The Experts below are selected from a list of 3786 Experts worldwide ranked by ideXlab platform
Joseph E. Ledoux - One of the best experts on this subject based on the ideXlab platform.
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Afferent specific regulation of cortical and subcortical synaptic input to the Lateral Amygdala by norepinephrine
2020Co-Authors: Luke R. Johnson, Joseph E. LedouxAbstract:The Lateral Amygdala (LA) has been extensively implicated in the neurobiology of conditioned fear paradigms. Norepinepherine (NE), especially its beta receptors, has been implicated in consolidation, reconsolidation and extinction of fear memories, and has been proposed as a potential treatment for PTSD (Berlau and McGaugh, NLM, 2006; Debiec and LeDoux, N, 2005)...
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Polysynaptic potentials within the Lateral Amygdala networks as indicators of reverberatory activity
2020Co-Authors: V. Doye Re, Luke R. Johnson, M. Nguyen, Hannah H. Alphs, Joseph E. LedouxAbstract:Synaptic plasticity in the Lateral Amygdala (LA) may underlie auditory fear conditioning. Hebb postulated that sustained activity in reverberating cellular ensembles can facilitate temporal coincidence detection. Our anatomical data show that LA neurons have extensive local axon colLaterals that are topographically organized and that could provide the anatomical basis for reverberatory activity...
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Propagating excitatory potentials within the fear conditioning circuit of the Lateral Amygdala
2020Co-Authors: Luke R. Johnson, Valerie Doyere, Hannah H. Alphs, Joseph E. LedouxAbstract:In the Hebbian postulate, transiently reverberating cellular ensembles can sustain activity to facilitate temporal coincidence detection. Auditory fear conditioning is believed to be formed in the Lateral Amygdala (LA), by way of plasticity at auditory input synapses on principal neurons. To evaluate the contribution of LA cellular ensembles in the formation of conditioned fear memories, we investigated the LA micro-circuitry by electrophysiological and anatomical approaches. Polysynaptic field potentials evoked in the LA by stimulation of auditory thalamus(MGm/PIN) or auditory cortical (TE3) afferents were analyzed in vitro and in vivo. In vivo, two potentials were identified following stimulation of either pathway. In vitro, these multiple potentials were revealed by adding 75uM Picrotoxin or 30uM Bicuculine, with the first potential peaking at 15-20 ms, followed by two additional potentials at 20 – 25 and 30 – 35 ms, respectively. These data show single stimulation events can result in multiple synchronized excitatory events within the Lateral Amygdala. In order to determine underlying mechanisms of auditory signal propagation, LA principal neuron axon colLateral trajectory patterns and morphology were analyzed. Neurons were found to have local axon colLaterals that are topographically organized. Each axon colLateral within the LA totaled 14.1 ± 2.73mm, had 29.8 ± 9.1 branch points and 1870.8 ± 1035 boutons (n=9). Electrophysiological and anatomical data show that a network of extensive axon colLaterals within the LA may facilitate preservation of auditory afferent signals.
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A recurrent network in the Lateral Amygdala: A mechanism for temporal coincidence detection
2020Co-Authors: Luke R. Johnson, Joseph E. Ledoux, Hannah H. Alphs, Adrián Ponce-alvarez, Leo M. Gribelyuk, Ladislau Albert, Bruce L. Brown, Valerie DoyereAbstract:Synaptic changes at sensory inputs to the dorsal nucleus of the Lateral Amygdala (LAd) play a key role in the acquisition and storage of associative fear memory. However, neither the temporal nor spatial architecture of the LAd network response to sensory signals is understood. We developed a method for the elucidation of network behavior. Using this approach, temporally patterned polysynaptic recurrent network responses were found in LAd (intra-LA), both in vitro and in vivo, in response to activation of thalamic sensory afferents. Potentiation of thalamic afferents resulted in a depression of intra-LA synaptic activity, indicating a homeostatic response to changes in synaptic strength within the LAd network. Additionally, the latencies of thalamic afferent triggered recurrent network activity within the LAd overlap with known later occurring cortical afferent latencies. Thus, this recurrent network may facilitate temporal coincidence of sensory afferents within LAd during associative learning.
