Second Messengers in Neuronal Growth and Degeneration

Author(s):  
Mark P. Mattson
2006 ◽  
Vol 84 (7) ◽  
pp. 687-694 ◽  
Author(s):  
John Cijiang He ◽  
Susana R. Neves ◽  
J. Dedrick Jordan ◽  
Ravi Iyengar

Neurite outgrowth is a complex differentiation process stimulated by many neuronal growth factors and transmitters and by electrical activity. Among these stimuli are ligands for G-protein-coupled receptors (GPCR) that function as neurotransmitters. The pathways involved in GPCR-triggered neurite outgrowth are not fully understood. Many of these receptors couple to Gαo, one of the most abundant proteins in the neuronal growth cones. We have studied the Go signaling network involved in neurite outgrowth in Neuro2A cells. Gαo can induce neurite outgrowth. The CB1 cannabinoid receptor, a Go/i-coupled receptor expressed endogenously in Neuro2A cells, triggers neurite outgrowth by activating Rap1, which promotes the Gαo-stimulated proteasomal degradation of Rap1GAPII. CB1-receptor-mediated Rap1 activation leads to the activation of a signaling network that includes the small guanosine triphosphate (GTP)ases Ral and Rac, the protein kinases Src, and c-Jun N-terminal kinase (JNK), which converge onto the activation of signal transducer and activator of transcription 3 (Stat3), a key transcription factor that mediates the gene expression process of neurite outgrowth in Neuro2A cells. This review describes current findings from our laboratory and also discusses alternative pathways that Go/i might mediate to trigger neurite outgrowth. We also analyze the role neurotransmitters, which stimulate Go/i to activate a complex signaling network controlling neurite outgrowth, play in regeneration after neuronal injury.


1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S44-S45
Author(s):  
A. PFEIFFER ◽  
B. NOELKE ◽  
H. ROCHLITZ
Keyword(s):  

Author(s):  
Gordon L. Fain

Sensory Transduction provides a thorough and easily accessible introduction to the mechanisms that each of the different kinds of sensory receptor cell uses to convert a sensory stimulus into an electrical response. Beginning with an introduction to methods of experimentation, sensory specializations, ion channels, and G-protein cascades, it provides up-to-date reviews of all of the major senses, including touch, hearing, olfaction, taste, photoreception, and the “extra” senses of thermoreception, electroreception, and magnetoreception. By bringing mechanisms of all of the senses together into a coherent treatment, it facilitates comparison of ion channels, metabotropic effector molecules, second messengers, and other components of signal pathways that are common themes in the physiology of the different sense organs. With its many clear illustrations and easily assimilated exposition, it provides an ideal introduction to current research for the professional in neuroscience, as well as a text for an advanced undergraduate or graduate-level course on sensory physiology.


1991 ◽  
Vol 261 (2) ◽  
pp. L188-L194 ◽  
Author(s):  
P. I. Plews ◽  
Z. A. Abdel-Malek ◽  
C. A. Doupnik ◽  
G. D. Leikauf

The endothelins (ET) are a group of isopeptides produced by a number of cells, including canine tracheal epithelial cells. Because these compounds are endogenous peptides that may activate eicosanoid metabolism, we investigated the effects of ET on Cl secretion in canine tracheal epithelium. Endothelin 1 (ET-1) was found to produce a dose-dependent change in short-circuit current (Isc) that increased slowly and reached a maximal value within 10-15 min. When isopeptides of ET were compared, 300 nM ET-1 and ET-2 produced comparable maximal increases in Isc, whereas ET-3 produced smaller changes in Isc (half-maximal concentrations of 2.2, 7.2, and 10.4 nM, respectively). Ionic substitution of Cl with nontransported anions, iodide and gluconate, reduced ET-1-induced changes in Isc. Furthermore, the response was inhibited by the NaCl cotransport inhibitor, furosemide. In paired tissues, ET-1 significantly increased mucosal net 36Cl flux without significant effect on 22Na flux. The increase in Isc induced by ET was diminished by pretreatment with indomethacin. The second messengers mediating the increase in Isc were investigated in cultured canine tracheal epithelial cells. ET-1 stimulated the release of [3H]arachidonate from membrane phospholipids, increased intracellular Ca2+ (occasionally producing oscillations), and increased adenosine 3',5'-cyclic monophosphate accumulation. The latter was diminished by indomethacin. Thus ET is a potent agonist of Cl secretion (with the isopeptides having the following potency: ET-1 greater than or equal to ET-2 greater than ET-3) and acts, in part, through a cyclooxygenase-dependent mechanism.


2001 ◽  
Vol 24 (2) ◽  
pp. 284-284 ◽  
Author(s):  
Terry Elliott

It is suggested that a connection between neurogenesis and brain part size is unsurprising. It is argued that neurogenesis cannot, however, be the only factor contributing to brain size. Highly individual post-natal experience radically shapes individual brains, leading to dramatic increases in brain size. The role of comparatively coarse statistical techniques in addressing these subtle biological issues is questioned.


2021 ◽  
Vol 60 ◽  
pp. 96-103
Author(s):  
Soo hun Yoon ◽  
Christopher M Waters
Keyword(s):  

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