A cAMP analog reverses contextual and tone memory deficits induced by a PKA inhibitor in Pavlovian fear conditioning

Nassireslami, Ehsan; Nikbin, Parmida; Payandemehr, Borna; Amini, Elham; Mohammadi, Mojdeh; Vakilzadeh, Glareh; Ghadiri, Tahereh; Noorbakhsh, Farshid; Sharifzadeh, Mohammad

doi:10.1016/j.pbb.2013.02.016

Cited by 17 publications

(9 citation statements)

References 63 publications

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“…For example, at the dorsolateral periaqueductal grey, inhibition of NMDA receptors, neuronal NOS, and soluble guanylyl cyclase attenuate contextual FC in rats [156], whereas activation of NMDA receptors in the medial prefrontal cortex has been found to be needed for the acquisition of both trace and contextual fear memories [157, 158]. The involvement of cAMP/PKA and nitric oxide/cGMP/PKG pathways in contextual fear learning and consolidation has been widely demonstrated by pharmacological and genetic approaches in hippocampus, amygdala and prefrontal cortex [159–165], and has the role of the transcription factor c-AMP-Responsive-Element binding [CREB; [166–168]. Cholinergic, serotoninergic and GABAergic signals have been also demonstrated to be crucial in contextual FC [160, 169–179].…”

Section: Behavioral Studiesmentioning

confidence: 99%

Behavioral assays with mouse models of Alzheimer's disease: Practical considerations and guidelines

Puzzo

Lee

Palmeri

et al. 2014

Biochemical Pharmacology

167

120

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In Alzheimer’s disease (AD) basic research and drug discovery, mouse models are essential resources for uncovering biological mechanisms, validating molecular targets and screening potential compounds. Both transgenic and non-genetically modified mouse models enable access to different types of AD-like pathology in vivo. Although there is a wealth of genetic and biochemical studies on proposed AD pathogenic pathways, as a disease that centrally features cognitive failure, the ultimate readout for any interventions should be measures of learning and memory. This is particularly important given the lack of knowledge on disease etiology – assessment by cognitive assays offers the advantage of targeting relevant memory systems without requiring assumptions about pathogenesis. A multitude of behavioral assays are available for assessing cognitive functioning in mouse models, including ones specific for hippocampal-dependent learning and memory. Here we review the basics of available transgenic and non-transgenic AD mouse models and detail three well-established behavioral tasks commonly used for testing hippocampal-dependent cognition in mice – contextual fear conditioning, radial arm water maze and Morris water maze. In particular, we discuss the practical considerations, requirements and caveats of these behavioral testing paradigms.

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Section: Behavioral Studiesmentioning

confidence: 99%

Behavioral assays with mouse models of Alzheimer's disease: Practical considerations and guidelines

Puzzo

Lee

Palmeri

et al. 2014

Biochemical Pharmacology

167

120

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“…Acute ethanol exposure affects neuronal membrane receptors and intracellular kinases. At intoxicating concentrations (50–100 mM), acute ethanol activates type 1 dopamine receptor (DR1), adenylate cyclase and cAMP dependent protein kinase A (PKA) (Rabin et al, 1992 ; Lovinger, 2002 ; Ferrani-Kile et al, 2003 ; Moonat et al, 2010 ; Coller and Hutchinson, 2012 ), a signaling pathway closely related to synaptic plasticity (Eftekharzadeh et al, 2012 ; Nassireslami et al, 2013 ). Acute ethanol can also activate other intracellular kinases such as Akt/protein kinase B (PKB) signaling pathway (Carter et al, 2008 ; Neasta et al, 2011 ; Zeng et al, 2012 ) and glycogen synthase kinase 3 beta (GSK3β), both are multifunctional serine/threonine kinases (French and Heberlein, 2009 ; Luo, 2009 ; Zeng et al, 2012 ; Shah et al, 2015 ), required for synaptic plasticity (Horwood et al, 2006 ; Ochs et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

Acute Ethanol Inhibition of γ Oscillations Is Mediated by Akt and GSK3β

Wang

Zhao

Liu

et al. 2016

Front. Cell. Neurosci.