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sensory specific associations stored in the Lateral Amygdala allow for selective alteration of fear memories
The Journal of Neuroscience, 2011Co-Authors: Lorenzo Diazmataix, Joseph E. Ledoux, Valerie Doyere, Jacek DebiecAbstract:Consolidated long-term fear memories become labile and can be disrupted after being reactivated by the presentation of the unconditioned stimulus (US). Whether this is due to an alteration of the conditioned stimulus (CS) representation in the Lateral Amygdala (LA) is not known. Here, we show in rats that fear memory reactivation through presentation of the aversive US, like CS presentation, triggers a process which, when disrupted, results in a selective depotentiation of CS-evoked neural responses in the LA in correlation with a selective suppression of CS-elicited fear memory. Thus, an aversive US triggers the reconsolidation of its associated predictor representation in LA. This new finding suggests that sensory-specific associations are stored in the Lateral Amygdala, allowing for their selective alteration by either element of the association.
Jane R. Taylor - One of the best experts on this subject based on the ideXlab platform.
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the striatal enriched protein tyrosine phosphatase gates long term potentiation and fear memory in the Lateral Amygdala
Biological Psychiatry, 2007Co-Authors: Surojit Paul, Irina Ruchkina, Natalie Tronson, Shawn Hakim, Michael W. Salter, Peter Olausson, Evan Mills, Deepa V Venkitaramani, Timothy Moran, Jane R. TaylorAbstract:Background Formation of long-term memories is critically dependent on extracellular-regulated kinase (ERK) signaling. Activation of the ERK pathway by the sequential recruitment of mitogen-activated protein kinases is well understood. In contrast, the proteins that inactivate this pathway are not as well characterized. Methods Here we tested the hypothesis that the brain-specific striatal-enriched protein tyrosine phosphatase (STEP) plays a key role in neuroplasticity and fear memory formation by its ability to regulate ERK1/2 activation. Results STEP co-localizes with the ERKs within neurons of the Lateral Amygdala. A substrate-trapping STEP protein binds to the ERKs and prevents their nuclear translocation after glutamate stimulation in primary cell cultures. Administration of TAT-STEP into the Lateral Amygdala (LA) disrupts long-term potentiation (LTP) and selectively disrupts fear memory consolidation. Fear conditioning induces a biphasic activation of ERK1/2 in the LA with an initial activation within 5 minutes of training, a return to baseline levels by 15 minutes, and an increase again at 1 hour. In addition, fear conditioning results in the de novo translation of STEP. Inhibitors of ERK1/2 activation or of protein translation block the synthesis of STEP within the LA after fear conditioning. Conclusions Together, these data imply a role for STEP in experience-dependent plasticity and suggest that STEP modulates the activation of ERK1/2 during Amygdala-dependent memory formation. The regulation of emotional memory by modulating STEP activity may represent a target for the treatment of psychiatric disorders such as posttraumatic stress disorder (PTSD), panic, and anxiety disorders.
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The Striatal-Enriched Protein Tyrosine Phosphatase Gates Long-Term Potentiation and Fear Memory in the Lateral Amygdala
Biological Psychiatry, 2007Co-Authors: Surojit Paul, Irina Ruchkina, Timothy D. Moran, Natalie Tronson, Shawn Hakim, Michael W. Salter, Peter Olausson, Evan Mills, Deepa V Venkitaramani, Jane R. TaylorAbstract:Background: Formation of long-term memories is critically dependent on extracellular-regulated kinase (ERK) signaling. Activation of the ERK pathway by the sequential recruitment of mitogen-activated protein kinases is well understood. In contrast, the proteins that inactivate this pathway are not as well characterized. Methods: Here we tested the hypothesis that the brain-specific striatal-enriched protein tyrosine phosphatase (STEP) plays a key role in neuroplasticity and fear memory formation by its ability to regulate ERK1/2 activation. Results: STEP co-localizes with the ERKs within neurons of the Lateral Amygdala. A substrate-trapping STEP protein binds to the ERKs and prevents their nuclear translocation after glutamate stimulation in primary cell cultures. Administration of TAT-STEP into the Lateral Amygdala (LA) disrupts long-term potentiation (LTP) and selectively disrupts fear memory consolidation. Fear conditioning induces a biphasic activation of ERK1/2 in the LA with an initial activation within 5 minutes of training, a return to baseline levels by 15 minutes, and an increase again at 1 hour. In addition, fear conditioning results in the de novo translation of STEP. Inhibitors of ERK1/2 activation or of protein translation block the synthesis of STEP within the LA after fear conditioning. Conclusions: Together, these data imply a role for STEP in experience-dependent plasticity and suggest that STEP modulates the activation of ERK1/2 during Amygdala-dependent memory formation. The regulation of emotional memory by modulating STEP activity may represent a target for the treatment of psychiatric disorders such as posttraumatic stress disorder (PTSD), panic, and anxiety disorders. © 2007 Society of Biological Psychiatry.
