Protein Kinase A Mediates the Modulation of the Slow Ca2+-Dependent K+Current,IsAHP, by the Neuropeptides CRF, VIP, and CGRP in Hippocampal Pyramidal Neurons

Haug, Trude M.; Storm, Johan F.

doi:10.1152/jn.2000.83.4.2071

Cited by 105 publications

(104 citation statements)

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“…CRF receptors are G protein-coupled, and their stimulation results in activation of adenylate cyclase and protein kinase A (28,29). It is possible that these signaling pathways link acute stress to increases in neuronal activity and A␤ levels.…”

Section: Discussionmentioning

confidence: 99%

Acute stress increases interstitial fluid amyloid-β via corticotropin-releasing factor and neuronal activity

Kang¹,

Cirrito²,

Dong³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

206

163

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Aggregation of the amyloid-␤ (A␤) peptide in the extracellular space of the brain is critical in the pathogenesis of Alzheimer's disease. A␤ is produced by neurons and released into the brain interstitial fluid (ISF), a process regulated by synaptic activity. To determine whether behavioral stressors can regulate ISF A␤ levels, we assessed the effects of chronic and acute stress paradigms in amyloid precursor protein transgenic mice. Isolation stress over 3 months increased A␤ levels by 84%. Similarly, acute restraint stress increased A␤ levels over hours. Exogenous corticotropin-releasing factor (CRF) but not corticosterone mimicked the effects of acute restraint stress. Inhibition of endogenous CRF receptors or neuronal activity blocked the effects of acute stress on A␤. Thus, behavioral stressors can rapidly increase ISF A␤ through neuronal activity in a CRF-dependent manner, and the results suggest a mechanism by which behavioral stress may affect Alzheimer's disease pathogenesis.Alzheimer's disease ͉ synaptic activity ͉ environmental stress ͉ microdialysis ͉ transgenic E vidence indicates that the aggregation and accumulation of the amyloid-␤ (A␤) peptide in the brain extracellular space is a key initiating event in the pathogenesis of Alzheimer's disease (AD) (1). A number of studies demonstrate that aggregation of A␤ is concentration-dependent (2). Increasing the amount of A␤ produced by 50% or specifically increasing the more fibrillogenic A␤ 42 either by APP gene dose or mutations in amyloid precursor protein (APP), PS1, or PS2, accelerates the onset of A␤ deposition and AD (3). Conversely, decreasing A␤ by decreasing cleavage of APP or by enhancing clearance of A␤ delays the onset of A␤ deposition (4). Thus, determining factors that regulate the levels of A␤ in the brain extracellular space, where it likely changes conformation and aggregates, may provide insight into AD pathogenesis and treatment.A␤ is produced in the brain primarily by neurons after cleavage of APP by ␤-and ␥-secretase (1). A␤ levels in the extracellular space are then influenced by factors regulating its release from neurons as well as postsecretory events such as transport and clearance. Recent evidence (5, 6) has shown that A␤ release from neurons is regulated by neuronal and specifically synaptic activity over minutes to hours. However, whether behavioral manipulations regulate synaptic activity and interstitial fluid (ISF) A␤ levels has not been addressed.Evidence in both humans and animals suggests that environmental stressors may increase risk for AD or AD pathology. In humans, persons without dementia who are prone to psychological distress are more likely to develop AD (7,8). Also, plasma levels of the stress hormone, cortisol, are correlated with the rate of dementia progression in patients with AD (9). In mouse models of AD, animals subjected to isolation stress over months had decreased learning performance and accelerated A␤ deposition (10). To explore the potential mechanisms and links between behavioral stressors and A...

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Section: Discussionmentioning

confidence: 99%

Acute stress increases interstitial fluid amyloid-β via corticotropin-releasing factor and neuronal activity

Kang¹,

Cirrito²,

Dong³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

206

163

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“…Increased cellular cAMP levels (58,59), promoting phosphorylation of cAMP-response element-binding protein transcription factor (41,60,61) is an attractive possibility, because cAMP-response element-binding protein is selectively activated in developing hippocampal neurons (62) and is involved in dendritic differentiation (63). The selective effects of CRF on proximal dendrites may be dictated by the selective distribution of CRF 1 at this age (Fig.…”

Section: Discussionmentioning

confidence: 99%

Modulation of dendritic differentiation by corticotropin-releasing factor in the developing hippocampus

