Overexpression of hippocampal Ca<sup>2+</sup>/calmodulin‐dependent protein kinase II improves spatial memory

Poulsen, David J.; Standing, D.; Bullshields, K.; Spencer, Kathryn B.; Micevych, Paul E.; Babcock, Alex M.

doi:10.1002/jnr.21163

Cited by 17 publications

(15 citation statements)

References 23 publications

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“…It is widely accepted that the CaMKII signaling pathway is critical for both declarative and non-declarative memory formation. For example, T286A mutation in αCaMKII severely impaired in the acquisition of spatial cognition, while overexpression of hippocampal CaMKII can improve performance in the Morris water maze task 41 43 . The T286A mutation in αCaMKII also impaired hippocampus-dependent contextual fear conditioning but not amygdala-dependent cued fear conditioning after using multiple tone–shock pairings training 44 .…”

Section: Discussionmentioning

confidence: 99%

Storage of passive motion pattern in hippocampal CA1 region depends on CaMKII/CREB signaling pathway in a motion sickness rodent model

Wang¹,

Liu²,

Pan³

et al. 2017

Sci Rep

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Sensory mismatch between actual motion information and anticipated sensory patterns (internal model) is the etiology of motion sickness (MS). Some evidence supports that hippocampus might involve the neural storage of the “internal model”. This study established an “internal model” acquisition-retention behavioral model using a repeated habituation rotation training protocol. We tried to identify the hippocampal subregion involved in “internal model” retention using chemical lesion methods. Hippocampal kinases (CaMK, CaMKIV, CREB and ERK1/2) phosphorylation in the target subregion was assayed and the effects of kinase inhibitors (KN93 or U0126) on “internal model” retention were investigated. The activities of potential kinases (CaMKII and CREB) were also examined in otoliths deficit het/het mice. In habituated rats, CA1 lesion reproduced MS-related behavioral responses on “internal model” retention day. Habituation training increased CaMKII and CREB activity but had no effect on CaMKIV and ERK1/2 activity in the CA1, while inhibition of CaMKII but not ERK1/2 impaired “internal model” retention. In het/het mice, CaMKII and CREB were not activated in the CA1 on the retention day. These results suggested that CaMKII/CREB pathway might potentially contribute to the storage of the “internal model” in the hippocampal CA1 after motion sickness induced by vestibular stimulation.

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Section: Discussionmentioning

confidence: 99%

Storage of passive motion pattern in hippocampal CA1 region depends on CaMKII/CREB signaling pathway in a motion sickness rodent model

Wang¹,

Liu²,

Pan³

et al. 2017

Sci Rep

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“…Further, CaMKIIα promotes synaptic formation, strengthening, and integration into existing neural circuits (Asrican et al, 2007; Matsuo et al, 2009; Miller et al, 2002; Zha et al, 2009). Like PSD-95, loss of CaMKIIα activity results in severe electrophysiological abnormalities associated with impaired synaptic plasticity and memory formation, while overexpression of CaMKIIα improves cognitive performance as assessed by Morris water maze testing (Elgersma et al, 2004; Giese et al, 1998; Miller et al, 2002; Poulsen et al, 2007; Silva et al, 1992). …”

Section: Discussionmentioning

confidence: 99%

Hippocampal dysregulation of synaptic plasticity-associated proteins with age-related cognitive decline

VanGuilder

Farley

Han

et al. 2011

Neurobiology of Disease

121

130

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Age-related cognitive decline occurs without frank neurodegeneration and is the most common cause of memory impairment in aging individuals. With increasing longevity, cognitive deficits, especially in hippocampus-dependent memory processes, are increasing in prevalence. Nevertheless, the neurobiological basis of age-related cognitive decline remains unknown. While concerted efforts have led to the identification of neurobiological changes with aging, few age-related alterations have been definitively correlated to behavioral measures of cognitive decline. In this work, adult (12 Months) and aged (28 months) rats were categorized by Morris water maze performance as Adult cognitively Intact, Aged cognitively Intact or Aged cognitively Impaired, and protein expression was examined in hippocampal synaptosome preparations. Previously described differences in synaptic expression of neurotransmission-associated proteins (Dnm1, Hpca, Stx1, Syn1, Syn2, Syp, SNAP25, VAMP2 and 14-3-3 eta, gamma, and zeta) were confirmed between Adult and Aged rats, with no further dysregulation associated with cognitive impairment. Proteins related to synaptic structural stability (MAP2, drebrin, Nogo-A) and activity-dependent signaling (PSD-95, 14-3-3θ, CaMKIIα) were up- and down-regulated, respectively, with cognitive impairment but were not altered with increasing age. Localization of MAP2, PSD-95, and CaMKIIα demonstrated protein expression alterations throughout the hippocampus. The altered expression of activity- and structural stability-associated proteins suggests that impaired synaptic plasticity is a distinct phenomenon that occurs with age-related cognitive decline, and demonstrates that cognitive decline is not simply an exacerbation of the aging phenotype.

