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Effects of Neurotrophic Factors in Glial Cells in the Central Nervous System: Expression and Properties in Neurodegeneration and Injury
Conclusion and Future Aspects This review summarizes available NTF expression data, compiles existing evidence on the effects of glial NTF signaling in healthy conditions and in disease models (Figure 1), and highlights the importance of this topic for future studies. The relationship between NTFs and glia is crucial for both the developing and adult brain. While some of these factors, such as NT-3 and CNTF, have highly potent effects on gliogenesis, others like BDNF and GDNF, are important for glia-mediated synapse formation. Neurotrophic factors play significant roles during neurodegenerative disorders. In many cases, ...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research

A single, clinically relevant dose of the GABAB agonist baclofen impairs visuomotor learning.
This article is protected by copyright. All rights reserved. PMID: 33085094 [PubMed - as supplied by publisher]
Source: The Journal of Physiology - October 21, 2020 Category: Physiology Authors: Johnstone A, Grigoras I, Petitet P, Capitão LP, Stagg CJ Tags: J Physiol Source Type: research

miR-149 reduces while let-7 elevates ASIC1a expression in vitro.
Authors: Jiang YQ, Zha XM Abstract Acid-sensing ion channel 1a (ASIC1a) is the key subunit that determines acid-activated currents in neurons. ASIC1a is important for neural plasticity, learning, and for multiple neurological diseases, including stroke, multiple sclerosis, and traumatic injuries. These findings underline the importance for better defining mechanisms that regulate ASIC1a expression. During the past decade, microRNA has emerged as one important group of regulatory molecules in controlling protein expression. However, little is known about whether microRNA regulates ASIC1a. Here, we assessed several m...
Source: International Journal of Physiology, Pathophysiology and Pharmacology - December 7, 2017 Category: Physiology Tags: Int J Physiol Pathophysiol Pharmacol Source Type: research