On the participation of hippocampal p38 mitogen-activated protein kinase in extinction and reacquisition of inhibitory avoidance memory

Rossato, Janine I.; Bevilaqua, Lia R.; Lima, Ramón Hypolito; Medina, Jorge H.; Izquierdo, Iván; Cammarota, Martı́n

doi:10.1016/j.neuroscience.2006.07.025

Cited by 41 publications

(26 citation statements)

References 76 publications

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“…It is unknown if the increase in p38 MAPK observed in our studies played a role in the CCL2-induced increase in synaptic network activity. Both p38 MAPK and CREB have been shown to play a key regulatory role in synaptic transmission, synaptic plasticity and memory mechanisms (Alonso et al, 2003;Brust et al, 2006;Butler et al, 2004;Josselyn and Nguyen, 2005;Rossato et al, 2006;Wang et al, 2007). Thus, these hippocampal synaptic functions may be an important target of CCL2 in the normal brain or during conditions associated with neuroinflammation and p38 MAPK may play a central role in the effects of CCL2 on these functions.…”

Section: Discussionmentioning

confidence: 99%

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells

Cho

Gruol

2008

Journal of Neuroimmunology

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Emerging evidence indicates that chemokines can regulate both the physiology and biochemistry of CNS neurons and glia. In the current study, Western blot analysis showed that in rat hippocampal neuronal/glial cultures the signal transduction pathway activated by CCL2, a chemokine expressed in the normal brain and at elevated levels during neuroinflammation, involves a G-protein coupled receptor, p38 MAPK as well as its immediate upstream kinase MKK3/6, and the downstream transcription factor CREB. ERK 1/2 and the transcription factors STAT1 and STAT3 do not play a prominent role. CCL2 also altered Ca 2+ influx and synaptic network activity in the hippocampal neurons. These results suggest an important role for p38 MAPK and CREB in hippocampal actions of CCL2.

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Section: Discussionmentioning

confidence: 99%

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells

Cho

Gruol

2008

Journal of Neuroimmunology

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“…Pharmacological inhibition of p38 immediately after training impairs both STM and LTM formation (Alonso et al 2003). Additionally, pharmacological block of p38 in hippocampal area CA1 impairs extinction of inhibitory avoidance memory (Rossato et al 2006). p38 activation by Ras-GRF1 has been implicated in the induction of long-term depression (LTD) (for review, see Feig 2011).…”

Section: Mapk Familymentioning

confidence: 99%

The roles of protein kinases in learning and memory

2013

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In the adult mammalian brain, more than 250 protein kinases are expressed, but only a few of these kinases are currently known to enable learning and memory. Based on this information it appears that learning and memory-related kinases either impact on synaptic transmission by altering ion channel properties or ion channel density, or regulate gene expression and protein synthesis causing structural changes at existing synapses as well as synaptogenesis. Here, we review the roles of these kinases in short-term memory formation, memory consolidation, memory storage, retrieval, reconsolidation, and extinction. Specifically, we discuss the roles of calcium/calmodulin-dependent kinase II (CaMKII

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“…For example, activation of MAPKs [223], SRC tyrosine kinases [214], protein synthesis [56], NMDA receptors, and protein kinase A (PKA) [224] are necessary for the consolidation of extinction learning. Neuronal changes in activity have been observed in the CA1 and dentate gyrus regions of the hippocampus as a result of extinction training following cocaine self-administration [220].…”

Section: Role In Extinction Learningmentioning

confidence: 99%

Neuroanatomical Structures Underlying the Extinction of Drug-Seeking Behavior

Cleva¹,

Gass²

2013

TOADDJ

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This review summarizes current knowledge about the neurobiological components underlying the extinction of drug-associated memories and how they may contribute to the treatment of drug addiction. Evidence suggests that extinction learning is not the forgetting, or unlearning, of the associations between external stimuli and drug effects, but that new reinforcer expectancies are necessary for extinction of drug-seeking behavior to take place. Several theories suggest that addiction is a disorder of learning and memory, and recent evidence indicates that the brain circuits, neurotransmitters, and signal transduction mechanisms that underlie drug addiction are similar to those that mediate learning and memory processes. According to these theories, drug addiction results from repeated drug use and the formation of lasting associations between a drug's effects, withdrawal symptoms, and the environmental cues and contexts within which they are experienced. Unfortunately, standard behavioral modification techniques, such as cue exposure therapy, have shown only moderate efficacy in reducing and/or extinguishing the salience of drug-associated cues and contexts. Therefore, a greater understanding of the neurobiological mechanisms involved in the extinction of drug-related memories could provide novel therapeutic interventions for the treatment of drug addiction.

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On the participation of hippocampal p38 mitogen-activated protein kinase in extinction and reacquisition of inhibitory avoidance memory

Cited by 41 publications

References 76 publications

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells

The roles of protein kinases in learning and memory

Neuroanatomical Structures Underlying the Extinction of Drug-Seeking Behavior

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