Neuroscience
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Hepatic encephalopathy (HE) represents a brain dysfunction caused by both acute and chronic liver failures, and its severity deeply affects the prognosis of patients with impaired liver function. In its pathophysiology, ammonia levels and glutamatergic system hyperactivity seem to play a pivotal role in the disruption of brain homeostasis. Here, we investigate important outcomes involved in behavioral performance, electroencephalographic patterns, and neurochemical parameters to better characterize the well-accepted animal model of acute liver failure (ALF) induced by subtotal hepatectomy (92% removal of tissue) that produces ALF. ⋯ The hepatectomized rats presented significant motor behavioral changes accompanied by important abnormalities in classical blood laboratory parameters of ALF, and EEG features suggestive of HE and deep disturbances in the brain glutamatergic system. Using an animal model of ALF induced via subtotal hepatectomy, this work provides a comprehensive and reliable experimental model that increases the opportunity for studying the effects of new treatment strategies to be explored in an unprecedented way. It also presents insights into the pathophysiology of HE in a reproducible model of ALF, which correlates important neurochemical and EEG aspects of the syndrome.
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We used force-matching tasks between the two hands to test predictions of the recently introduced scheme of perception based on the concept of iso-perceptual manifold (IPM) in the combined afferent-efferent space of neural signals. The main hypothesis was that accuracy and variability of individual finger force matching would be worse in a four-finger task compared to one-finger tasks. The subjects produced accurate force levels under visual feedback by pressing with either all four fingers or by one of the fingers of a hand (task-hand). ⋯ Matching hypothetical commands to fingers, rather than finger forces, could be responsible for the consistent force overshoots. Indices of inter-trial variance affecting and unaffecting total force showed strong stabilization of total force in the task-hand but not in the match-hand in support of an earlier hypothesis on the importance of visual feedback for force stabilization. No differences were seen between the right and left hands suggesting that the dynamic dominance hypothesis may not be generalizable to perceptual phenomena.
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Intracortical inhibitory modulation seems crucial for an intact motor control and motor learning. However, the influence of long(er) term training on short-interval intracortical inhibition (SICI) is scarcely investigated. With respect to balance, it was previously shown that with increasing postural task difficulty, SICI decreased but the effect of balance training (BT) is unknown. ⋯ The present study confirms previous findings of task-specific modulation of SICI when balancing. More importantly, training was shown to increase SICI and this increase was correlated with changes in balance performance. Thus, changes in SICI seem to be involved not only for the control but also when adapting upright posture with training.
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Human bipedal balance control is proposed to be the integrated activity of distributed neural areas. There is growing understanding about the cortical involvement in this highly automated behavior. While evidence exists for cortical activity temporally linked to reactive balance control, little is known about the functional interaction of potential cortical regions. ⋯ The results suggest that there might exist a balance control cortical network while standing and rapid, transient, and frequency-specific reorganization occurs in this network during reactive balance control events. This reorganization was characterized by an increased number of short-range connections between neighboring areas and increased strength between connections in delta, theta, alpha, and beta frequency bands during PEP N1 compared to baseline. To our knowledge, this is the first study to report the existence of functional cortical networks during reactive balance control with potential implications on assessing impaired balance associated with various neural diseases.
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Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β and tau proteins, which are believed to lead to neural damage that translates into brain dysfunction and cognitive deficits. Brain dysfunction can be evaluated by measuring single-neuron activity (spikes), global neural activity (local field potentials, LFPs) and the interaction between them. Considering that the dynamic interactions between the hippocampal pyramidal cells and lateral septum are important for proper structure function, we used the complete septo-hippocampal preparation from 30-day-old controls and J20-AD transgenic mice to record changes in spiking activity from the lateral septum and its relationship with LFP activity from the CA1 area. ⋯ Similarly, the LFP- LFP coherence between CA1 and septum in the theta range showed lower values in J20 animals. Importantly, alterations were found before any detectable signs of cognitive deficits. Our data indicate that the disruption in the communication between hippocampus and rostral lateral septum is an early event in AD pathology and may contribute to the deficits observed during AD.