Impaired Synaptic Plasticity and cAMP Response Element-Binding Protein Activation in Ca<sup>2+</sup>/Calmodulin-Dependent Protein Kinase Type IV/Gr-Deficient Mice

Ho, Nga; Liauw, Jason; Blaeser, Frank; Feng, Wei; Hanissian, Silva H.; Muglia, Lisa M.; Wozniak, David F.; Nardi, A.; Arvin, Kara L.; Holtzman, David M.; Linden, David J.; Zhuo, Min; Muglia, Louis J.; Chatila, Talal A.

doi:10.1523/jneurosci.20-17-06459.2000

Cited by 237 publications

(238 citation statements)

References 72 publications

(79 reference statements)

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“…Cooperation between NMDA receptors and L-type calcium channels can occur to enhance CREB signaling (Nakazawa and Murphy, 1999;Rajadhyaksha et al, 1999), but depending on the stimulus conditions, activation of a single pathway can also take place (Hardingham et al, 2002). Our work has focused on studying how mild depolarizations lead to CREB phosphorylation and CRE-dependent transcription via CaM/CaMKIV activation, because this is the signaling pathway responsible for CREB regulation after synaptic activity at multiple stimulus frequencies and is a critical mediator of plasticity in vivo (Ho et al, 2000;Ribar et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Within the hippocampus and other brain regions, CREB activation after brief stimulation (Յ3 min) is primarily mediated by calcium entry via L-type calcium channels (with a smaller component attributable to NMDA receptors) (Sheng et al, 1991;Deisseroth et al, 1996;Mermelstein et al, 2000). Calcium influx through L-type channels activates calmodulin (CaM), leading to phosphorylation of CREB on Ser 133 by CaMdependent protein kinases Tokumitsu et al, 1995;Bito et al, 1996;Ahn et al, 1999;Ho et al, 2000;Ribar et al, 2000;Kang et al, 2001). Phosphorylation of CREB promotes its interaction with CREB binding protein (CBP) or a similar coactivator, leading to CRE-dependent transcription (Parker et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

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Interactions with PDZ Proteins Are Required for L-Type Calcium Channels to Activate cAMP Response Element-Binding Protein-Dependent Gene Expression

et al. 2003

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After brief periods of heightened stimulation, calcium entry through L-type calcium channels leads to activation of the transcription factor cAMP response element-binding protein (CREB) and CRE-dependent transcription. Many of the details surrounding the mechanism by which L-type calcium channels are privileged in signaling to CREB, to the exclusion of other calcium entry pathways, has remained unclear. We hypothesized that the PDZ interaction sequence contained within the last four amino acids of the calcium channel

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Interactions with PDZ Proteins Are Required for L-Type Calcium Channels to Activate cAMP Response Element-Binding Protein-Dependent Gene Expression

et al. 2003

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“…The battery included the following tests using previously published protocols. 13,14 1. Walking initiation: each mouse was placed in the center of a square (21 3 21 cm) outlined on a smooth black tabletop, and the latency for initiating movement out of the square (placing all four limbs outside the square) was timed in seconds.…”

Section: Neurobehavioral Testingmentioning

confidence: 99%

“…On day 8 of the experiment (five days after the last weight-drop/sham-impact session), the mice were evaluated on the MWM using a procedure similar to previously published methods. 14 Briefly, this task involved training mice to navigate to a platform in a pool (100 cm wide 3 30 cm deep) of opaque water to escape out of the water. All trials were monitored by a video camera mounted above the pool, and data were recorded using a computerized tracking system (Polytrak; San Diego Instruments, San Diego, CA) that measured the escape path length (distance traveled to find the platform) and escape latency (time to find the platform).…”

Section: Platform Test: Each Mouse Was Timed (In Seconds)mentioning

confidence: 99%

Multiple Episodes of Mild Traumatic Brain Injury Result in Impaired Cognitive Performance in Mice

