Neuroscience
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The concentration of the multifunctional protein clusterin is reduced in the plasma of subjects with degenerative scoliosis (DS) and carpal tunnel syndrome (CTS) but elevated in the cerebrospinal fluid of neuropathic pain patients successfully treated with spinal cord stimulation. The present work tries to increase the knowledge of pain-associated changes of plasma and brain clusterin by using an animal model of neuropathy. We studied the effects of sciatic nerve ligation on mechanical allodynia (von Frey test), anxiety (elevated plus maze test), plasma clusterin (enzyme-linked immunosorbent assay) and clusterin expression in the nucleus accumbens (NAC) and prefrontal cortex (PFC) of adult male Wistar rats (western blot). ⋯ Animals with nerve ligation showed mechanical allodynia, anxiety and a marked downregulation of clusterin in the mitochondrial fraction of the prefrontal cortex. Animals fed on HF also exhibited a slight increase of the sensitivity to mechanical stimuli and anxiety; however, the diet did not potentiate the effects of nerve ligation. The results did not confirm a parallelism between neuropathy, obesity and alterations of plasma levels of clusterin, but strongly suggest that the protein could be involved in the functional reorganization of the prefrontal cortex which has been recently reported in chronic pain conditions.
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Chronic inflammation might correlate with the formation of α-synuclein oligomers, subsequently leading to dopaminergic (DA) neuronal death in Parkinson's disease (PD). As major components of chronic inflammation, NOD-like receptor protein 3 (NLRP3) inflammasomes play a crucial role in PD via caspase 1 activation, primarily induced by mitochondrial damage. NLRP3 binds to apoptosis-associated speck-like protein containing a CARD (PYCARD/ASC), and forms inflammasomes in the brain. ⋯ Mutations to PRKN (encoding Parkin) are the most common cause of autosomal recessive familial and sporadic early-onset PD. Evidence has confirmed a relationship between Parkin and NLRP3 inflammasomes. In this review, we summarize the current understanding of NLRP3 inflammasomes and their role in PD progression, and discuss their regulation by Parkin.
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Reciprocal connection between the ventral tegmental area (VTA) and the hippocampus forms a loop that controls information entry into long-term memory. Compared with the widely studied VTA dopamine system, VTA glutamate terminals are anatomically dominant in the hippocampus and less understood. The current study employs anterograde and retrograde labeling of VTA dopamine and glutamate neurons to map the distribution of their terminals within the layers of the hippocampus. ⋯ Conversely, activation of VTA glutamate neurons increased CA1 network firing rate and burst rate. In addition, VTA glutamate inputs reduced the interspike and interburst intervals for putative CA1 neurons. Taken together, we deduced that layer-specific distribution of presynaptic dopamine and glutamate terminals in the hippocampus determinines VTA modulation (dopamine) or regulation (glutamate) of excitability in the CA1 neural network.
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Perceiving the sensory consequences of our actions with a delay alters the interpretation of these afferent signals and impacts motor learning. For reaching movements, delayed visual feedback of hand position reduces the rate and extent of visuomotor adaptation, but substantial adaptation still occurs. Moreover, the detrimental effect of visual feedback delay on reach motor learning-selectively affecting its implicit component-can be mitigated by prior habituation to the delay. ⋯ Although habituation minimized awareness of the delay, no improvement in adaptation to the spectral perturbation was observed. Thus, short-term habituation to auditory feedback delays is not effective in reducing the negative impact of delay on speech auditory-motor adaptation. Combined with previous findings, the strong negative effect of delay and the absence of an influence of delay awareness suggest the involvement of predominantly implicit learning mechanisms in speech.
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Resting state functional connectivity can be leveraged to investigate bilingual individual differences in cognitive control of language; however, thus far no report is provided on how the connectivity profiles of brain functional networks at rest point to different language control behavior in bilinguals. In order to address this gap in state-of-the-art research we did a functional connectivity analysis on the resting state data acquired via multiband EPI to investigate three resting state networks of interest namely, the frontoparietal network (FPN), the salience network (SN), and the default mode network (DMN), which are related to cognitive control, between two groups of Dutch-English bilinguals based on how they performed in a language switching task. ⋯ As regards these results, we claim that the primary somatosensory cortex has a dual function in coupling with the dorsolateral prefrontal cortex and the inferior parietal cortex in the FPN, and in fact, in what characterizes bilingual individual differences in cognitive control of language in healthy participants. The results of this study provide a model for future research in cognitive control of language and may serve as a reference in clinical neuroscience when bilinguals are diagnosed with dysfunction in cognitive control.