Journal of neurochemistry
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Journal of neurochemistry · Feb 2009
ReviewCommunication between neurons and astrocytes: relevance to the modulation of synaptic and network activity.
Neuromodulation is a fundamental process in the brain that regulates synaptic transmission, neuronal network activity and behavior. Emerging evidence demonstrates that astrocytes, a major population of glial cells in the brain, play previously unrecognized functions in neuronal modulation. ⋯ For example, recent findings show that astrocytes play crucial roles in the control of Hebbian plasticity, the regulation of neuronal excitability and the induction of homeostatic plasticity. This review discusses the importance of astrocyte-to-neuron signaling in different aspects of neuronal function from the activity of single synapses to that of neuronal networks.
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Journal of neurochemistry · Feb 2009
Fibronectin stimulates TRPV1 translocation in primary sensory neurons.
Extracellular matrix (ECM) molecules are highly variable in their composition and receptor recognition. Their ubiquitous expression profile has been linked to roles in cell growth, differentiation, and survival. Recent work has identified certain ECM molecules that serve as dynamic signal modulators, versus the more-recognized role of chronic modulation of signal transduction. ⋯ This FN-induced increase in TRPV1 sensitivity to activation is coupled by an increase in plasma membrane expression of TRPV1, as well as an increase in tyrosine phosphorylation of TRPV1 in TG neurons. Furthermore, TG neurons cultured on FN demonstrated an increase in capsaicin-mediated Ca(2+) accumulation relative to neurons cultured on poly-D-lysine. Data presented from these studies indicate that FN stimulates tyrosine-phosphorylation-dependent translocation of the TRPV1 receptor to the plasma membrane, identifying FN as a critical component of the ECM capable of sensory neuron sensitization.
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Journal of neurochemistry · Feb 2009
CREB activation in the rapid, intermediate, and delayed ischemic preconditioning against hypoxic-ischemia in neonatal rat.
Ischemic preconditioning (IP) is a defense program in which exposure to sublethal ischemia followed by a period of reperfusion results in subsequent resistance to severe ischemic insults. Very few in vivo IP models have been established for neonatal brain. We examined whether rapid, intermediate, and delayed IP against hypoxic-ischemia (HI) could be induced in neonatal brain, and if so, whether the IP involved phosphorylation of cAMP response element-binding protein (pCREB) after HI. ⋯ The increases of caspase-3 and calpain-mediated proteolysis of a-spectrin post-HI were significantly reduced only in 22-h IP group. Furthermore, all three IP groups had long-term neuroprotection at behavioral and pathological levels compared with no-IP group. In conclusion, IP, rapid, intermediate, or delayed, in neonatal rat brain activates CREB, up-regulates Bcl-2, induces extensive brakes on caspase-dependent and -independent apoptosis after HI, and provides long-term neuroprotection.