Fear memory and the amygdala: insights from a molecular perspective

Stork, Oliver; Pape, Hans‐Christian

doi:10.1007/s00441-002-0656-2

Cited by 20 publications

(13 citation statements)

References 86 publications

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“…In fact, several conserved regulatory amino acid motifs indicate that the Ndr2 protein is a site of convergence for Ca 2ϩ /S100, protein kinase A, and mitogen-activated protein kinase signaling pathways, all of which are involved in neurite outgrowth in PC12 cells (22)(23)(24)(25), as well as amygdalar processes during fear memory consolidation (reviewed in Ref. 4).…”

Section: Discussionmentioning

confidence: 99%

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Neuronal Functions of the Novel Serine/Threonine Kinase Ndr2

Stork

Zhdanov

Kudersky

et al. 2004

Journal of Biological Chemistry

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We have identified a novel member of the Ndr subfamily of serine/threonine protein kinases, Ndr2, as a gene product that is induced in the mouse amygdala during fear memory consolidation and examined a possible function of this kinase in neural differentiation. Expression of Ndr2 mRNA was detected in various cortical and subcortical brain regions, as well as non-neuronal tissues. Its expression in the amygdala was increased 6 h after Pavlovian fear conditioning training and returned to control levels within 24 h. To study intracellular localization and functions of Ndr2, EGFP::Ndr2 fusion proteins were expressed in rat pheochromocytoma (PC12) cells and acutely isolated cortical neurons, thereby revealing an association of Ndr2 with the actin cytoskeleton in somata, neurites and filopodia, in spines and at sites of cell contact. Co-precipitation and pulldown experiments support this finding. Evidence for an involvement of Ndr2 in actin-mediated cellular functions further comes from the observation of decreased cell spreading and changes in neurite outgrowth that were associated with protein serine phosphorylation in transfected PC12 cells. Together, our data suggest that Ndr2 is an interesting candidate gene for the regulation of structural processes in differentiating and mature neuronal cells.Stimulus-dependent modifications of cell structure and connectivity in the central nervous system are basic elements of long term memory formation. Protein kinases and protein phosphatases are key regulators of these processes, which they control and co-ordinate through the phosphorylation and/or dephosphorylation of neurotransmitter receptors and ion channels, cytoskeleton elements, cell surface molecules, and transcription factors (1).We have employed a classic fear conditioning paradigm to isolate candidate genes involved in memory-related functions in the brain (2). Fear conditioning is highly amenable to cellular and molecular approaches to learning and memory, because conditioned subjects (a) very quickly learn to associate a previously neutral sensory stimulus (conditional stimulus) and an aversive, unconditional stimulus during fear conditioning training and (b) develop a robust and easily measurable long term memory after a single training session. Moreover, the neuronal circuits and cellular mechanisms that underlie classic fear conditioning have been investigated in detail (reviewed in Ref.3). These conceptual and technical advantages have allowed researchers to show that, among other factors, protein kinase A, mitogen-activated protein kinase and calcium/calmodulin-dependent kinases are critical for fear conditioning (summarized in Ref. 4). Some of these protein kinase activities could even be tracked down to the amygdala (5-7). Recent evidence further suggests an involvement of Rho-mediated signaling pathways and the Rho-associated kinase (p160 ROCK ) in amygdala plasticity after fear conditioning (8). This pathway may be of particular importance, because it controls actinmediated changes in dendrite and spine...

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Section: Discussionmentioning

confidence: 99%

“…These conceptual and technical advantages have allowed researchers to show that, among other factors, protein kinase A, mitogen-activated protein kinase and calcium/calmodulin-dependent kinases are critical for fear conditioning (summarized in Ref. 4). Some of these protein kinase activities could even be tracked down to the amygdala (5-7).…”

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confidence: 99%

Neuronal Functions of the Novel Serine/Threonine Kinase Ndr2

Stork

Zhdanov

Kudersky

et al. 2004

Journal of Biological Chemistry

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“…41 Notably, deterioration of the amygdala can explain both mildly fearful expression recognition deficit and precocious memory impairment in a-MCI patients, because of its projections to prefrontal cortex and hippocampal complex, forming the neural network for emotional memory. 42,43 Indeed, the role of amygdala is also well established in consolidation of memory of fearful cues, 44 and is suggested by studies supporting the cholinergic model in AD. 45 In this context, it is of interest that amygdala receives a major cholinergic projection from the nucleus basalis of Meynert.…”

Section: Discussionmentioning

confidence: 99%

Facial Emotion Recognition Deficit in Amnestic Mild Cognitive Impairment and Alzheimer Disease

Spoletini

Marra

Iulio

et al. 2008

The American Journal of Geriatric Psychiatry

126

139

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“…Similar training procedures can be used in laboratory animals and human volunteers and current data suggest a large degree of similarity in neural mechanisms across species. A number of excellent recent reviews are available providing more detailed treatment of various aspects of the anatomy, physiology, and molecular biology of FC than space here permits (e.g., Blair, et al, 2001;Davis, 2000;Fanselow & Poulos, 2005;Goosens & Maren, 2002;Kim & Jung, 2006;Maren 2000;Medina, et al, 2002;Pare, Quirk & LeDoux, 2004;Stork & Pape, 2002).…”

Section: Introductionmentioning

confidence: 99%

Macromolecular synthesis, distributed synaptic plasticity, and fear conditioning

Helmstetter

Parsons

Gafford

2008

Neurobiology of Learning and Memory

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Recent work from a number of laboratories has provided new and important insights about how gene expression is altered by experience and how these molecular changes may provide a substrate for the long-term storage of new memories. Here we review a series of recent studies using aversive Pavlovian conditioning in rats as a well characterized model system in which experience-dependent alterations in gene expression can be manipulated and quantified within a specific neural circuit. We highlight some of the issues involved in using broad-spectrum inhibitors of mRNA and protein synthesis to study cellular changes underlying the formation and long-term stability of memory and discuss the idea that these changes occur over widespread, behaviorally-defined, networks of cells. We also discuss the idea that the maintenance of memory and its susceptibly to disruption after retrieval may relate to local protein synthesis in dendrites. Finally, a series of recent experiments from our laboratory studying the role of a specific signaling pathway (mTOR) which regulates translational processes and memory formation in the amygdala and hippocampus during fear conditioning are reviewed.

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Fear memory and the amygdala: insights from a molecular perspective

Cited by 20 publications

References 86 publications

Neuronal Functions of the Novel Serine/Threonine Kinase Ndr2

Neuronal Functions of the Novel Serine/Threonine Kinase Ndr2

Facial Emotion Recognition Deficit in Amnestic Mild Cognitive Impairment and Alzheimer Disease

Macromolecular synthesis, distributed synaptic plasticity, and fear conditioning

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