Fear memories induce a switch in stimulus response and signaling mechanisms for long-term potentiation in the lateral amygdala

2004 ◽  
Vol 20 (2) ◽  
pp. 549-556 ◽  
Author(s):  
Bradley W. Schroeder ◽  
Patricia Shinnick-Gallagher
Keyword(s):  
Long Term Potentiation ◽  
Lateral Amygdala ◽  
Stimulus Response ◽  
Signaling Mechanisms ◽  
Term Potentiation

scholarly journals Knockdown of MicroRNA-1 in the Hippocampus Ameliorates Myocardial Infarction Induced Impairment of Long-Term Potentiation

2018 ◽  
Vol 50 (4) ◽  
pp. 1601-1616 ◽  
Author(s):  
Ji-Chao Ma ◽  
Ming-Jing Duan ◽  
Ke-Xin Li ◽  
Das Biddyut ◽  
Shuai Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sham Group ◽  
Long Term Potentiation ◽  
Stimulus Response ◽  
Protein Levels ◽  
Term Potentiation ◽  
Passive And Active Avoidance ◽  
Related Proteins

Backgrounds/Aims: It has been reported that myocardial infarction (MI) is a risk factor for vascular dementia. However, the molecular mechanism remains largely unknown. Methods: MI mice were generated by ligation of the left coronary artery (LCA) for 4 weeks. Passive and active avoidance tests were performed to evaluate the cognitive ability of MI mice. A theta-burst stimulation (TBS) protocol was applied to elicit long-term potentiation (LTP) of the perforant pathway-dentate gyrus synapse (PP-DG). Western blot analysis was employed to assess protein levels. Results: In this study, we demonstrated that after 4 weeks of MI, C57BL/6 mice had significantly impaired memory. Compared with the sham group, in vivo physiological recording in the MI group revealed significantly decreased amplitude of population spikes (PS) with no effect on the latency and duration of the stimulus-response curve. The amplitude of LTP was markedly decreased in the MI group compared with the sham group. Further examination showed that the expression of the TBS-LTP-related proteins BDNF, GluA1 and phosphorylated GluA1 were all decreased in the MI group compared with those in the sham group. Strikingly, all these changes were prevented by hippocampal stereotaxic injection of an anti-miR-1 oligonucleotide fragment carried by a lentivirus vector (lenti-pre-AMO-1). Conclusion: MI induced cognitive decline and TBS-LTP impairment, and decreased BDNF and GluA1 phosphorylation levels from overexpression of miR-1ated were involved in this process.

scholarly journals Antagonism of lateral amygdala alpha1-adrenergic receptors facilitates fear conditioning and long-term potentiation

2010 ◽  
Vol 17 (10) ◽  
pp. 489-493 ◽  
Author(s):  
S. C. Lazzaro ◽  
M. Hou ◽  
C. Cunha ◽  
J. E. LeDoux ◽  
C. K. Cain
Keyword(s):  
Fear Conditioning ◽  
Adrenergic Receptors ◽  
Long Term Potentiation ◽  
Lateral Amygdala ◽  
Term Potentiation

scholarly journals Fast and flexible sequence induction in spiking neural networks via rapid excitability changes

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Rich Pang ◽  
Adrienne L Fairhall
Keyword(s):  
Neural Networks ◽  
Cognitive Flexibility ◽  
Long Term Potentiation ◽  
Spiking Neural Networks ◽  
Intrinsic Excitability ◽  
Stimulus Response ◽  
Term Potentiation ◽  
Spiking Network ◽  
Sequence Induction

Cognitive flexibility likely depends on modulation of the dynamics underlying how biological neural networks process information. While dynamics can be reshaped by gradually modifying connectivity, less is known about mechanisms operating on faster timescales. A compelling entrypoint to this problem is the observation that exploratory behaviors can rapidly cause selective hippocampal sequences to ‘replay’ during rest. Using a spiking network model, we asked whether simplified replay could arise from three biological components: fixed recurrent connectivity; stochastic ‘gating’ inputs; and rapid gating input scaling via long-term potentiation of intrinsic excitability (LTP-IE). Indeed, these enabled both forward and reverse replay of recent sensorimotor-evoked sequences, despite unchanged recurrent weights. LTP-IE ‘tags’ specific neurons with increased spiking probability under gating input, and ordering is reconstructed from recurrent connectivity. We further show how LTP-IE can implement temporary stimulus-response mappings. This elucidates a novel combination of mechanisms that might play a role in rapid cognitive flexibility.

