Gene expression of the small GTP-binding proteins RhoA, RhoB, Rac1, and Cdc42 in adult rat brain

Olenik, Claudia; Barth, Holger; Just, Ingo; Aktories, Klaus; Meyer, Dieter

doi:10.1016/s0169-328x(97)00270-2

Cited by 66 publications

(50 citation statements)

References 28 publications

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“…The expression of NADPH oxidase originally was characterized in phagocytic neutrophils of the immune system (Shatwell and Segal, 1996). However, there is evidence that NADPH oxidase and Rac1 also are expressed in the brain and, in particular, the hippocampus (Olenik et al, 1997;Mizuki et al, 1998). Interestingly, Rac1 is one of the proteins that has been shown to be associated with NMDA receptor multiprotein complexes (Husi et al, 2000), making it a candidate for regulation after the induction of LTP.…”

Section: Discussionmentioning

confidence: 99%

Potentiation of Hippocampal Synaptic Transmission by Superoxide Requires the Oxidative Activation of Protein Kinase C

Knapp¹,

2002

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Recent evidence suggests that reactive oxygen species (ROS), including superoxide, are not only neurotoxic but function as small messenger molecules in normal neuronal processes such as synaptic plasticity. Consistent with this idea, we show that brief incubation of hippocampal slices with the superoxidegenerating system xanthine/xanthine oxidase (X/XO) produces a long-lasting potentiation of synaptic transmission in area CA1. We found that X/XO-induced potentiation was associated with a persistent superoxide-dependent increase in autonomous PKC activity that could be isolated via DEAE column chromatography. The X/XO-induced potentiation was blocked by the inhibition of PKC, indicating that the superoxidedependent increase in autonomous PKC activity was necessary for the potentiation. We also found that X/XO-induced potentiation and long-term potentiation (LTP) occluded one another, suggesting that these forms of plasticity share similar cellular mechanisms. In further support of this idea, we found that a persistent, superoxide-dependent increase in autonomous PKC activity isolated via DEAE column chromatography also was associated with LTP. Taken together, our findings indicate that X/XO-induced potentiation and LTP share similar cellular mechanisms, including superoxide-dependent increases in autonomous PKC activity. Finally, our findings suggest that superoxide, in addition to its well known role as a neurotoxin, also can be considered a small messenger molecule critical for normal neuronal signaling.

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Section: Discussionmentioning

confidence: 99%

Potentiation of Hippocampal Synaptic Transmission by Superoxide Requires the Oxidative Activation of Protein Kinase C

Knapp¹,

2002

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“…Rho is present in the crude membrane fraction of bovine brain (Yamamoto et al 1988). RhoA, rhoB, rac1, and cdc42 are found expressed throughout the nervous system; mRNA can be found in hippocampus, cerebellum, brainstem, thalamus, and neocortex (Olenik et al 1997). This widespread expression suggests a critical involvement of the rho GTPases in neuronal function.…”

Section: Rho Gtpases: Organizers Of Actin Structuresmentioning

confidence: 98%

Signaling mechanisms that regulate actin‐based motility processes in the nervous system

Meyer

Feldman

2002

Journal of Neurochemistry

172

108

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Actin-based motility is critical for nervous system development. Both the migration of neurons and the extension of neurites require organized actin polymerization to push the cell membrane forward. Numerous extracellular stimulants of motility and axon guidance cues regulate actin-based motility through the rho GTPases (rho, rac, and cdc42). The rho GTPases reorganize the actin cytoskeleton, leading to stress fiber, filopodium, or lamellipodium formation. The activity of the rho GTPases is regulated by a variety of proteins that either stimulate GTP uptake (activation) or hydrolysis (inactivation). These proteins potentially link extracellular signals to the activation state of rho GTPases. Effectors downstream of the rho GTPases that directly influence actin polymerization have been identified and are involved in neurite development.The Arp2/3 complex nucleates the formation of new actin branches that extend the membrane forward. Ena/VASP proteins can cause the formation of longer actin filaments, characteristic of growth cone actin morphology, by preventing the capping of barbed ends. Actin-depolymerizing factor (ADF)/cofilin depolymerizes and severs actin branches in older parts of the actin meshwork, freeing monomers to be re-incorporated into actively growing filaments. The signaling mechanisms by which extracellular cues that guide axons to their targets lead to direct effects on actin filament dynamics are becoming better understood. Keywords: actin-depolymerizing factor (ADF)/cofilin, actinrelated protein Arp2/3, ena/VASP, LIM kinase, rho GTPase.

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“…Among the numerous regulatory elements participating in this equilibrium, the Rho family of proteins plays a central role, as they link extracellular signals to a variety of intracellular effectors. These small GTPases (i.e., RhoA, Cdc42, and Rac1) are highly expressed in brain (Olenik et al, 1997) and differentially regulate spine morphology during neuronal development (Nakayama et al, 2000;Penzes and Rafalovich, 2012). Stimulation of the RhoA/RhoA kinase (ROCK) pathway has been proposed to drive actin polymerization and spine growth during LTP, whereas Rac/Cdc42/p21-activated kinase (PAK) signaling seems to be important for F-actin stabilization and maintenance of structural plasticity Murakoshi et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Activity-Dependent Rapid Local RhoA Synthesis Is Required for Hippocampal Synaptic Plasticity

Briz¹,

Zhu²,

Wang³

et al. 2015

J. Neurosci.

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Dendritic protein synthesis and actin cytoskeleton reorganization are important events required for the consolidation of hippocampal LTP and memory. However, the temporal and spatial relationships between these two processes remain unclear. Here, we report that treatment of adult rat hippocampal slices with BDNF or with tetraethylammonium (TEA), which induces a chemical form of LTP, produces a rapid and transient increase in RhoA protein levels. Changes in RhoA were restricted to dendritic spines of CA3 and CA1 and require de novo protein synthesis regulated by mammalian target of rapamycin (mTOR). BDNF-mediated stimulation of RhoA activity, cofilin phosphorylation, and actin polymerization were completely suppressed by protein synthesis inhibitors. Furthermore, intrahippocampal injections of RhoA antisense oligodeoxynucleotides inhibited theta burst stimulation (TBS)-induced RhoA upregulation in dendritic spines and prevented LTP consolidation. Addition of calpain inhibitors after BDNF or TEA treatment maintained RhoA levels elevated and prolonged the effects of BDNF and TEA on actin polymerization. Finally, the use of isoform-selective calpain inhibitors revealed that calpain-2 was involved in RhoA synthesis, whereas calpain-1 mediated RhoA degradation. Overall, this mechanism provides a novel link between dendritic protein synthesis and reorganization of the actin cytoskeleton in hippocampal dendritic spines during LTP consolidation.

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Gene expression of the small GTP-binding proteins RhoA, RhoB, Rac1, and Cdc42 in adult rat brain

Cited by 66 publications

References 28 publications

Potentiation of Hippocampal Synaptic Transmission by Superoxide Requires the Oxidative Activation of Protein Kinase C

Potentiation of Hippocampal Synaptic Transmission by Superoxide Requires the Oxidative Activation of Protein Kinase C

Signaling mechanisms that regulate actin‐based motility processes in the nervous system

Activity-Dependent Rapid Local RhoA Synthesis Is Required for Hippocampal Synaptic Plasticity

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