Neuroscience
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Optic neuropathies comprise a group of disorders in which the axons of retinal ganglion cells (RGCs), the retinal projection neurons conveying visual information to the brain, are damaged. This results in visual impairment or even blindness, which is irreversible as adult mammals lack the capacity to repair or replace injured or lost neurons. Despite intensive research, no efficient treatment to induce axonal regeneration in the central nervous system (CNS) is available yet. ⋯ Interestingly, the pattern of the autophagic response in the axons followed the spatiotemporal window of axonal regrowth, which suggests that autophagy is ongoing at the growth cones. Pharmacological inhibition of the recycling pathway resulted in accelerated RGC target reinnervation, possibly linked to increased mechanistic target of rapamycin (mTOR) activity, known to stimulate axonal regrowth. Taken together, these intriguing findings underline that further research is warranted to decipher if modulation of autophagy could be an effective therapeutic method to induce CNS regeneration.
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Elevation of CSF Sortilin Following Subarachnoid Hemorrhage in Patients and Experimental Model Rats.
Subarachnoid hemorrhage (SAH) can cause acute neuronal injury and chronic neurocognitive deficits; biomarkers reflecting its associated neuronal injury are of potential prognostic value. Sortilin, a member of the vacuolar protein sorting 10p (Vps10p) family, is enriched in neurons and is likely involved in neurodegenerative diseases. Here, we explored sortilin in the cerebrospinal fluid (CSF) as a potential biomarker for early neuronal injury after SAH. ⋯ In immunohistochemistry, the pattern of sortilin labeling in the brain was largely comparable between the SAH and control rats, whereas an increased astrocytic GFAP immunolabeling was evident in the former. Together, these results suggest that SAH can cause an early and remarkable rise of sortilin products in CSF, likely reflecting neuronal change. Sortilin could be further explored as a potential biomarker in some brain disorders.
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Theta rhythm recorded as an extracellular synchronous field potential is generated in a number of brain sites including the hippocampus. The physiological occurrence of hippocampal theta rhythm is associated with the activation of a number of structures forming the ascending brainstem-hippocampal synchronizing pathway. ⋯ The posterior hypothalamic area plays an important role in movement control, place-learning, memory processing, emotion and arousal. In the light of multiplicity of functions of the posterior hypothalamic area and the influence of theta field oscillations on a number of neural processes, it is the authors' intent to summarize the data concerning the involvement of the supramammillary nucleus and posterior hypothalamic nuclei in the modulation of limbic theta rhythmicity as well as the ability of these brain structures to independently generate theta rhythmicity.
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It is well known that the central nervous system (CNS) is a complex neuronal network and its function depends on the balance between excitatory and inhibitory neurons. Disruption of the excitatory/inhibitory (E/I) balance is the main cause for the majority of the CNS diseases. In this review, we will discuss roles of the inhibitory system in the CNS diseases. ⋯ The GABAergic system consists of GABA, GABA transporters, GABAergic receptors and GABAergic neurons. Changes in any of these components may contribute to the dysfunctions of the CNS. In this review, we will synthesize studies which demonstrate how the GABAergic system participates in the pathogenesis of the CNS disorders, which may provide a new idea that might be used to treat the CNS diseases.