Neuroscience
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Detecting errors in one's own and other's actions is a crucial ability for learning and adapting behavior to everchanging, highly volatile environments. Studies in healthy people demonstrate that monitoring errors in one's own and others' actions are underpinned by specific neural systems that are dysfunctional in a variety of neurological disorders. In this review, we first briefly discuss the main findings concerning error detection and error awareness in healthy subjects, the current theoretical models, and the tasks usually applied to investigate these processes. ⋯ Also theta activity was reduced in some neurological groups, but consistent evidence on the oscillatory activity has not been provided thus far. Behaviorally, we did not observe relevant patterns of pronounced dysfunctional (post-) error processing. Finally, we discuss limitations of the existing literature, conclusive points, open questions and new possible methodological approaches for clinical studies.
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Chronic nonspecific low back pain (cNLBP) is a leading contributor to disease burden worldwide that is difficult to treat due to its nonspecific aetiology and complexity. The amygdala is a complex of structurally and functionally heterogeneous nuclei that serve as a key neural substrate for the interactions between pain and negative affective states. However, whether the functions of amygdalar subcomponents are differentially altered in cNLBP remains unknown. ⋯ Both groups exhibited stronger effective connectivity from the left amygdala to the right amygdala. In summary, these findings not only suggested altered rsFC of the amygdala-mPFC pathway in cNLBP but also implicated an abnormal direction of information processing between the amygdala and mPFC in these patients. Our results further highlight the involvement of the amygdala in the neuropathology of cNLBP.
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The centrally-projecting Edinger-Westphal nucleus (EWcp) has been shown to contribute to regulation of multiple functions, including responses to stress and fear, attention, food consumption, addiction, body temperature and maternal behaviors. However, receptors involved in regulation of these behaviors through EWcp remain poorly characterized. On the other hand, the oxytocin peptide (OXT) is also known to regulate a substantial number of physiological responses and behaviors. ⋯ A follow up study showed that injection of OXT (2.3 or 7.7 mg/kg, IP) is accompanied by a decrease in body temperature. Since EWcp is known to be involved in regulation of body temperature, we hypothesize that OXT's effects on body temperature could be mediated through the EWcp. The contribution of OXTR in EWcp to regulation of various functions of EWcp and OXT needs to be deciphered.
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Fear of falling increases conscious control of balance and postural threat warrants accurate anticipatory motor commands for keeping a safe body posture. This study examines the anticipatory (APAs) and compensatory (CPAs) postural adjustments generated in response to an external perturbation while individuals are positioned at two different altitudes (2 cm and 80 cm) from the floor level. The main result indicates that due to the perceived emotional threat, different agonist and antagonist muscles synergies (R and C-Indexes) are manifested, particularly during the anticipatory phase. ⋯ Interestingly, the APAs strategies were modified under different postural threats by controlling the agonist-antagonist muscles at different joints of lower extremity. For CPAs the reciprocal activation was less applied compared to muscles co-activation to unsure larger margin for compensatory adjustments as needed and re-establish the postural stability. The results indicate that when facing to a postural threat, the CNS modulates the anticipatory and compensatory phases of postural adjustments to minimize the risk of falling.
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Defective mitophagy and mitochondrial dysfunction have been linked to aging and Alzheimer's disease (AD). β2-Adrenergic receptor (ADRB2) is critical for mitochondrial and cognitive function. However, researchers have not clearly determined whether ADRB2 activation ameliorates defective mitophagy and cognitive deficits in individuals with AD. Here, we observed that the activation of ADRB2 by clenbuterol (Clen, ADRB2 agonist, 2 mg/kg/day) ameliorated amyloid-β-induced (Aβ1-42 bilateral intracerebral infusion, 2 μl, 5 μg/μl) memory deficits. ⋯ Finally, we established that Clen improved mitophagy and attenuated mitochondrial dysfunction, and tau pathology in mice by activating the ADRB2/Akt/PINK1 signaling pathway. Conversely, the inhibition of ADRB2 by propranolol (βAR antagonist, 10 μM) blocked the Clen-mediated improvements in pathological changes in N2a cells. The results from the present study indicate that ADRB2 activation may be a therapeutic strategy for AD.