Hanschristian Pape - One of the best experts on this subject based on the ideXlab platform.
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interictal like network activity and receptor expression in the epileptic human Lateral Amygdala
Brain, 2011Co-Authors: Stephanie Graebenitz, Olga Kedo, Erwin-josef Speckmann, Ali Gorji, Heinz Panneck, Volkmar Hans, Axel Schleicher, Karl Zilles, Nicola Palomerogallagher, Hanschristian PapeAbstract:While the Amygdala is considered to play a critical role in temporal lobe epilepsy, conclusions on underlying pathophysiological mechanisms have been derived largely from experimental animal studies. Therefore, the present study aimed to characterize synaptic network interactions, focusing on spontaneous interictal-like activity, and the expression profile of transmitter receptors in the human Lateral Amygdala in relation to temporal lobe epilepsy. Electrophysiological recordings, obtained intra-operatively in vivo in patients with medically intractable temporal lobe epilepsy, revealed the existence of interictal activity in Amygdala and hippocampus. For in vitro analyses, slices were prepared from surgically resected specimens, and sections from individual specimens were used for electrophysiological recordings, receptor autoradiographic analyses and histological visualization of major amygdaloid nuclei for verification of recording sites. In the Lateral Amygdala, interictal-like activity appeared as spontaneous slow rhythmic field potentials at an average frequency of 0.39Hz, which occurred at different sites with various degrees of synchronization in 33.3% of the tested slices. Pharmacological blockade of glutamate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, but not N -methyl-d-aspartate receptors, abolished interictal-like activity, while the γ-aminobutyric acid A-type receptor antagonist bicuculline resulted in a dampening of activity, followed by highly synchronous patterns of slow rhythmic activity during washout. Receptor autoradiographic analysis revealed significantly higher α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, kainate, metabotropic glutamate type 2/3, muscarinic type 2 and adrenoceptor α1 densities, whereas muscarinergic type 3 and serotonergic type 1A receptor densities were lower in the Lateral Amygdala from epileptic patients in comparison to autopsy controls. Concerning γ-aminobutyric acid A-type receptors, agonist binding was unaltered whereas antagonist binding sites were downregulated in the epileptic Lateral Amygdala, suggesting an altered high/low-affinity state ratio and concomitant reduced pool of total γ-aminobutyric acid A-type receptors. Together these data indicate an abnormal pattern of receptor densities and synaptic function in the Lateral nucleus of the Amygdala in epileptic patients, involving critical alterations in glutamate and γ-aminobutyric acid receptors, which may give rise to domains of spontaneous interictal discharges contributing to seizure activity in the Amygdala. * Abbreviations : AMPA : α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid APV : DL-2-amino-5-phosphono-valerate CNQX : 6-cyano-7-nitro-quinoxaline-2,3-dione CSF : cerebrospinal fluid EEG : electroencephalogram GABA : aminobutyric acid MRI : magnetic resonance imaging NMDA : N -methyl-d-aspartate ns : not significant
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Interictal-like network activity and receptor expression in the epileptic human Lateral Amygdala.
Brain : a journal of neurology, 2011Co-Authors: Stephanie Graebenitz, Olga Kedo, Erwin-josef Speckmann, Ali Gorji, Heinz Panneck, Volkmar Hans, Nicola Palomero-gallagher, Axel Schleicher, Karl Zilles, Hanschristian PapeAbstract:While the Amygdala is considered to play a critical role in temporal lobe epilepsy, conclusions on underlying pathophysiological mechanisms have been derived largely from experimental animal studies. Therefore, the present study aimed to characterize synaptic network interactions, focusing on spontaneous interictal-like activity, and the expression profile of transmitter receptors in the human Lateral Amygdala in relation to temporal lobe epilepsy. Electrophysiological recordings, obtained intra-operatively in vivo in patients with medically intractable temporal lobe epilepsy, revealed the existence of interictal activity in Amygdala and hippocampus. For in vitro analyses, slices were prepared from surgically resected specimens, and sections from individual specimens were used for electrophysiological recordings, receptor autoradiographic analyses and histological visualization of major amygdaloid nuclei for verification of recording sites. In the Lateral Amygdala, interictal-like activity appeared as spontaneous slow rhythmic field potentials at an average frequency of 0.39 Hz, which occurred at different sites with various degrees of synchronization in 33.3% of the tested slices. Pharmacological blockade of glutamate α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, but not N-methyl-D-aspartate receptors, abolished interictal-like activity, while the γ-aminobutyric acid A-type receptor antagonist bicuculline resulted in a dampening of activity, followed by highly synchronous patterns of slow rhythmic activity during washout. Receptor autoradiographic analysis revealed significantly higher α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, kainate, metabotropic glutamate type 2/3, muscarinic type 2 and adrenoceptor α(1) densities, whereas muscarinergic type 3 and serotonergic type 1A receptor densities were lower in the Lateral Amygdala from epileptic patients in comparison to autopsy controls. Concerning γ-aminobutyric acid A-type receptors, agonist binding was unaltered whereas antagonist binding sites were downregulated in the epileptic Lateral Amygdala, suggesting an altered high/low-affinity state ratio and concomitant reduced pool of total γ-aminobutyric acid A-type receptors. Together these data indicate an abnormal pattern of receptor densities and synaptic function in the Lateral nucleus of the Amygdala in epileptic patients, involving critical alterations in glutamate and γ-aminobutyric acid receptors, which may give rise to domains of spontaneous interictal discharges contributing to seizure activity in the Amygdala.
