IQ-Motif Proteins Influence Intracellular Free Ca<sup>2+</sup>in Hippocampal Neurons Through Their Interactions With Calmodulin

Kubota, Yoshihisa; Putkey, John A.; Shouval, Harel Z.; Waxham, M. Neal

doi:10.1152/jn.00876.2007

Cited by 27 publications

(35 citation statements)

References 46 publications

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“…These results reinforce that Ng plays a critical role in controlling the Ca 2ϩ /CaM signaling pathway and, when the Ca 2ϩ -buffering capacity of CaM is considered, also plays a role in establishing free Ca 2ϩ levels inside cells (4,24). Given these properties, it is not surprising that Ng has been documented as a key molecule regulating the induction of Ca 2ϩ -dependent plasticity (38) in the nervous system and has been implicated in a growing number of neurological disorders (39 -46).…”

supporting

confidence: 73%

Neurogranin Alters the Structure and Calcium Binding Properties of Calmodulin

Hoffman¹,

Chandrasekar²,

Wang³

et al. 2014

Journal of Biological Chemistry

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Background:Neurogranin is an IQ motif protein that binds to both apo-and calcium-saturated calmodulin. Results: Neurogranin makes contacts with both the N-and C-domains of calmodulin that functionally leads to altered calcium binding kinetics. Conclusion:The availability and calcium saturation of calmodulin is determined by neurogranin. Significance: Neurogranin plays a major role in controlling the intracellular calcium-calmodulin-signaling pathway.

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supporting

confidence: 73%

Neurogranin Alters the Structure and Calcium Binding Properties of Calmodulin

Hoffman¹,

Chandrasekar²,

Wang³

et al. 2014

Journal of Biological Chemistry

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“…First, binding of Pep-19 to CaM has been shown to increase the rates of association and dissociation of calcium to CaM by as much as 40-to 50-fold (25,27). Models have predicted that this would reduce the increase in free calcium and rapidly saturate and release Ca 2ϩ from the C-domain of CaM during high frequency stimulation (14,25). The PMCA pump is strongly regulated by the C-domain of CaM, and its rate of calcium efflux is enhanced by Ͼ30-fold when bound to calcium loaded CaM (23).…”

Section: Discussionmentioning

confidence: 99%

Regional differences in hippocampal calcium handling provide a cellular mechanism for limiting plasticity

Simons

Escobedo

Yasuda

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

119

148

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Although much is known about the mechanisms underlying synaptic plasticity, the cellular mechanisms that negatively regulate plasticity in some brain regions are considerably less studied. One region where neurons do not reliably express long-term potentiation (LTP) is the CA2 subfield of the hippocampus. Given the connection between synaptic plasticity and increases in postsynaptic [Ca 2؉ ], and that CA2 neurons express a large number of calcium-regulating proteins, we tested the hypothesis that the relative lack of LTP in CA2 results from differences in the calcium dynamics of these neurons. By measuring calcium-dependent fluorescence transients in dendritic spines, we show that CA2 neurons have smaller action potential-evoked intracellular Ca 2؉ transients because of a higher endogenous Ca 2؉ -buffering capacity and significantly higher rates of Ca 2؉ extrusion when compared with CA1 and CA3 neurons. CA2 ͉ hippocampus ͉ synaptic plasticity

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“…Together, these data indicated that CA2 pyramidal neurons possess the intracellular machinery required to support induction of NMDAR-dependent LTP, but that the higher calcium buffering and extrusion in CA2 neurons normally prevents such plasticity from occurring. Although CA2 neurons do not selectively express high levels of specific calcium pumps or exchangers relative to other regions in the hippocampus that could account for the increased rates of extrusion observed, they are highly enriched in the calmodulin-regulating protein Pep-19 (Gerendasy 1999;Kubota et al 2008). Pyramidal cells in CA1 do not normally express high levels of Pep-19, but to test whether Pep-19 regulates calcium extrusion, Simons et al (2009) introduced into CA1 neurons a functional analog of Pep-19, camstatin, which successfully produced a plasticity-resistant phenotype in CA1 similar to pyramidal neurons in CA2 (Fig.…”

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New insights into the regulation of synaptic plasticity from an unexpected place: Hippocampal area CA2

2012

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The search for molecules that restrict synaptic plasticity in the brain has focused primarily on sensory systems during early postnatal development, as critical periods for inducing plasticity in sensory regions are easily defined. The recent discovery that Schaffer collateral inputs to hippocampal area CA2 do not readily support canonical activity-dependent long-term potentiation (LTP) serves as a reminder that the capacity for synaptic modification is also regulated anatomically across different brain regions. Hippocampal CA2 shares features with other similarly "LTP-resistant" brain areas in that many of the genes linked to synaptic function and the associated proteins known to restrict synaptic plasticity are expressed there. Add to this a rich complement of receptors and signaling molecules permissive for induction of atypical forms of synaptic potentiation, and area CA2 becomes an ideal model system for studying specific modulators of brain plasticity. Additionally, recent evidence suggests that hippocampal CA2 is instrumental for certain forms of learning, memory, and social behavior, but the links between CA2-enriched molecules and putative CA2-dependent behaviors are only just beginning to be made. In this review, we offer a detailed look at what is currently known about the synaptic plasticity in this important, yet largely overlooked component of the hippocampus and consider how the study of CA2 may provide clues to understanding the molecular signals critical to the modulation of synaptic function in different brain regions and across different stages of development.

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IQ-Motif Proteins Influence Intracellular Free Ca²⁺in Hippocampal Neurons Through Their Interactions With Calmodulin

Cited by 27 publications

References 46 publications

Neurogranin Alters the Structure and Calcium Binding Properties of Calmodulin

Neurogranin Alters the Structure and Calcium Binding Properties of Calmodulin

Regional differences in hippocampal calcium handling provide a cellular mechanism for limiting plasticity

New insights into the regulation of synaptic plasticity from an unexpected place: Hippocampal area CA2

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IQ-Motif Proteins Influence Intracellular Free Ca2+in Hippocampal Neurons Through Their Interactions With Calmodulin

Cited by 27 publications

References 46 publications

Neurogranin Alters the Structure and Calcium Binding Properties of Calmodulin

Neurogranin Alters the Structure and Calcium Binding Properties of Calmodulin

Regional differences in hippocampal calcium handling provide a cellular mechanism for limiting plasticity

New insights into the regulation of synaptic plasticity from an unexpected place: Hippocampal area CA2

Contact Info

Product

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About

IQ-Motif Proteins Influence Intracellular Free Ca²⁺in Hippocampal Neurons Through Their Interactions With Calmodulin