Neuroscience
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In recent years, a growing body of research has addressed the nature and mechanism of material perception. Material perception entails perceiving and recognizing a material, surface quality or internal state of an object based on sensory stimuli such as visual, tactile, and/or auditory sensations. This process is ongoing in every aspect of daily life. ⋯ Our main focus is on vision, but every sensory modality is involved in material perception. Information obtained through different sensory modalities is closely linked in material perception. Such cross-modal processing is another important feature of material perception, and will also be covered in this review.
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Review
Brain Stem Neural Circuits of Horizontal and Vertical Saccade Systems and Their Frame of Reference.
Sensory signals for eye movements (visual and vestibular) are initially coded in different frames of reference but finally translated into common coordinates, and share the same final common pathway, namely the same population of extraocular motoneurons. From clinical studies in humans and lesion studies in animals, it is generally accepted that voluntary saccadic eye movements are organized in horizontal and vertical Cartesian coordinates. However, this issue is not settled yet, because neural circuits for vertical saccades remain unidentified. ⋯ Comparing well-known vestibuloocular pathways with our findings of commissural excitation and inhibition between both superior colliculi, we proposed that the saccade system uses the same frame of reference as the vestibuloocular system, common semicircular canal coordinate. This proposal is mainly based on marked similarities (1) between output neural circuitry from one superior colliculus to extraocular motoneurons and that from a respective canal to its innervating extraocular motoneurons, (2) of patterns of commissural reciprocal inhibitions between upward saccade system on one side and downward system on the other, and between anterior canal system on one side and posterior canal system on the other, and (3) between the neural circuits of saccade and quick phase of vestibular nystagmus sharing brainstem burst neurons. In support of the proposal, commissural excitation of the superior colliculi may help to maintain Listing's law in saccades in spite of using semicircular canal coordinate.
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Intracranial hypertension, which often follows a severe brain injury, is usually treated with intravenous (i.v.) application of hyperosmolar solutions. The mechanism of intracranial cerebrospinal fluid (CSF) pressure decrease after such a treatment is still unclear. The aim of this article was to try to explain the mechanism of CSF pressure reduction after i.v. hyperosmolar mannitol bolus in regard to the changes in CSF volume. ⋯ This shift, without significant volume change inside the cranium, causes a predominant decrease of CSF volume in the spinal part of the system, which in turn leads to lowering of the CSF pressure. Spinal CSF volume decrease is enabled by the extensibility of the spinal dura, this way providing the possibility for CSF volume redistribution inside the CSF system, together with CSF pressure decrease. This mechanism of mannitol action is in accordance with the new hypothesis of CSF physiology.
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The hallmark of human evolution encompasses the dramatic increase in brain size and complexity. The intricate interplays of micro-RNAs (miRNAs) and their target genes are indispensable in brain development. Sequence divergence in distinct structural regions of Brain-specific precursor miRNAs (pre-miRNAs) and its consequence in the production of corresponding mature miRNAs in human are unknown. ⋯ Further analysis revealed that presence of certain motif and nucleotide preference in the Brain-specific pre-miRNAs may favor DROSHA and DICER to ameliorate miRNA processing. The higher processing efficiency of human Brain-specific miRNAs was reflected as an elevated production of corresponding mature miRNAs in the human brain. Finally, re-construction of gene-regulatory network uncovers different pathways driven by Brain-specific miRNAs that may contribute to the development of brain in human.
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Postnatal ethanol exposure has been shown to cause persistent defects in hippocampal synaptic plasticity and disrupt learning and memory processes. However, the mechanisms responsible for these abnormalities are less well studied. We evaluated the influence of postnatal ethanol exposure on several signaling and epigenetic changes and on expression of the activity-regulated cytoskeletal (Arc) protein in the hippocampus of adult offspring under baseline conditions and after a Y-maze spatial memory (SP) behavior (activity). ⋯ ChIP results suggested that reduced H3K14ac and H4K8ac in the Arc gene promoter is because of impaired CBP, and increased H3K9me2 is due to the enhanced recruitment of G9a. The CB1R antagonist and a G9a/GLP inhibitor, which were shown to rescue postnatal ethanol-triggered synaptic plasticity and learning and memory deficits, were able to prevent the negative effects of ethanol on activity-dependent signaling, epigenetics and Arc expression. Together, these findings provide a molecular mechanism involving signaling and epigenetic cascades that collectively are responsible for the neurobehavioral deficits associated with an animal model of fetal alcohol spectrum disorders (FASD).