Protein kinase C mediates memory consolidation of taste avoidance conditioning in Lymnaea stagnalis

Takigami, Satoshi; Sunada, Hiroshi; Lukowiak, Ken; Kuzirian, Alan M.; Alkon, Daniel L.; Sakakibara, Manabu

doi:10.1016/j.nlm.2014.02.011

Cited by 14 publications

(9 citation statements)

References 60 publications

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“…PKCα has an organized linear configuration consisting of N-terminal pseudosubstrate domains, a kinase domain, targeting domains, and inhibitory regulatory domains [23]. PKCα provides biochemical and structural support for synaptic architecture through activation of protein synthesis and has been associated with memory capacity [24, 25]. PKCβ has a distinct active site with a Cα backbone surrounded by supportive side chains [26].…”

Section: Background Of Pkc In the Central Nervous Systemmentioning

confidence: 99%

Common Mechanisms of Alzheimer's Disease and Ischemic Stroke: The Role of Protein Kinase C in the Progression of Age-Related Neurodegeneration

Lucke‐Wold

Turner

Logsdon

et al. 2014

JAD

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Ischemic stroke and Alzheimer’s disease (AD), despite being distinct disease entities, share numerous pathophysiological mechanisms such as those mediated by inflammation, immune exhaustion, and neurovascular unit compromise. An important shared mechanistic link is acute and chronic changes in protein kinase C (PKC) activity. PKC isoforms have widespread functions important for memory, blood-brain barrier maintenance, and injury repair that change as the body ages. Disease states accelerate PKC functional modifications. Mutated forms of PKC can contribute to neurodegeneration and cognitive decline. In some cases the PKC isoforms are still functional but are not successfully translocated to appropriate locations within the cell. The deficits in proper PKC translocation worsen stroke outcome and amyloid-β toxicity. Cross talk between the innate immune system and PKC pathways contribute to the vascular status within the aging brain. Unfortunately, comorbidities such as diabetes, obesity, and hypertension disrupt normal communication between the two systems. The focus of this review is to highlight what is known about PKC function, how isoforms of PKC change with age, and what additional alterations are consequences of stroke and AD. The goal is to highlight future therapeutic targets that can be applied to both the treatment and prevention of neurologic disease. Although the pathology of ischemic stroke and AD are different, the similarity in PKC responses warrants further investigation, especially as PKC-dependent events may serve as an important connection linking age-related brain injury.

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Section: Background Of Pkc In the Central Nervous Systemmentioning

confidence: 99%

Common Mechanisms of Alzheimer's Disease and Ischemic Stroke: The Role of Protein Kinase C in the Progression of Age-Related Neurodegeneration

Lucke‐Wold

Turner

Logsdon

et al. 2014

JAD

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“…Additionally, because they possess relatively simple nervous systems with identifiable neurons, it has been possible to study at the single neuron level the changes underlying learning and memory. Another important advantage possessed by these systems is that because they have an open circulatory system the concentrations of peptides and sugars in the hemolymph are thought to be similar to those in the CNS (Lee et al, 2012;Lukowiak, Sunada, Teskey, Lukowiak, & Dalesman, 2014;Matsuo, Kawaguchi, Yamagishi, Amano, & Ito, 2010;Naskar, Wan, & Kemenes, 2014;Noboa & Gillette, 2013;Otsuka et al, 2013;Walker, Campodonico, Cavallo, & Farley, 2010;Takigami et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

An increase in insulin is important for the acquisition conditioned taste aversion in Lymnaea

Mita¹,

Yamagishi²,

Fujito³

et al. 2014

Neurobiology of Learning and Memory

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“…10,11 Specifically, molluscan insulin-related peptide II and protein kinase C are thought to play a role in the LTM formation of conditioned taste aversion. 12,17 The observed increase in the synthesis of HSPs in the central nervous system of L. stagnalis, following exposure to thermal stress, suggests that these proteins may play a role in LTM formation in relation to a thermal stimulus. Thus, further investigation of the role of HSPs in memory formation is warranted.…”

mentioning

confidence: 98%

Time-related expression profiles for heat shock protein gene transcripts (HSP40, HSP70) in the central nervous system ofLymnaea stagnalisexposed to thermal stress

Foster

Lukowiak

Henry

2015

Communicative & Integrative Biology

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Organisms exposed to environmental stressors respond by rapidly synthesising a suite of highly conserved proteins called heat shock proteins (HSPs). Environmental stress can also enhance and/or block memory formation, with long-term memory formation requiring gene activation and protein synthesis. Thermal stress in the pond snail Lymnaea stagnalis can enhance memory formation, and, in this study, the effect of thermal stress on HSP gene expression in the nervous system was investigated. Time-related expression profiles for HSP40 and HSP70 indicated rapid (<30 min) induction for both transcripts. For HSP40, induction was <20 fold relative to control and expression returned to control levels within 8 h, whereas HSP70 induction was >100 fold and expression did not return to control levels within 8 h.

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Protein kinase C mediates memory consolidation of taste avoidance conditioning in Lymnaea stagnalis

Cited by 14 publications

References 60 publications

Common Mechanisms of Alzheimer's Disease and Ischemic Stroke: The Role of Protein Kinase C in the Progression of Age-Related Neurodegeneration

Common Mechanisms of Alzheimer's Disease and Ischemic Stroke: The Role of Protein Kinase C in the Progression of Age-Related Neurodegeneration

An increase in insulin is important for the acquisition conditioned taste aversion in Lymnaea

Time-related expression profiles for heat shock protein gene transcripts (HSP40, HSP70) in the central nervous system ofLymnaea stagnalisexposed to thermal stress

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