Neuroscience
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Nicotine is known to have enhancing effects on some aspects of attention and cognition. As for the pre-attentive processes of detecting sensory changes, nicotine has significant effects on the auditory and visual systems implying that its pre-attentive effect is common among sensory modalities. The purpose of the present study was to elucidate whether acute nicotine administration has enhancing effects in the somatosensory system. ⋯ Effects of nicotine on the cortical response in the primary (S1) and secondary (S2) somatosensory cortices were investigated. Results showed that nicotine failed to affect the S1 response while it significantly increased the amplitude of S2 activity in the hemisphere ipsilateral to the stimulation, and shortened the peak latency of S2 activity in both hemispheres. Since cortical responses in the present study represent a pre-attentive automatic process to encode new somatosensory events, the results suggest that nicotine can exert beneficial cognitive effects without a direct impact on attention and that the effect of nicotine on the automatic change-detecting system is common across sensory modalities.
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Stanniocalcin 1 (STC1), originally described as an antihypercalcemic hormone in fish, is highly expressed in differentiated mammalian neurons. Mild hypoxic treatment and focal cerebral ischemia induce upregulation of STC1 in the brain. These findings prompted us to investigate whether STC1 contributes to neuroprotection after ischemia and whether STC1 is required for development of ischemic tolerance. ⋯ Ischemic STC1(-/-) mice showed significantly lower Il-6 mRNA expression than ischemic WT mice. Evans Blue fluorescence levels showed no difference in between WT and STC1(-/-) mice under evaluated conditions, thus BBB integrity is preserved despite STC1 deficiency. STC1 was not crucial for the development of ischemic tolerance triggered by HPC or for preserving BBB integrity but may be involved in functional recovery after stroke.
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Mechanism of hyperphagia contributing to obesity in brain-derived neurotrophic factor knockout mice.
Global-heterozygous and brain-specific homozygous knockouts (KOs) of brain-derived neurotrophic factor (BDNF) cause late- and early-onset obesity, respectively, both involving hyperphagia. Little is known about the mechanism underlying this hyperphagia or whether BDNF loss from peripheral tissues could contribute to overeating. Since global-homozygous BDNF-KO is perinatal lethal, a BDNF-KO that spared sufficient brainstem BDNF to support normal health was utilized to begin to address these issues. ⋯ This could imply that augmentation of vago-vagal digestive reflexes occurred (e.g., accommodation), which would support increased meal size and possibly increased meal number by reducing the increase in intragastric pressure produced by a given amount of ingesta. Additionally, vagal sensory neuron number in BDNF-KO mice was altered in a manner consistent with the increased meal-induced activation of the DMV. These results suggest reduced BDNF causes satiety and satiation deficits that support hyperphagia, possibly involving augmentation of vago-vagal reflexes mediated by central pathways or vagal afferents regulated by BDNF levels.
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Although respiratory complications are a major cause of morbidity/mortality in many neural injuries or diseases, little is known concerning mechanisms whereby deficient myelin impairs breathing, or how patients compensate for such changes. Here, we tested the hypothesis that respiratory and forelimb motor functions are impaired in a rat model of focal dorsolateral spinal demyelination (ethidium bromide, EB). Ventilation, phrenic nerve activity and horizontal ladder walking were performed 7-14 days post-C2 injection of EB or vehicle (SHAM). ⋯ This ratio was significantly reduced 7 days post-EB versus SHAM during baseline conditions, and versus SHAM and 14-day groups during chemoreceptor activation. Limb function ipsilateral to EB was impaired 7 days post-EB and partially recovered by 14 days post-EB. EB provides a reversible model of focal, spinal demyelination, and may be a useful model to study mechanisms of functional impairment and recovery via motor plasticity, or the efficacy of new therapeutic interventions to reduce severity or duration of disease.
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Leptin microinjections into the nucleus of the solitary tract (NTS) have been shown to elicit sympathoexcitatory responses, and potentiate the cardiovascular responses to activation of the chemoreflex. In this study, experiments were done in Sprague-Dawley rats initially to provide a detailed mapping within the NTS complex of cells containing immunoreactivity to the long form of the leptin receptor (Ob-Rb). In a second series, this NTS region containing Ob-Rb immunoreactive cells was explored for single units antidromically activated by stimulation of pressor sites in the rostral ventrolateral medulla (RVLM). ⋯ In addition, 17 of these leptin responsive neurons were excited by the intra-carotid injections of KCN (80 μg/0.1 ml). Furthermore, the excitatory response of these single units to KCN was potentiated (59-83%) immediately following the leptin injection. These data indicate that leptin responsive neurons in NTS mediate chemoreceptor afferent information to pressor sites in the RVLM, and suggest that leptin may act as a facilitator on neuronal circuits within the NTS that potentiates the sympathoexcitatory responses elicited during the reflex activation of arterial chemoreceptors.