Perceptual Correlate of Nociceptive Long-Term Potentiation (LTP) in Humans Shares the Time Course of Early-LTP

2006 ◽  
Vol 96 (6) ◽  
pp. 3551-3555 ◽  
Author(s):  
Thomas Klein ◽  
Walter Magerl ◽  
Rolf-Detlef Treede
Keyword(s):  
Healthy Subjects ◽  
Time Course ◽  
Pain Perception ◽  
Long Term Potentiation ◽  
Afferent Input ◽  
High Frequency Stimulation ◽  
Stimulus Response ◽  
Term Potentiation ◽  
Relay Nucleus

As in neocortex and hippocampus, neurons in the dorsal horn of the spinal cord develop long-term potentiation of synaptic efficacy (LTP) on high-frequency stimulation (HFS) of their afferent input, although how long LTP lasts in this nociceptive relay nucleus has not yet been addressed. Here we studied neurogenic hyperalgesia, a perceptual correlate of nociceptive LTP, in 13 healthy subjects, after HFS (5 × 1 s at 100 Hz) of superficial cutaneous afferents. HFS led to a mean upward shift of the stimulus–response function for pinprick-evoked pain (punctate mechanical hyperalgesia) in all subjects by a factor of 2.5 ( P < 0.001) that lasted undiminished for the initial 1-h observation period. Follow-up tests until the next day revealed that this type of neurogenic hyperalgesia decayed with a t1/2 of 3.3 h (99% CI: 3.1–3.5 h) and disappeared completely within 25.4 h (99% CI: 20.4–31.6 h). Touch-evoked pain (dynamic mechanical allodynia) developed in eight of 13 subjects, decayed with a t1/2 of 2.9 h from the maximum and disappeared within 9.3 h. These findings suggest that a single HFS session induces nociceptive LTP in healthy subjects that corresponds to early-LTP (LTP1), implying primarily posttranslational mechanisms for this type of plasticity of human pain perception.

scholarly journals cGMP-dependent kinase I supports formation of associative fear memory and long-term potentiation in the lateral amygdala

2007 ◽  
Vol 7 (S1) ◽  
Author(s):  
Cindy Paul ◽  
Pascal Weinmeister ◽  
Robert Feil ◽  
Franz Hofmann ◽  
Thomas Kleppisch
Keyword(s):  
Long Term Potentiation ◽  
Fear Memory ◽  
Lateral Amygdala ◽  
Term Potentiation

scholarly journals The Striatal-Enriched Protein Tyrosine Phosphatase Gates Long-Term Potentiation and Fear Memory in the Lateral Amygdala

2007 ◽  
Vol 61 (9) ◽  
pp. 1049-1061 ◽  
Author(s):  
Surojit Paul ◽  
Peter Olausson ◽  
Deepa V. Venkitaramani ◽  
Irina Ruchkina ◽  
Timothy D. Moran ◽  
...  
Keyword(s):  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Long Term Potentiation ◽  
Fear Memory ◽  
Lateral Amygdala ◽  
Protein Tyrosine ◽  
Term Potentiation

scholarly journals Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala

2019 ◽  
Vol 20 (17) ◽  
pp. 4310 ◽  
Author(s):  
Susanne Meis ◽  
Thomas Endres ◽  
Thomas Munsch ◽  
Volkmar Lessmann
Keyword(s):  
Synaptic Transmission ◽  
Long Term Potentiation ◽  
Fear Learning ◽  
Inhibitory Synapses ◽  
Lateral Amygdala ◽  
Term Potentiation ◽  
Gabaergic Synapses ◽  
Bdnf Signaling ◽  
The Impact

Brain-derived neurotrophic factor (BDNF) has previously been shown to play an important role in glutamatergic synaptic plasticity in the amygdala, correlating with cued fear learning. While glutamatergic neurotransmission is facilitated by BDNF signaling in the amygdala, its mechanism of action at inhibitory synapses in this nucleus is far less understood. We therefore analyzed the impact of chronic BDNF depletion on GABAA-mediated synaptic transmission in BDNF heterozygous knockout mice (BDNF+/−). Analysis of miniature and evoked inhibitory postsynaptic currents (IPSCs) in the lateral amygdala (LA) revealed neither pre- nor postsynaptic differences in BDNF+/− mice compared to wild-type littermates. In addition, long-term potentiation (LTP) of IPSCs was similar in both genotypes. In contrast, facilitation of spontaneous IPSCs (sIPSCs) by norepinephrine (NE) was significantly reduced in BDNF+/− mice. These results argue against a generally impaired efficacy and plasticity at GABAergic synapses due to a chronic BDNF deficit. Importantly, the increase in GABAergic tone mediated by NE is reduced in BDNF+/− mice. As release of NE is elevated during aversive behavioral states in the amygdala, effects of a chronic BDNF deficit on GABAergic inhibition may become evident in response to states of high arousal, leading to amygdala hyper-excitability and impaired amygdala function.

scholarly journals Phosphorylation of ERK/MAP kinase is required for long-term potentiation in anatomically restricted regions of the lateral amygdala in vivo

2008 ◽  
Vol 15 (2) ◽  
pp. 55-62 ◽  
Author(s):  
G. E. Schafe ◽  
M. W. Swank ◽  
S. M. Rodrigues ◽  
J. Debiec ◽  
V. Doyere
Keyword(s):  
Map Kinase ◽  
Long Term Potentiation ◽  
Lateral Amygdala ◽  
Term Potentiation
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