Neuroscience
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Chronic psychosocial stress modulates brain antioxidant systems and causes neuroinflammation that plays a role in the pathophysiology of depression. Although the antidepressant fluoxetine (FLX) represents the first-line treatment for depression and the atypical antipsychotic clozapine (CLZ) is considered as a second-line treatment for psychotic disorders, the downstream mechanisms of action of these treatments, beyond serotonergic or dopaminergic signaling, remain elusive. We examined behavioral changes, glutathione (GSH)-dependent defense and levels of proinflammatory mediators in the prefrontal cortex (PFC) of adult male Wistar rats exposed to 21days of chronic social isolation (CSIS). ⋯ In conclusion, prefrontal cortical GSH depletion and the proinflammatory response underlying depressive- and anxiety-like states induced by CSIS were prevented by FLX. The protective effect of CLZ, which was equally effective as FLX on the behavioral level, was limited to proinflammatory components. Hence, different mechanisms underlie the protective effects of these two drugs in CSIS rats.
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Functional magnetic resonance imaging (fMRI) is based on neurovascular coupling, which allows inferring neuronal activity from hemodynamic changes. Spinal fMRI has been used to examine pain processes, although spinal neurovascular coupling has never been investigated. In addition, fluctuations in mean arterial pressure (MAP) occur during nociceptive stimulation and this may affect neurovascular coupling. ⋯ This indicates that spinal hemodynamic changes reflect neuronal activity even when large fluctuations in MAP occur. This contrasts with results from previous studies on cerebral neurovascular coupling and suggests that spinal autoregulation might allow better adaptation to sudden MAP changes than cerebral autoregulation. Although assessment of the coupling between spinal neuronal activity and BOLD signal remains to be investigated, this study supports the use of spinal fMRI, based on the tight coupling between SCBF and LFP.
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It is still unclear if muscle synergies reflect neural strategies or mirror the underlying mechanical constraints. Therefore, this study aimed to verify the consistency of muscle groupings between the synergies based on the linear envelope (LE) of muscle activities and those incorporating the time-frequency (TF) features of the electromyographic (EMG) signals. Twelve healthy participants performed six 20-m walking trials at a comfort and fast self-selected speed, while the activity of eleven lower limb muscles was recorded by means of surface EMG. ⋯ When accounting the reconstruction level of the initial dataset, a new TF synergy emerged. This new synergy dissociated the activity of the rectus femoris from those of the vastii muscles (synergy #1) and from the one of the tensor fascia latae (synergy #5). Overall, extracting TF muscle synergies supports the neural origin of muscle synergies and provides an opportunity to distinguish between prescriptive and descriptive muscle synergies.
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Corticotropin-releasing hormone release is the final common pathway of stress-associated neuroendocrine responses. This study tested how corticotropin-releasing hormone modulates airway vagal preganglionic neurons. Airway vagal preganglionic neurons in neonatal rats were retrogradely labeled with fluorescent dye and identified in medullary slices, and their responses to corticotropin-releasing hormone (200nmolL-1) were examined using whole-cell patch clamp. ⋯ The responses induced by corticotropin-releasing hormone were prevented by Antalarmin hydrochloride (50μmolL-1), an antagonist of type 1 corticotropin-releasing hormone receptors, but insensitive to Astressin 2B (200nmolL-1), an antagonist of type 2 corticotropin-releasing hormone receptors. These results suggest that corticotropin-releasing hormone excites airway vagal preganglionic neurons via activation of its type 1 receptors at multiple sites, which includes a direct postsynaptic excitatory action and presynaptic facilitation of both glutamatergic and GABAergic inputs. In stress, corticotropin-releasing hormone might be able to activate the airway vagal nerves and, consequently, participate in induction or exacerbation of airway disorders.