Neuroscience
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Few animal studies focus on consequences of nicotine postnatal exposure, particularly through lactation. We have recently shown that forced nicotine drinking elevates maternal care, paradoxically provoking arousal and stress in pups. Present work aimed to evaluate the specific contribution of altered maternal cares, compared to the sequelae merely due to nicotine effects. ⋯ Brain analyses at adulthood suggest that, in prefrontal cortex, nicotine per se reduced serotonin, while the maternal overcare reduced CHRN-B2 gene-expression. As a whole, unescapable nicotine-enhanced maternal care could have an impact on the offspring arousal by acting on prefrontal CHRN-B2 gene-expression. When present results are translated to consequences of non-voluntary exposure in humans, we propose that children receiving altered attentions by a smoking caregiver might undergo a neuro-behavioural development biased towards emotional shyness.
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Coagulation factor XII (FXII) is synthesized in the liver and secreted into the circulation, where it initiates the contact activation system. Although typically thought to be restricted to the circulation, FXII protein has been found in the brain of Alzheimer's disease (AD) and multiple sclerosis patients. Moreover, activation of the contact system has been detected in the cerebrospinal fluid of these patients as well as in the brain of healthy and AD individuals. ⋯ We show that a recombinant version of this shorter FXII protein is activated by plasma kallikrein, reciprocally activates prekallikrein, and converts pro-hepatocyte growth factor (HGF) to active HGF in vitro. HGF-Met signaling plays a role in neuronal development and survival, and its dysregulation has been implicated in neurodevelopmental disorders and neurodegeneration. Taken together, our results show that a short isoform of FXII mRNA is expressed in the brain and raise the possibility that brain-derived FXII may be involved in HGF-Met signaling in neurons.
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Randomized Controlled Trial
Effects of Transcranial Static Magnetic Stimulation on Motor Cortex Evaluated by Different TMS Waveforms and Current Directions.
Transcranial static magnetic stimulation (tSMS) modulates cortical excitability probably by interacting with the GABA-glutamate intracortical balance. Different transcranial magnetic stimulation (TMS) waveforms probe distinct GABA-mediated cortical inhibition networks. The goal of the present work is to further characterize tSMS-induced changes in motor cortex reactivity and inhibition-excitation (I/E) balance. ⋯ MEP amplitude increased compared to sham with monoAP TMS, with no clear changes in general intracortical I/E balance. Biphasic TMS was not able to capture any effects of tSMS. The results show that the effects of tSMS on cortical excitability and inhibition involve specific interneuron circuits that are selectively activated by monoPA TMS.
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Randomized Controlled Trial
Fronto-Parietal Brain Areas Contribute to the Online Control of Posture during a Continuous Balance Task.
Neuroimaging studies have provided evidence for the involvement of frontal and parietal cortices in postural control. However, the specific role of these brain areas for postural control remains to be known. Here, we investigated the effects of disruptive transcranial magnetic stimulation (TMS) over supplementary motor areas (SMA) during challenging continuous balance task in healthy young adults. ⋯ Importantly, cTBS over SMA compared to sham stimulation altered EEG power within the identified fronto-parietal regions. These findings suggest that the changes in activation within distant fronto-parietal brain areas following cTBS over SMA contributed to the altered postural behavior. Our study confirms a critical role of AC, CG, and both PPC regions in calibrating online postural responses during a challenging continuous balance task.
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Ketogenic diet is reported to protect against cognitive decline, drug-resistant epilepsy, Alzheimer's Disease, damaging effect of ischemic stroke and many neurological diseases. Despite mounting evidence that this dietary treatment works, the exact mechanism of its protective activity is largely unknown. Ketogenic diet acts systemically, not only changing GABA signaling in neurons, but also influencing the reliance on mitochondrial respiration, known to be disrupted in many neurological diseases. ⋯ In the brain astrocytes are believed to be the sole neural cells capable of fatty oxidation. Here we try to explain that not exclusively neurons, but also morphological changes of astroglia and/or microglia due to different metabolic state are important for the mechanism underlying the protective role of ketogenic diet. By quantifying different parameters describing cellular morphology like ramification index or fractal dimension and using Principal Component Analysis to discover the regularities between them, we demonstrate that in normal adult rat brain, ketogenic diet itself is able to change glial morphology, indicating an important role of these underappreciated cells in the brain metabolism.