Brain research
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Friedreich's ataxia (FRDA) is the most common form of hereditary ataxia. In addition to proximal spinal cord and brain stem atrophy, mild to moderate atrophy of the cerebellum has been reported in advanced FRDA. The aim of this study was to examine dysfunction in motor-related areas involved in the execution of finger tapping tasks in individuals with FRDA, and to investigate functional re-organization of cortico-cerebellar, cortico-striatal and parieto-frontal loops as a result of the cerebellar pathology. ⋯ Although the pattern of the BOLD signal from the putamen was different during the self-paced regular finger tapping task to the other tasks in controls, in individuals with FRDA there was no distinction of the signal between the tasks suggesting that primary cerebellar pathology may cause secondary basal ganglia dysregulation. While individuals with FRDA tapped at a slightly lower rate (0.59Hz) compared with controls (0.74Hz) they showed significantly decreased activity of the SMA and the inferior parietal lobule, which may suggest disruption to the fronto-parietal connections. These findings suggest that the motor impairments in individuals with FRDA result from dysfunction extending beyond the spinal cord and cerebellum to include sub-cortical and cortical brain regions.
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Hyperoside is a flavonoid compound and widely used in clinic to relieve pain and improve cardiovascular functions. However, the effects of hyperoside on ischemic neurons and the molecular mechanisms remain unclear. Here, we used an in vitro ischemic model of oxygen-glucose deprivation followed by reperfusion (OGD-R) to investigate the protective effects of hyperoside on ischemic neuron injury and further explore the possible related mechanisms. ⋯ Meanwhile, hyperoside lessened iNOS expression induced by OGD-R via inhibition of NF-κB activation. Furthermore, ameliorating of ERK, JNK and Bcl-2 family-related apoptotic signaling pathways were also involved in the neuroprotection of hyperoside. Taken together, these studies revealed that hyperoside had protective effects on neuronal ischemia-reperfusion impairment, which was related to the regulation of nitric oxide signaling pathway.
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Our previous study has shown that activating peripheral μ-receptors is necessary for switching the bronchopulmonary C-fibers (PCFs)-mediated rapid shallow breathing (RSB) into an apnea by systemic administration of fentanyl. The brainstem nuclei, such as the medial nucleus tractus solitarius (mNTS) and the pre-Botzinger complex (PBC), are required for completing the PCF-mediated respiratory reflexes. Moreover, these areas contain abundant μ-receptors and their activation prolongs expiratory duration (T(E)). Thus, we asked if central μ-receptors, especially those in the mNTS and PBC, are involved in fully expressing this RSB-apnea switch by fentanyl. In anesthetized rats, the cardiorespiratory responses to right atrial injection of phenylbiguanide (PBG, 3-6μg/kg) were repeated after: (1) fentanyl (iv), a μ-receptor agonist, alone (8μg/kg, iv); (2) fentanyl following microinjection of naloxone methiodide (NXM, an opioid receptor antagonist) into the cisterna magna (10μg/4μl); (3) the bilateral mNTS (10mM, 20nl); or (4) PBC (10mM, 20nl). Our results showed that PBG shortened T(E) by 37±6% (RSB, from 0.41±0.05 to 0.26±0.03s, P<0.01), but it markedly prolonged T(E) by 5.8-fold (an apnea, from 0.50±0.04s to 2.9±0.57s, P<0.01) after fentanyl (iv). Pretreatment with NXM injected into the cisterna magna or the PBC, but not the mNTS, prevented the fentanyl-induced switch. This study, along with our previous results mentioned above, suggests that although peripheral μ-receptors are essential for triggering the fentanyl-induced switch, central μ-receptors, especially those in the PBC, are required to fully exhibit such switch. ⋯ Our results suggest that the activation of central μ-receptors, especially those in the pre-Botzinger complex, is required for switching the pulmonary C-fiber-mediated rapid shallow breathing into an apnea by systemic administration of fentanyl.
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Craving is an important factor in relapse to drug abuse, and cue-induced craving is an especially powerful form of this construct. Neuroimaging methods have been utilized to study drug cue-induced craving and neural correlates in the human brain. However, very few studies have focused on characterizing craving and the neural responses to heroin-related cues in short-term abstinent heroin-dependent patients. ⋯ The abstinence duration correlated positively with brain activation in the left caudate and right parahippocampal gyrus. In conclusion, the cue-reactivity paradigm significantly activated neural responses in the mesolimbic dopamine (DA) system and prefrontal cortex (PFC) and induced increased craving in short-term abstinent heroin-dependent patients. We suggest that these response patterns characterize the high vulnerability of relapse in short-term abstinent heroin-dependent subjects.
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We examined whether somatosensory activity could be modulated by the observation of bodily experiences. For this purpose, somatosensory-evoked potentials elicited by non-painful stimulation were recorded when subjects were viewing a hand penetrated by a needle, touched by a cotton swab or at resting without stimulation. ⋯ Moreover, enhanced P50 amplitudes during observation of both pain and touch in others were associated with increased unpleasant ratings induced by the video clips, as well as with high scores in a perspective taking scale (IRI). These findings provide support for the involvement of an attentional bottom-up mechanism which could be responsible to enhance sensory processing of somatic information when observing bodily experiences in others irrespective of whether they are painful or not.