Chen

Bender²,

Brunson³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

162

165

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The interplay of environmental and genetic factors in the developmental organization of the hippocampus has not been fully elucidated. The neuropeptide corticotropin-releasing factor (CRF) is released from hippocampal interneurons by environmental signals, including stress, to increase synaptic efficacy. In the early postnatal hippocampus, we have previously characterized a transient population of CRF-expressing Cajal-Retzius-like cells. Here we queried whether this stress-activated neuromodulator influences connectivity in the developing hippocampal network. Using mice deficient in the principal hippocampal CRF receptor [CRF 1(؊͞؊)] and organotypic cultures grown in the presence of synthetic CRF, or CRF receptor antagonists, we found robust effects of CRF on dendritic differentiation in hippocampal neurons. In CRF 1(؊͞؊) mice, the dendritic trees of hippocampal principal cells were exuberant, an effect that was induced in normal hippocampi in vitro by the presence of CRF 1 antagonists. In both cases, total dendritic length and dendritic branching were significantly increased. In contrast, exogenous synthetic CRF blunted the dendritic growth in hippocampal organotypic cultures. Taken together, these findings suggest that endogenous CRF, if released excessively by previous early postnatal stress, might influence neuronal connectivity and thus function of the immature hippocampus.corticotropin-releasing hormone ͉ stress ͉ corticotropin-releasing factor receptor ͉ neuropeptide ͉ Cajal-Retzius cells T he developmental organization of the hippocampal network is a complex process, requiring the interplay of genetic and environmental factors. Establishment of basic hippocampal connectivity is governed by genetically determined mechanisms, including the coordinated activation of transcription factors (1-3), and the expression of both local and more generally acting guidance molecules (4-6). Once the basic elements are in place, refinement of connectivity is achieved through environmental stimuli that influence neuronal activity (7-9). Among the elements that contribute to developmental organization of the hippocampus are the Cajal-Retzius (CR) cells (10, 11). CR cells, found in hippocampal marginal zones, release reelin, an extracellular matrix protein required for layer formation and positioning of cortical neurons (12, 13). Because lack of reelin causes perturbation of cortical lamination (14), control of neuronal positioning has been considered the major function of CR cells. However, recent results suggest additional roles for CR cells that are independent of reelin (15-18).We have previously characterized a subset of CR cells that do not express reelin but release the neuropeptide corticotropinreleasing factor (CRF).ʈ CRF functions primarily as a regulator of the neuroendocrine stress response (19,20) but is also widely expressed within the central nervous system, where it acts as a neuromodulator (21)(22)(23)(24) 5-dimethyl-N,N-dipropyl-pyrazolo[2,3-a]pyrimidin-7-amine, previously R121919} were 0.1 or 1 M (for G...

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“…In particular, the suppression of sAHP in CA1 pyramidal neurons appears to be mainly mediated by the level of the second messenger cAMP and the candidate kinase for synaptic tagging PKA (Haug and Storm, 2000;Storm, 1993, 1995). Furthermore, recent evidence suggests that CREB activity, which is known to be downstream of such inputs (Berke and Hyman, 2000), might mediate sustained changes in intrinsic excitability (Dong et al, 2006;Han et al, 2006;Lopez de Armentia et al, 2007).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…It is well known that DG granular neurons have a prominent sAHP and that this current is block by adrenergic and dopaminergic activation. Several studies have also showed that the reduction of the AHP facilitates synaptic plasticity phenomena (Cohen et al, 1999;Fuenzalida et al, 2007;Haug and Storm, 2000;Sah and Bekkers, 1996). Therefore, a reduction of the sAHP produced by β-adrenergic metabotropic receptors in granular neurons can reduce the threshold required to achieve L-LTP in glutamatergic inputs and contribute to behavioral LTP-reinforcement.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited 10 years later

Barco

Armentia

Alarcón

2008

Neuroscience & Biobehavioral Reviews

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Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited ten years later, Neuroscience and Biobehavioral Reviews (2008Reviews ( ), doi:10.1016Reviews ( /j.neubiorev.2008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.A c c e p t e d m a n u s c r i p t A c c e p t e d m a n u s c r i p tThe STC hypothesis revisited 2 Abstract A decade ago, the synaptic tagging hypothesis was proposed to explain how newly synthesized plasticity products can be specifically targeted to active synapses. A growing number of studies have validated the seminal findings that gave rise to this model, as well as contributed to unveil and expand the range of mechanisms underlying late-associativity and neuronal computation.Here, we will review what it was learnt during this past decade regarding the cellular and molecular mechanisms underlying synaptic tagging and synaptic capture. The accumulated experimental evidence has widened the theoretical framework set by the synaptic tagging and capture (STC) model and introduced concepts that were originally considered part of alternative models for explaining synapse-specific LTP. As a result, we believe that the STC model, now improved and expanded with these new ideas and concepts, still represents the most compelling hypothesis to explain late-associativity in synapse-specific plasticity processes. We will also discuss the impact of this model in our view of the integrative capability of neurons and associative learning. wordsKeywords: synaptic plasticity; LTP; associative learning; neuronal computation; synaptic tagging; synaptic capture; metaplasticity A c c e p t e d m a n u s c r i p tThe STC hypothesis revisited 3 Contents

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Protein Kinase A Mediates the Modulation of the Slow Ca²⁺-Dependent K⁺Current,I_sAHP, by the Neuropeptides CRF, VIP, and CGRP in Hippocampal Pyramidal Neurons

Cited by 105 publications

References 105 publications

Acute stress increases interstitial fluid amyloid-β via corticotropin-releasing factor and neuronal activity

Acute stress increases interstitial fluid amyloid-β via corticotropin-releasing factor and neuronal activity

Modulation of dendritic differentiation by corticotropin-releasing factor in the developing hippocampus

Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited 10 years later

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