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gabaergic interneurons in the mouse Lateral Amygdala a classification study
Journal of Neurophysiology, 2010Co-Authors: Ludmila Sosulina, Stephanie Graebenitz, Hanschristian PapeAbstract:Whole cell patch-clamp recordings were performed in GABAergic interneurons labeled by green fluorescent protein (GFP) in the Lateral Amygdala (LA) in vitro from glutamic acid decarboxylase 67 (GAD6...
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Cortical spreading depression modulates synaptic transmission of the rat Lateral Amygdala
European Journal of Neuroscience, 2008Co-Authors: Shahab Dehbandi, Hanschristian Pape, Erwin-josef Speckmann, Ali GorjiAbstract:Clinical and pathophysiological evidence connects migraine and the Amygdala. Cortical spreading depression (CSD) plays a causative role in the generation of aura symptoms. However, the role of CSD in the pathophysiology of other symptoms of migraine needs to be investigated. An in vitro brain slice technique was used to investigate CSD effects on tetanus-induced long-term potentiation (LTP) in the Lateral Amygdala (LA) of the combined rat Amygdala-hippocampus-cortex slices. More than 75% of CSD induced in temporal cortex propagated to LA. Induction of CSD in combined Amygdala-hippocampus-cortex slices in which CSD propagated from neocortex to LA significantly augmented LTP in LA. LTP was inhibited when CSD travelled only in the neocortical tissues. Separation of the Amygdala from the remaining neocortical part of the slice, in which CSD propagation was limited to the neocortex, increased LTP close to the control levels. Pharmacological manipulations of the slices, in which CSD reached LA, revealed the involvement of NMDA and AMPA glutamate subreceptors as well as dopamine D2 receptors in the enhancement of LTP in LA. However, neither blocking of GABA receptors nor activation of dopamine D1 receptors affected LTP in these slices. The results indicate the disturbances of LA synaptic transmission triggered by propagation of CSD. This perturbation of LA synaptic transmission induced by CSD may relate to some symptoms occurring during migraine attacks.
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Classification of projection neurons and interneurons in the rat Lateral Amygdala based upon cluster analysis.
Molecular and Cellular Neuroscience, 2006Co-Authors: Ludmila Sosulina, Susanne Meis, Gerald Seifert, Christian Steinhäuser, Hanschristian PapeAbstract:Neurons in the rat Lateral Amygdala in situ were classified based upon electrophysiological and molecular parameters, as studied by patch-clamp, single-cell RT-PCR and unsupervised cluster analyses. Projection neurons (class I) were characterized by low firing rates, frequency adaptation and expression of the vesicular glutamate transporter (VGLUT1). Two classes were distinguished based upon electrotonic properties and the presence (IB) or absence (IA) of vasointestinal peptide (VIP). Four classes of glutamate decarboxylase (GAD67) containing interneurons were encountered. Class III reflected "classical" interneurons, generating fast spikes with no frequency adaptation. Class II neurons generated fast spikes with early frequency adaptation and differed from class III by the presence of VIP and the relatively rare presence of neuropeptide Y (NPY) and somatostatin (SOM). Class IV and V were not clearly separated by molecular markers, but by membrane potential values and spike patterns. Morphologically, projection neurons were large, spiny cells, whereas the other neuronal classes displayed smaller somata and spine-sparse dendrites.
