Neuroscience
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Songbirds possess mirror neurons (MNs) activating during the perception and execution of specific features of songs. These neurons are located in high vocal center (HVC), a premotor nucleus implicated in song perception, production and learning, making worth to inquire their properties and functions in vocal recognition and imitative learning. By integrating a body of brain and behavioral data, we discuss neurophysiology, anatomical, computational properties and possible functions of songbird MNs. ⋯ At the functional level, we discuss whether songbird MNs are involved in others' song recognition, by dissecting the function of recognition in various different but possible overlapping processes: action-oriented perception, discriminative-oriented perception and identification of the signaler. We conclude that songbird MNs may be involved in recognizing other singer's vocalizations, while their role in imitative learning still require to solve how auditory feedback are used to correct own vocal performance to match the tutor song. Finally, we compare songbird and human mirror responses, hypothesizing a case of convergent evolution, and proposing new experimental directions.
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Spatial relations (SRs: coordinate/metric vs categorical/non metric) and frames of reference (FoRs: egocentric/body vs allocentric/external element) represent the building blocks underlying any spatial representation. In the present 7-T fMRI study we have identified for the first time the neural correlates of the spatial representations emerging from the combination of the two dimensions. The direct comparison between the different spatial representations revealed a bilateral fronto-parietal network, mainly right sided, that was more involved in the egocentric categorical representations. ⋯ Finally, a smaller part of this bilateral network (i.e. Calcarine Sulcus and Lingual Gyrus), along with the right Supramarginal and Inferior Frontal gyri, supported the allocentric coordinate representations. The fact that some areas were more involved in a spatial representation than in others reveals how our brain builds adaptive spatial representations in order to effectively react to specific environmental needs and task demands.
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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by selective loss of motor neurons. Statins are widely used as cholesterol-lowering drugs and significantly reduce the risk of cardiovascular and cerebrovascular diseases. Increasing evidence indicates the protective effects of statins against certain neurodegenerative diseases. ⋯ Conversely, these outcomes were completely reversed by co-incubation with mevalonate, farnesyl pyrophosphate (FPP) or geranylgeranyl pyrophosphate (GGPP) but not cholesterol. In addition, inhibition of geranylgeranyl transferase I by GGTI-286 led to similar alterations in cell viability and autophagic marker levels. These results indicated that the cytotoxic effect of simvastatin on NSC34-hSOD1G93A cells might be due to the aggravation of autophagic flux impairment through the inhibition of GGPP synthesis.
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Stress is a non-specific, systemic, physiological response of the body to strong internal and external environmental stimuli. Accumulating evidence has suggested that stress, particularly chronic restraint stress (CRS), can reduce pain threshold and increase pain sensitivity. However, pathogenic and therapeutic mechanisms underlying CRS remain unclear. ⋯ Notably, only the intrathecal injection improved PWMT and TFL. Additionally, an intraperitoneal injection of rapamycin, an mTOR inhibitor, failed to induce any behavioral changes, whereas a single intrathecal injection of rapamycin improved abnormal CRS-induced PWMT and TFL. In conclusion, CRS can induce abnormal pain sensitivity, probably by altering the BDNF-mTOR signaling pathway in the spinal cord.
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Benzodiazepines are one of the most commonly prescribed anxiolytic drugs in America, and between 2006 and 2015 prescription rates increased by an estimated 27.1%. Weight gain is a common side effect of these drugs and it may result from increased feeding caused by drug-enhanced food palatability. We investigated the role of specific GABAA receptor subtypes involved with benzodiazepine-induced food consumption through third ventricle injections of L-838,417, a partial agonist of GABAA α2, α3, and α5 subunits, and a full antagonist of the α1 receptor subunit. ⋯ These results indicate that nuclei in proximity to the ventricles respond to GABAA α2, α3, or α5 activation to induce motivation to feed, absent of α1 receptor subunit activation. Furthermore, activation of the α1 subunit is not necessary for benzodiazepine hyperphagia and may instead contribute to the oromotor depressant and sedative properties of classic benzodiazepine agonists. Hypothalamic nuclei such as the paraventricular nucleus may be involved in the benzodiazepine-increased motivation to feed, while the parabrachial nucleus of the hindbrain could contribute to benzodiazepine-induced enhancement of taste palatability.