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“…The application of CaMKII inhibitors, such as KN-62 or KN-93, or genetic disruption of the CaMKII gene can block LTP (Malinow et al 1989;Otmakhov et al 1997;Hinds et al 1998;Yamagata et al 2009). Conversely, the injection or viral expression of a constitutively active form of CaMKII leads to the improvement of spatial memory (Poulsen et al 2007), in enhancement of AMPAR-mediated synaptic transmission and occludes further induction of LTP (McGladeMcCulloh et al 1993;Pettit et al 1994;Lledo et al 1995). This enhancement in AMPAR conductance has been proposed to occur through an increase in synaptic trafficking of GluA1 subunits, as well as phosphorylation of GluA1 at Ser831 (Shi et al 1999;Hayashi et al 2000;Broutman and Baudry 2001;Esteban et al 2003;Oh et al 2006).…”

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confidence: 99%

Long-term potentiation can be induced in the CA1 region of hippocampus in the absence of αCaMKII T286-autophosphorylation

2014

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a-calcium/calmodulin-dependent protein kinase (aCaMKII) T286-autophosphorylation provides a short-term molecular memory that was thought to be required for LTP and for learning and memory. However, it has been shown that learning can occur in aCaMKII-T286A mutant mice after a massed training protocol. This raises the question of whether there might be a form of LTP in these mice that can occur without T286 autophosphorylation. In this study, we confirmed that in CA1 pyramidal cells, LTP induced in acute hippocampal slices, after a recovery period in an interface chamber, is strictly dependent on postsynaptic aCaMKII autophosphorylation. However, we demonstrated that aCaMKII-autophosphorylation-independent plasticity can occur in the hippocampus but at the expense of synaptic specificity. This nonspecific LTP was observed in mutant and wild-type mice after a recovery period in a submersion chamber and was independent of NMDA receptors. Moreover, when slices prepared from mutant mice were preincubated during 2 h with rapamycin, high-frequency trains induced a synapse-specific LTP which was added to the nonspecific LTP. This specific LTP was related to an increase in the duration and the amplitude of NMDA receptor-mediated response induced by rapamycin.The formation of memories is believed to be achieved through strengthening of synaptic communication between two simultaneously active neurons, a phenomenon called long-term potentiation (LTP). For several years, numerous studies have sought to better understand the molecular mechanisms of synaptic plasticity and LTP, and in particular the role of calcium-calmodulin-dependent protein kinase II (CaMKII), one of the most important postsynaptic components in glutamatergic synapses. Indeed, CaMKII is both necessary and sufficient for LTP induction. The application of CaMKII inhibitors, such as KN-62 or KN-93, or genetic disruption of the CaMKII gene can block LTP (Malinow et al. 1989;Otmakhov et al. 1997;Hinds et al. 1998;Yamagata et al. 2009). Conversely, the injection or viral expression of a constitutively active form of CaMKII leads to the improvement of spatial memory (Poulsen et al. 2007), in enhancement of AMPAR-mediated synaptic transmission and occludes further induction of LTP (McGladeMcCulloh et al. 1993;Pettit et al. 1994;Lledo et al. 1995). This enhancement in AMPAR conductance has been proposed to occur through an increase in synaptic trafficking of GluA1 subunits, as well as phosphorylation of GluA1 at Ser831 (Shi et al. 1999;Hayashi et al. 2000;Broutman and Baudry 2001;Esteban et al. 2003;Oh et al. 2006). Besides its role in synaptic transmission, CaMKII is also involved in the structural plasticity of spines, and more specifically in activity-dependent spine growth following NMDAR activation (Okamoto et al. 2009;Pi et al. 2010). Moreover, it seems that CaMKII-dependent processes involved in hippocampal LTP in CA1 synapses are quite general since the kinase also affects in vivo plasticity in different brain regions (Wu and Cline 1998;Zou and Cline 1999). ...

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Overexpression of hippocampal Ca²⁺/calmodulin‐dependent protein kinase II improves spatial memory

Cited by 17 publications

References 23 publications

Storage of passive motion pattern in hippocampal CA1 region depends on CaMKII/CREB signaling pathway in a motion sickness rodent model

Storage of passive motion pattern in hippocampal CA1 region depends on CaMKII/CREB signaling pathway in a motion sickness rodent model

Hippocampal dysregulation of synaptic plasticity-associated proteins with age-related cognitive decline

Long-term potentiation can be induced in the CA1 region of hippocampus in the absence of αCaMKII T286-autophosphorylation

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Overexpression of hippocampal Ca2+/calmodulin‐dependent protein kinase II improves spatial memory

Cited by 17 publications

References 23 publications

Storage of passive motion pattern in hippocampal CA1 region depends on CaMKII/CREB signaling pathway in a motion sickness rodent model

Storage of passive motion pattern in hippocampal CA1 region depends on CaMKII/CREB signaling pathway in a motion sickness rodent model

Hippocampal dysregulation of synaptic plasticity-associated proteins with age-related cognitive decline

Long-term potentiation can be induced in the CA1 region of hippocampus in the absence of αCaMKII T286-autophosphorylation

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Overexpression of hippocampal Ca²⁺/calmodulin‐dependent protein kinase II improves spatial memory