Neuroscience
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This study examined the effect of neuron-endothelial coupling on the survival of neurons after ischemia and the possible mechanism underlying that effect. Whole-cell patch-clamp experiments were performed on cortical neurons cultured alone or directly cocultured with brain microvascular endothelial cells (BMEC). Propidium iodide (PI) and NeuN staining were performed to examine neuronal death following oxygen and glucose deprivation (OGD). ⋯ These results indicate that vascular endothelial cells assist neurons to prevent hypoxic injury via inhibiting neuronal IA by production of NO in the direct neuron-BMEC coculture system. These results further provide direct evidence of functional coupling between neurons and vascular endothelial cells. This study clearly demonstrates that vascular endothelial cells play beneficial roles in the pathophysiological processes of neurons after hypoxic injury, suggesting that the improvement of neurovascular coupling or functional remodeling may become an important therapeutic target for preventing brain injury.
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The dorsal diencephalic conduction system (DDC) is an important pathway of the brain reward circuitry, linking together forebrain and midbrain structures. The present work was aimed at describing the effect of a DDC lesion on the distribution of Fos-like immunoreactivity (FLIR) following intracranial self-stimulation (ICSS) of the lateral hypothalamus (LH). Rats were implanted with monopolar electrodes and divided into three groups; the first two groups were trained to self-stimulate at the LH, whereas the third group received no stimulation and served as a control. ⋯ As previously shown, a lesion at the DDC resulted in significant attenuations of the rewarding effectiveness of LH stimulation. Results also show a higher FLIR in several reward-related areas following LH stimulation, especially in the hemisphere ipsilateral to the stimulation electrode. Compared to non-lesioned rats, lesioned animals had lower FLIR in certain brain regions, suggesting that those regions that were activated by the rewarding stimulation may be functionally interconnected with the DDC.
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Numerous intrinsic currents are known to collectively shape neuronal membrane potential dynamics, or neuronal signatures. Although how sets of currents shape specific signatures such as spiking characteristics or oscillations has been studied individually, it is less clear how a neuron's suite of currents jointly shape its entire set of signatures. Biophysical conductance-based models of neurons represent a viable tool to address this important question. ⋯ We illustrate the methodology using two example case rodent pyramidal neurons, from the lateral amygdala and the hippocampus. The methodology also helped reveal that a single-core compartment model could capture multiple neuronal properties. Such biophysical single-compartment models have potential to improve the fidelity of large network models.
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Although there is little overlap in core diagnostic criteria for ADHD and Autism Spectrum Disorder (ASD), ASD symptoms are estimated to co-occur in children with ADHD in 20-50% of cases. As motor control deficits are common to both disorders, we investigated the impact of ASD symptoms on ocular motor control in children with Attention Deficit Hyperactivity Disorder-Combined Type (ADHD-CT), using a cued saccade paradigm sensitive to cerebellar ocular motor impairment in ASD. ⋯ Our results revealed that saccade profiles of the ADHD-CT group showed a pattern of hypermetria and altered main sequence. As the cerebellum is crucially involved in the regulation of saccade parameters, we propose that this pattern of deficit in ADHD-CT is consistent with the widely reported morphological abnormalities in ocular motor vermis (cerebellar lobules VI-VII) in ADHD-CT and ASD.
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Intracranial atherosclerotic stenosis (ICAS) is one of the most common causes of stroke worldwide and, in particular, has been implicated as a leading cause of recurrent ischemic stroke. We adapted a rat model of atherosclerosis to study brain intracranial atherosclerosis, and further investigated the effect of omega-3 fatty acids (O3FA) in attenuating development of ICAS. ⋯ Long-term O3FA dietary supplementation prevents the development of intracranial atherosclerosis. This O3FA effect appears to be mediated by its prevention of macrophage infiltration into the vessel wall, therefore reducing inflammation and intimal thickening. While similar effects in humans need to be determined, O3FA dietary supplement shows promising results in the prevention of ICAS.