The protein kinase C phosphorylation site on GAP‐43 differentially regulates information storage

Holahan, Matthew R.; Routtenberg, Aryeh

doi:10.1002/hipo.20486

Cited by 35 publications

(41 citation statements)

References 13 publications

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“…First, it enhances learning on a working and spatial memory version of the delayed matching-to-place task in the radial arm maze (Routtenberg et al 2000) but not on purely spatial tasks, such as contextual fear conditioning or the water maze (Holahan and Routtenberg 2008). However, it favors the extinction of contextual fear memory and enhances reversal learning in the radial arm maze (Holahan and Routtenberg 2008). Overexpression of a pseudophosphorylated GAP43 does not affect spatial learning but enhances contextual fear memory and blocks its extinction (Holahan and Routtenberg 2008).…”

Section: +mentioning

confidence: 99%

“…Consistently, GAP43 overexpression has an effect on memory. First, it enhances learning on a working and spatial memory version of the delayed matching-to-place task in the radial arm maze (Routtenberg et al 2000) but not on purely spatial tasks, such as contextual fear conditioning or the water maze (Holahan and Routtenberg 2008). However, it favors the extinction of contextual fear memory and enhances reversal learning in the radial arm maze (Holahan and Routtenberg 2008).…”

Section: +mentioning

confidence: 99%

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Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

2012

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Major brain functions depend on neuronal processes that favor the plasticity of neuronal circuits while at the same time maintaining their stability. The mechanisms that regulate brain plasticity are complex and engage multiple cascades of molecular components that modulate synaptic efficacy. Protein kinases (PKs) and phosphatases (PPs) are among the most important of these components that act as positive and negative regulators of neuronal signaling and plasticity, respectively. In these cascades, the PP protein phosphatase 2B or calcineurin (CaN) is of particular interest because it is the only Ca 2+ -activated PP in the brain and a major regulator of key proteins essential for synaptic transmission and neuronal excitability. This review describes the primary properties of CaN and illustrates its functions and modes of action by focusing on several representative targets, in particular glutamate receptors, striatal enriched protein phosphatase (STEP), and neuromodulin (GAP43), and their functional significance for synaptic plasticity and memory.

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Section: +mentioning

confidence: 99%

Section: +mentioning

confidence: 99%

Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

2012

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“…GAP-43 homozygous deficit mice die shortly after birth (Strittmatter et al, 1995, Maier et al, 1999, while homozygous GAP-43 overexpressing mice show enhanced learning and synaptic plasticity (Routtenberg et al, 2000). Also, transgenic GAP-43 overexpressing mice exhibit deficit spatial learning (Holahan and Routtenberg, 2008) when observed in radial arm maze, Morris water maze and contextual fear conditioning. However, Holahan and Routtenberg (2008) demonstrated that the phosphorylation state of GAP-43 plays a key role in the regulation of its activity.…”

Section: Discussionmentioning

confidence: 99%

“…Also, transgenic GAP-43 overexpressing mice exhibit deficit spatial learning (Holahan and Routtenberg, 2008) when observed in radial arm maze, Morris water maze and contextual fear conditioning. However, Holahan and Routtenberg (2008) demonstrated that the phosphorylation state of GAP-43 plays a key role in the regulation of its activity. Significant memory impairments was observed in heterozygous GAP-43 knockout mice with levels reduced by one-half, but with normal levels of synaptophysin (Rekart et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

A single neonatal exposure to perfluorohexane sulfonate (PFHxS) affects the levels of important neuroproteins in the developing mouse brain

Lee

Viberg

2013

NeuroToxicology

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A single neonatal exposure to perfluorohexane sulfonate (PFHxS) affects the levels of important neuroproteins in the developing mouse brain. , 37: 190-196 Neurotoxicology AbstractPerfluorohexane sulfonate (PFHxS) is an industrial chemical and belongs to the group of perfluorinated compounds (PFCs). It has recently been shown to cause developmental neurobehavioral defects in mammals. These compounds are commonly used in products such as surfactant and protective coating due to their ability to repel water-and oil stains. PFCs are globally found in the environment as well as in human umbilical cord blood, serum and breast milk. In a previous study on other well-known PFCs i.e. PFOS and PFOA, it was shown that neonatal exposure caused altered neuroprotein levels in the hippocampus and cerebral cortex in neonatal male mice. The present study show that neonatal exposure to PFHxS, during the peak of the brain growth spurt, can alter neuroprotein levels e.g. CaMKII, GAP-43, synaptophysin and tau, which are essential for normal brain development in mice. This was measured for both males and females, in hippocampus and cerebral cortex. The results suggest that PFHxS may act as a developmental neurotoxicant and the effects are similar to that of PFOS and PFOA, but also to other substances such as PCBs, PBDEs and Bisphenol A.

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“…The overall behavioral memory functions associated with each of these lines has been reported; 104 G-Phos mice showed enhanced …”

Section: Relationship To Memory Storagementioning

confidence: 99%

GAP-43 in synaptic plasticity: molecular perspectives

Holahan¹

2015

RRBC

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Abstract:The growth-associated protein, GAP-43 (also known as F1, neuromodulin, B-50), participates in the developmental regulation of axonal growth and neural network formation via protein kinase C-mediated regulation of cytoskeletal elements. Transgenic overexpression of GAP-43 can result in the formation of new synapses, neurite outgrowth, and synaptogenesis after injury. In a number of adult mammalian species, GAP-43 has been implicated in the regulation of synaptic transmission and plasticity, such as long-term potentiation, drug sensitization, and changes in memory processes. This review examines the molecular and biochemical attributes of GAP-43, its distribution in the central nervous system, subcellular localization, role in neurite outgrowth and development, and functions related to plasticity, such as those occurring during long-term potentiation, memory formation, and drug sensitization.

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The protein kinase C phosphorylation site on GAP‐43 differentially regulates information storage

Cited by 35 publications

References 13 publications

Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

A single neonatal exposure to perfluorohexane sulfonate (PFHxS) affects the levels of important neuroproteins in the developing mouse brain

GAP-43 in synaptic plasticity: molecular perspectives

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