, suggesting potential neuronal functions for NIF-1. ⋯ Furthermore, activity-induced Ca(2+) influx, which is critical for neuronal morphogenesis, stimulated the nuclear localization of NIF-1 in cortical neurons. Suppression of NIF-1 expression reduced the up-regulation of neuronal activity-dependent gene transcription. These findings collectively suggest that NIF-1 directs neuronal morphogenesis during early developmental stages through modulating activity-dependent gene transcription.
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Recent research suggests an involvement of pro-opiomelanocortin (POMC) gene products (e.g., beta-endorphin) in modulating cocaine-induced reward and addiction-like behaviors in rodents. In this study, we investigated whether chronic "binge" cocaine and its withdrawal altered POMC gene expression in the brain of rats. Male Fischer rats were treated with two different chronic (14-day) "binge" pattern cocaine administration regimens (three injections at 1-h intervals, i.p.): steady-dose (45mg/kg/day) and escalating-dose (90mg/kg on the last day). ⋯ In contrast, after acute (1-day) withdrawal from chronic "binge" escalating-dose regimen, but not steady-dose regimen, there were increased hypothalamic POMC mRNA levels that persisted into 14days of protracted withdrawal. To study the role of the endogenous opioid systems in the cocaine withdrawal effects, we administered a single naloxone injection (1mg/kg) that caused elevated POMC mRNA levels observed 24h later in cocaine naïve rats, but it did not lead to further increases in cocaine-withdrawn rats. Our results suggest that during withdrawal from chronic "binge" escalating-dose cocaine: (1) there was a persistent increase in hypothalamic POMC gene expression; and (2) hyposensitivity of the POMC gene expression to naloxone indicates altered opioidergic tone at or above the hypothalamic level.