Karl Deisseroth - One of the best experts on this subject based on the ideXlab platform.
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the central Amygdala controls learning in the Lateral Amygdala
Nature Neuroscience, 2017Co-Authors: Kai Yu, Sandra Ahrens, Xian Zhang, Hillary Schiff, Charu Ramakrishnan, Lief E Fenno, Karl DeisserothAbstract:Experience-driven synaptic plasticity in the Lateral Amygdala is thought to underlie the formation of associations between sensory stimuli and an ensuing threat. However, how the central Amygdala participates in such a learning process remains unclear. Here we show that PKC-δ-expressing central Amygdala neurons are essential for the synaptic plasticity underlying learning in the Lateral Amygdala, as they convey information about the unconditioned stimulus to Lateral Amygdala neurons during fear conditioning.
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the central Amygdala controls learning in the Lateral Amygdala
bioRxiv, 2017Co-Authors: Kai Yu, Sandra Ahrens, Xian Zhang, Hillary Schiff, Charu Ramakrishnan, Lief E Fenno, Karl Deisseroth, Pengcheng Zhou, Liam Paninski, Bo LiAbstract:Both the Lateral and the central nuclei of the Amygdala are required for adaptive behavioral responses to environmental cues predicting threats. While experience-driven synaptic plasticity in the Lateral Amygdala is thought to underlie the formation of association between a sensory stimulus and an ensuing threat, how the central Amygdala participates in such learning process remains unclear. Here we show that a specific class of central Amygdala neurons, the protein kinase C-δ-expressing neurons, is essential for the synaptic plasticity underlying learning in the Lateral Amygdala, as it is required for Lateral Amygdala neurons to respond to unconditioned stimulus, and furthermore carries information about the unconditioned stimulus to instruct learning. Our results uncover an Amygdala functional organization that may play a key role in diverse learning processes.
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optical activation of Lateral Amygdala pyramidal cells instructs associative fear learning
Proceedings of the National Academy of Sciences of the United States of America, 2010Co-Authors: Joshua P Johansen, Joseph E. Ledoux, Karl Deisseroth, Marie H Monfils, Hiroki Hamanaka, Rudy Behnia, Hugh T BlairAbstract:Humans and animals can learn that specific sensory cues in the environment predict aversive events through a form of associative learning termed fear conditioning. This learning occurs when the sensory cues are paired with an aversive event occuring in close temporal proximity. Activation of Lateral Amygdala (LA) pyramidal neurons by aversive stimuli is thought to drive the formation of these associative fear memories; yet, there have been no direct tests of this hypothesis. Here we demonstrate that viral-targeted, tissue-specific expression of the light-activated channelrhodopsin (ChR2) in LA pyramidal cells permitted optical control of LA neuronal activity. Using this approach we then paired an auditory sensory cue with optical stimulation of LA pyramidal neurons instead of an aversive stimulus. Subsequently presentation of the tone alone produced behavioral fear responses. These results demonstrate in vivo optogenetic control of LA neurons and provide compelling support for the idea that fear learning is instructed by aversive stimulus-induced activation of LA pyramidal cells.
Valerie Doyere - One of the best experts on this subject based on the ideXlab platform.
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Propagating excitatory potentials within the fear conditioning circuit of the Lateral Amygdala
2020Co-Authors: Luke R. Johnson, Valerie Doyere, Hannah H. Alphs, Joseph E. LedouxAbstract:In the Hebbian postulate, transiently reverberating cellular ensembles can sustain activity to facilitate temporal coincidence detection. Auditory fear conditioning is believed to be formed in the Lateral Amygdala (LA), by way of plasticity at auditory input synapses on principal neurons. To evaluate the contribution of LA cellular ensembles in the formation of conditioned fear memories, we investigated the LA micro-circuitry by electrophysiological and anatomical approaches. Polysynaptic field potentials evoked in the LA by stimulation of auditory thalamus(MGm/PIN) or auditory cortical (TE3) afferents were analyzed in vitro and in vivo. In vivo, two potentials were identified following stimulation of either pathway. In vitro, these multiple potentials were revealed by adding 75uM Picrotoxin or 30uM Bicuculine, with the first potential peaking at 15-20 ms, followed by two additional potentials at 20 – 25 and 30 – 35 ms, respectively. These data show single stimulation events can result in multiple synchronized excitatory events within the Lateral Amygdala. In order to determine underlying mechanisms of auditory signal propagation, LA principal neuron axon colLateral trajectory patterns and morphology were analyzed. Neurons were found to have local axon colLaterals that are topographically organized. Each axon colLateral within the LA totaled 14.1 ± 2.73mm, had 29.8 ± 9.1 branch points and 1870.8 ± 1035 boutons (n=9). Electrophysiological and anatomical data show that a network of extensive axon colLaterals within the LA may facilitate preservation of auditory afferent signals.