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Hippocampal network oscillations at gamma band frequency (γ, 30–80 Hz) are closely associated with higher brain functions such as learning and memory. Acute ethanol exposure at intoxicating concentrations (≥50 mM) impairs cognitive function. This study aimed to determine the effects and the mechanisms of acute ethanol exposure on γ oscillations in an in vitro model. Ethanol (25–100 mM) suppressed kainate-induced γ oscillations in CA3 area of the rat hippocampal slices, in a concentration-dependent, reversible manner. The ethanol-induced suppression was reduced by the D1R antagonist SCH23390 or the PKA inhibitor H89, was prevented by the Akt inhibitor triciribine or the GSk3β inhibitor SB415286, was enhanced by the NMDA receptor antagonist D-AP5, but was not affected by the MAPK inhibitor U0126 or PI3K inhibitor wortmanin. Our results indicate that the intracellular kinases Akt and GSk3β play a critical role in the ethanol-induced suppression of γ oscillations and reveal new cellular pathways involved in the ethanol-induced cognitive impairment.

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“…Some studies have reported that the cAMP/PKA/CREB signaling pathway critically contributes to the neuronal synaptic plasticity in the processes of pain and memory [15, 27, 38]. Being a crucial second messenger, cAMP is involved in varies types of learning and memory processes and long-term synaptic plasticity [17, 39]. Years ago, it was found that increased levels of cAMP in sensory neurons indeed lead to a transient enhancement of transmitter release in the synaptic connection between sensory and motor neurons, which was regarded as a biochemical mechanism for short-term and long-term changes [13, 40].…”

Section: Discussionmentioning

confidence: 99%

“…The inhibition of PKA activity reduces the phosphorylation of CREB [26, 45]. Other studies have indicated that different degrees of emotional/fear memories can be abolished by PKA deficiencies and that the cAMP/PKA signaling pathway is important for memory consolidation [15, 39]. The mechanical allodynia caused by inflammation and nerve injury can be inhibited by microinjections of PKA inhibitor [19, 46].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of the cAMP/PKA/CREB Pathway Contributes to the Analgesic Effects of Electroacupuncture in the Anterior Cingulate Cortex in a Rat Pain Memory Model

et al. 2016

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Pain memory is considered as endopathic factor underlying stubborn chronic pain. Our previous study demonstrated that electroacupuncture (EA) can alleviate retrieval of pain memory. This study was designed to observe the different effects between EA and indomethacin (a kind of nonsteroid anti-inflammatory drugs, NSAIDs) in a rat pain memory model. To explore the critical role of protein kinase A (PKA) in pain memory, a PKA inhibitor was microinjected into anterior cingulate cortex (ACC) in model rats. We further investigated the roles of the cyclic adenosine monophosphate (cAMP), PKA, cAMP response element-binding protein (CREB), and cAMP/PKA/CREB pathway in pain memory to explore the potential molecular mechanism. The results showed that EA alleviates the retrieval of pain memory while indomethacin failed. Intra-ACC microinjection of a PKA inhibitor blocked the occurrence of pain memory. EA reduced the activation of cAMP, PKA, and CREB and the coexpression levels of cAMP/PKA and PKA/CREB in the ACC of pain memory model rats, but indomethacin failed. The present findings identified a critical role of PKA in ACC in retrieval of pain memory. We propose that the proper mechanism of EA on pain memory is possibly due to the partial inhibition of cAMP/PKA/CREB signaling pathway by EA.

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A cAMP analog reverses contextual and tone memory deficits induced by a PKA inhibitor in Pavlovian fear conditioning

Cited by 17 publications

References 63 publications

Behavioral assays with mouse models of Alzheimer's disease: Practical considerations and guidelines

Behavioral assays with mouse models of Alzheimer's disease: Practical considerations and guidelines

Acute Ethanol Inhibition of γ Oscillations Is Mediated by Akt and GSK3β

Inhibition of the cAMP/PKA/CREB Pathway Contributes to the Analgesic Effects of Electroacupuncture in the Anterior Cingulate Cortex in a Rat Pain Memory Model

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