Creeley¹,

Wozniak²,

Bayly³

et al. 2004

Acad Emergency Med

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Objectives: Results from recent studies on animal models of concussion suggest that multiple, rather than single, episodes of mild traumatic brain injury result in impaired cognitive performance in mice. The objective of the present study was to administer multiple impacts to the heads of mice while directly measuring the force of the impacts to determine how these parameters are related to transient loss of consciousness, cognitive deficits, and potential neuropathologic effects. Methods: Seven-week-old male C57BL/6 mice were randomly assigned to experimental conditions involving three impacts (weight-drop method) to the head to induce mild traumatic brain injury or to sham control procedures. Some impacted (n ¼ 10) and sham control (n ¼ 10) mice were evaluated behaviorally and tested for spatial learning using the Morris water maze (MWM), whereas other impacted (n ¼ 10) and sham control (n ¼ 5) mice were used for histopathologic analysis. Results: The mean (6SD) force of impact was 19 (63.5) N. Impacted mice took longer to regain consciousness compared with sham control mice (p \ 0.0005). Behavioral test results showed that the groups did not differ on activity or sensorimotor tests or during cued trials in the MWM. Impacted mice exhibited impaired spatial learning performance during place trials in the MWM (p \ 0.05). Silver staining revealed a contra-coup type of injury involving ventral brain structures in contact with or in close proximity to the skull. Conclusions: This multiple-impact model, delivered within a specifiable force range, results in transient, reversible loss of consciousness, a contra-coup brain injury, and cognitive impairment. Key words: traumatic brain injury; concussion; memory; cognition; mice. ACADEMIC EMERGENCY MED-ICINE 2004; 11:809-819. It is not clear whether mild traumatic brain injury (TBI) causes demonstrable long-term cognitive impairment in humans. A number of earlier epidemiologic studies suggest that this may be the case, but the use of retrospective designs, lack of appropriate control groups, and an inability to correct for several confounding factors did not allow for a straightforward interpretation of the results. [1][2][3][4] More recently, a number of studies of athletes who have experienced a sports-related concussion suggest that symptomatology and cognitive impairment can last for one week 5 and, in some cases, up to three months. 6 Animal models have been used to study the behavioral and neuropathologic sequelae associated with TBI. [7][8][9][10] In three of these studies, in which slightly different murine models of mild TBI were used, the results suggested that mild single impacts did not produce discernible learning/memory deficits when behavioral testing was conducted more than three days after impact. [8][9][10] In contrast, multiple mild impacts have usually been found to produce significant effects on behavior, but the nature of these changes has been inconsistent across studies. For example, DeFord et al. 10 reported that multiple mild impacts ...

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“…Both describe deficits in CREB phosphorylation and cerebellar defects, affecting either latephase of long-term depression (43) or the number and size (44) of Purkinje cells. These studies confirm the importance of this kinase during cerebellar function and development.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotection by Neurotrophic Factors and Membrane Depolarization Is Regulated by Calmodulin Kinase IV

Pérez-García

Gou-Fàbregas

Pablo

et al. 2008

Journal of Biological Chemistry

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Impaired Synaptic Plasticity and cAMP Response Element-Binding Protein Activation in Ca²⁺/Calmodulin-Dependent Protein Kinase Type IV/Gr-Deficient Mice

Cited by 237 publications

References 72 publications

Interactions with PDZ Proteins Are Required for L-Type Calcium Channels to Activate cAMP Response Element-Binding Protein-Dependent Gene Expression

Interactions with PDZ Proteins Are Required for L-Type Calcium Channels to Activate cAMP Response Element-Binding Protein-Dependent Gene Expression

Multiple Episodes of Mild Traumatic Brain Injury Result in Impaired Cognitive Performance in Mice

Neuroprotection by Neurotrophic Factors and Membrane Depolarization Is Regulated by Calmodulin Kinase IV

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Impaired Synaptic Plasticity and cAMP Response Element-Binding Protein Activation in Ca2+/Calmodulin-Dependent Protein Kinase Type IV/Gr-Deficient Mice

Cited by 237 publications

References 72 publications

Interactions with PDZ Proteins Are Required for L-Type Calcium Channels to Activate cAMP Response Element-Binding Protein-Dependent Gene Expression

Interactions with PDZ Proteins Are Required for L-Type Calcium Channels to Activate cAMP Response Element-Binding Protein-Dependent Gene Expression

Multiple Episodes of Mild Traumatic Brain Injury Result in Impaired Cognitive Performance in Mice

Neuroprotection by Neurotrophic Factors and Membrane Depolarization Is Regulated by Calmodulin Kinase IV

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Impaired Synaptic Plasticity and cAMP Response Element-Binding Protein Activation in Ca²⁺/Calmodulin-Dependent Protein Kinase Type IV/Gr-Deficient Mice