Effects of post-training infusions of a mitogen-activated protein kinase kinase inhibitor into the hippocampus or entorhinal cortex on short- and long-term retention of inhibitory avoidance

Walz, Roger; Roesler, Rafaël; Barros, Daniela M.; Souza, Márcia María de; Rodrigues, C.; Sant’Anna, Marcia Kauer; Quevedo, Joao L De; Choi, Humberto; Neto, Waldemar Pires Ferreira; Silva, T. L. DeDavid E; Medina, Jorge H.; Izquierdo, Iván

doi:10.1097/00008877-199912000-00003

Cited by 61 publications

(41 citation statements)

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“…It is not known how U0126 impaired the retrieval of one-trial inhibitory avoidance for such a long time after administration. However, a similar effect has been reported with the MEK inhibitor PD098059, which impairs long-term memory 21 h after administration (Walz et al, 1999). The memoryenhancing effect of rolipram is only maintained for 60 min after single injection .…”

Section: Discussionsupporting

confidence: 70%

Inhibition of the Phosphodiesterase 4 (PDE4) Enzyme Reverses Memory Deficits Produced by Infusion of the MEK Inhibitor U0126 into the CA1 Subregion of the Rat Hippocampus

Zhang

Zhao

Huang

et al. 2004

Neuropsychopharmacol

134

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Cyclic AMP-specific phosphodiesterase 4 (PDE4), which is an integral component of NMDA receptor-mediated cAMP signaling, is involved in the mediation of memory processes. Given that NMDA receptors also mediate MEK/mitogen-activated protein kinase (MAPK, ERK) signaling, which is involved in synaptic plasticity, and that some PDE4 subtypes are phosphorylated and regulated by ERK, it was of interest to determine if PDE4 is involved in MEK/ERK signaling-mediated memory. It was found that rolipram, a PDE4-selective inhibitor, reversed the amnesic effect in the radial-arm maze test of the MEK inhibitor U0126 administered into the CA1 subregion of the rat hippocampus. Consistent with this, rolipram, either by peripheral administration or direct intra-CA1 infusion, enhanced the retrieval of long-term memory impaired by intra-CA1 infusion of U0126 using the step-through inhibitory avoidance test. The same dose of rolipram did not affect U0126-induced reduction of phospho-ERK1/2 levels in the CA1 subregion. However, in primary cultures of rat cerebral cortical neurons, pretreatment with U0126 increased PDE4 activity; this was correlated with the U0126-induced reduction of phospho-ERK1/2 levels. These results suggest that MEK/ERK signaling plays an inhibitory role in regulating PDE4 activity in the brain; this may be a novel mechanism by which MEK/ERK signaling mediates memory. PDE4 is likely to be an important link between the cAMP/PKA and MEK/ERK signaling pathways in the mediation of memory.

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Section: Discussionsupporting

confidence: 70%

Inhibition of the Phosphodiesterase 4 (PDE4) Enzyme Reverses Memory Deficits Produced by Infusion of the MEK Inhibitor U0126 into the CA1 Subregion of the Rat Hippocampus

Zhang

Zhao

Huang

et al. 2004

Neuropsychopharmacol

134

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“…Similarly, gustatory memory is associated with activation of ERK (56). These observations illustrate a role for ERK activation in a variety of models of memory, and this recurrent theme has recently been extended to inhibitory avoidance learning (635,636). The theme also extends across species, since ERK activation is essential for learned responses in Aplysia.…”

Section: B Erkmentioning

confidence: 68%

Long-Term Potentiation and Memory

Lynch

2004

Physiological Reviews

1,684

1,098

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Lynch, MA. Long-Term Potentiation and Memory. Physiol Rev 84: 87–136, 2004; 10.1152/physrev.00014.2003.—One of the most significant challenges in neuroscience is to identify the cellular and molecular processes that underlie learning and memory formation. The past decade has seen remarkable progress in understanding changes that accompany certain forms of acquisition and recall, particularly those forms which require activation of afferent pathways in the hippocampus. This progress can be attributed to a number of factors including well-characterized animal models, well-defined probes for analysis of cell signaling events and changes in gene transcription, and technology which has allowed gene knockout and overexpression in cells and animals. Of the several animal models used in identifying the changes which accompany plasticity in synaptic connections, long-term potentiation (LTP) has received most attention, and although it is not yet clear whether the changes that underlie maintenance of LTP also underlie memory consolidation, significant advances have been made in understanding cell signaling events that contribute to this form of synaptic plasticity. In this review, emphasis is focused on analysis of changes that occur after learning, especially spatial learning, and LTP and the value of assessing these changes in parallel is discussed. The effect of different stressors on spatial learning/memory and LTP is emphasized, and the review concludes with a brief analysis of the contribution of studies, in which transgenic animals were used, to the literature on memory/learning and LTP.

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“…Izquierdo and his colleagues have shown that bilateral infusion of PD098059 into the dorsal hippocampus 180 mins following training significantly impaired avoidance performance when tested 24 hrs later (Walz, Roesler, Barros et al, 1999). This effect was replicated again in the hippocampus (Walz et al, 2000), as well as in other brain structures such as the amygdala, entorhinal and parietal cortices at different time intervals following conditioning (Walz, Roesler, Barros, et al, 1999;Walz, Roesler, Quevedo et al, 1999;Walz, et al, 2000), suggesting differences in time-specificity of critical MAPK activation in different cortical structures. The same researchers also examined hippocampal MAPK involvement in the expression of inhibitory learning shortly after training compared to long-term memory expression.…”

Section: The Role Of Mapk In the Acquisition Of Conditioned Fearmentioning

confidence: 95%

The Role of Mitogen-Activated Protein Kinase in Treatment Strategies for Fear and Drug Addiction

Brown¹,

Lawrence²,

Kim³

2012

Advances in Protein Kinases

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Effects of post-training infusions of a mitogen-activated protein kinase kinase inhibitor into the hippocampus or entorhinal cortex on short- and long-term retention of inhibitory avoidance

Cited by 61 publications

References 0 publications

Inhibition of the Phosphodiesterase 4 (PDE4) Enzyme Reverses Memory Deficits Produced by Infusion of the MEK Inhibitor U0126 into the CA1 Subregion of the Rat Hippocampus

Inhibition of the Phosphodiesterase 4 (PDE4) Enzyme Reverses Memory Deficits Produced by Infusion of the MEK Inhibitor U0126 into the CA1 Subregion of the Rat Hippocampus

Long-Term Potentiation and Memory

The Role of Mitogen-Activated Protein Kinase in Treatment Strategies for Fear and Drug Addiction

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