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A recurrent network in the Lateral Amygdala: A mechanism for temporal coincidence detection
2020Co-Authors: Luke R. Johnson, Joseph E. Ledoux, Hannah H. Alphs, Adrián Ponce-alvarez, Leo M. Gribelyuk, Ladislau Albert, Bruce L. Brown, Valerie DoyereAbstract:Synaptic changes at sensory inputs to the dorsal nucleus of the Lateral Amygdala (LAd) play a key role in the acquisition and storage of associative fear memory. However, neither the temporal nor spatial architecture of the LAd network response to sensory signals is understood. We developed a method for the elucidation of network behavior. Using this approach, temporally patterned polysynaptic recurrent network responses were found in LAd (intra-LA), both in vitro and in vivo, in response to activation of thalamic sensory afferents. Potentiation of thalamic afferents resulted in a depression of intra-LA synaptic activity, indicating a homeostatic response to changes in synaptic strength within the LAd network. Additionally, the latencies of thalamic afferent triggered recurrent network activity within the LAd overlap with known later occurring cortical afferent latencies. Thus, this recurrent network may facilitate temporal coincidence of sensory afferents within LAd during associative learning.
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sensory specific associations stored in the Lateral Amygdala allow for selective alteration of fear memories
The Journal of Neuroscience, 2011Co-Authors: Lorenzo Diazmataix, Joseph E. Ledoux, Valerie Doyere, Jacek DebiecAbstract:Consolidated long-term fear memories become labile and can be disrupted after being reactivated by the presentation of the unconditioned stimulus (US). Whether this is due to an alteration of the conditioned stimulus (CS) representation in the Lateral Amygdala (LA) is not known. Here, we show in rats that fear memory reactivation through presentation of the aversive US, like CS presentation, triggers a process which, when disrupted, results in a selective depotentiation of CS-evoked neural responses in the LA in correlation with a selective suppression of CS-elicited fear memory. Thus, an aversive US triggers the reconsolidation of its associated predictor representation in LA. This new finding suggests that sensory-specific associations are stored in the Lateral Amygdala, allowing for their selective alteration by either element of the association.
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A recurrent network in the Lateral Amygdala: a mechanism for coincidence detection.
Frontiers in Neural Circuits, 2008Co-Authors: Luke R. Johnson, Joseph E. Ledoux, Hannah H. Alphs, Adrián Ponce-alvarez, Leo M. Gribelyuk, Ladislau Albert, Bruce L. Brown, Valerie DoyereAbstract:Synaptic changes at sensory inputs to the dorsal nucleus of the Lateral Amygdala (LAd) play a key role in the acquisition and storage of associative fear memory. However, neither the temporal nor spatial architecture of the LAd network response to sensory signals is understood. We developed a method for the elucidation of network behavior. Using this approach, temporally patterned polysynaptic recurrent network responses were found in LAd (intra-LA), both in vitro and in vivo, in response to activation of thalamic sensory afferents. Potentiation of thalamic afferents resulted in a depression of intra-LA synaptic activity, indicating a homeostatic response to changes in synaptic strength within the LAd network. Additionally, the latencies of thalamic afferent triggered recurrent network activity within the LAd overlap with known later occurring cortical afferent latencies. Thus, this recurrent network may facilitate temporal coincidence of sensory afferents within LAd during associative learning.
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synapse specific reconsolidation of distinct fear memories in the Lateral Amygdala
Nature Neuroscience, 2007Co-Authors: Jacek Debiec, Valerie Doyere, Marie H Monfils, Glenn E Schafe, Joseph E. LedouxAbstract:When reactivated, memories enter a labile, protein synthesis–dependent state, a process referred to as reconsolidation. Here, we show in rats that fear memory retrieval produces a synaptic potentiation in the Lateral Amygdala that is selective to the reactivated memory, and that disruption of reconsolidation is correlated with a reduction of synaptic potentiation in the Lateral Amygdala. Thus, both retrieval and reconsolidation alter memories via synaptic plasticity at selectively targeted synapses.
