scholarly journals Fast and Flexible Sequence Induction In Spiking Neural Networks Via Rapid Excitability Changes

2018 ◽  
Author(s):  
Rich Pang ◽  
Adrienne Fairhall
Keyword(s):  
Neural Networks ◽  
Cognitive Flexibility ◽  
Structural Changes ◽  
Network Dynamics ◽  
Long Term Potentiation ◽  
Recurrent Network ◽  
Task Demands ◽  
Stimulus Response ◽  
Term Potentiation ◽  
Sequence Induction

AbstractCognitive flexibility, the adaptation of mental processing to changes in task demands, is thought to depend on biological neural networks’ ability to rapidly modulate the dynamics governing how they process information. While extensive work has elucidated how network dynamics can be reshaped by slowly occurring structural changes, e.g. the gradual modification of recurrent synaptic patterns, much less is known about how dynamics might be reconfigured over faster timescales of seconds. One compelling example of rapid and selective modulation of network dynamics potentially involved in cognitive flexibility is observed in rodent hippocampus, where short bouts of exploratory behavior cause new activity sequences to preferentially “replay” during subsequent awake rest periods without continued sensory input. Fast mechanisms for selectively biasing sequential activity through networks, however, remain unknown. Using a spiking neural network model, we asked whether a simplified version of sequence replay could arise from three biophysically plausible components: recurrent, spatially organized connectivity; homogeneous, stochastic “gating” inputs; and rapid, activity-dependent scaling of gating input strengths, based on a phenomenon known as long-term potentiation of intrinsic excitability (LTP-IE). Indeed, these enabled both forward and reverse replay of flexible sequences reflecting recent behavior, despite unchanged recurrent weights. Specifically, activation-triggered LTP-IE “tags” neurons in the recurrent network by increasing their spiking probability when gating input is applied, and the sequential ordering of spikes is reconstructed by the existing recurrent connectivity. In a proof-of-concept demonstration, we also show how LTP-IE-based sequences can implement temporary stimulus-response mappings in a straightforward manner. These results elucidate a simple yet previously unexplored combination of biological mechanisms that converge in hippocampus and suffice for fast and flexible reconfiguration of sequential network dynamics, suggesting their potential role in cognitive flexibility over rapid timescales.

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.

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 Selective Presynaptic Propagation of Long-Term Potentiation in Defined Neural Networks

2000 ◽  
Vol 20 (9) ◽  
pp. 3233-3243 ◽  
Author(s):  
Hui-zhong W. Tao ◽  
Li I. Zhang ◽  
Guo-qiang Bi ◽  
Mu-ming Poo
Keyword(s):  
Neural Networks ◽  
Long Term Potentiation ◽  
Term Potentiation

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.

Is learning involved in plasticity in nociceptive regulation?

1997 ◽  
Vol 20 (3) ◽  
pp. 452-453
Author(s):  
Kjell Hole ◽  
Frode Svendsen ◽  
Arne Tjølsen
Keyword(s):  
Spinal Cord ◽  
Structural Changes ◽  
Long Term Potentiation ◽  
Field Potentials ◽  
Term Potentiation ◽  
C Fibre ◽  
Plastic Changes ◽  
Spinal Cord Function

Plastic changes in spinal cord function like neuronal wind-up and increased receptive field are too short-lived to explain chronic pain without structural changes. It is possible that learning could be a mechanism for longlasting changes in nociceptive regulation. A learning process localized to the spinal cord has been shown to be important for the development of tolerance to the analgetic effect of ethanol, suggesting that nociceptive control systems may be changed by learning. Long term potentiation (LTP) is regarded as a useful model of learning and memory. LTP-like changes have been observed in in vitro preparations from the spinal cord and in spinal cord field potentials. Recently a long term increase in spinal A-β and C-fibre evoked responses after painful stimulation has been observed. [coderre & katz, dickenson, wiesenfeld-hallin et al.]

scholarly journals Long-Term Plasticity of Neurotransmitter Release: Emerging Mechanisms and Contributions to Brain Function and Disease

2018 ◽  
Vol 41 (1) ◽  
pp. 299-322 ◽  
Author(s):  
Hannah R. Monday ◽  
Thomas J. Younts ◽  
Pablo E. Castillo
Keyword(s):  
Brain Function ◽  
Neurotransmitter Release ◽  
Structural Changes ◽  
Novelty Detection ◽  
Long Term Potentiation ◽  
Inhibitory Synapses ◽  
Term Potentiation ◽  
The Central Nervous System ◽  
Circuit Function

Long-lasting changes of brain function in response to experience rely on diverse forms of activity-dependent synaptic plasticity. Chief among them are long-term potentiation and long-term depression of neurotransmitter release, which are widely expressed by excitatory and inhibitory synapses throughout the central nervous system and can dynamically regulate information flow in neural circuits. This review article explores recent advances in presynaptic long-term plasticity mechanisms and contributions to circuit function. Growing evidence indicates that presynaptic plasticity may involve structural changes, presynaptic protein synthesis, and transsynaptic signaling. Presynaptic long-term plasticity can alter the short-term dynamics of neurotransmitter release, thereby contributing to circuit computations such as novelty detection, modifications of the excitatory/inhibitory balance, and sensory adaptation. In addition, presynaptic long-term plasticity underlies forms of learning and its dysregulation participates in several neuropsychiatric conditions, including schizophrenia, autism, intellectual disabilities, neurodegenerative diseases, and drug abuse.

scholarly journals Structural changes at dendritic spine synapses during long-term potentiation

2003 ◽  
Vol 358 (1432) ◽  
pp. 745-748 ◽  
Author(s):  
Kristen M. Harris ◽  
John C. Fiala ◽  
Linnaea Ostroff
Keyword(s):  
Dendritic Spines ◽  
Dendritic Spine ◽  
Structural Changes ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Structural Basis ◽  
Immature Rat ◽  
Term Potentiation ◽  
New Findings

Two key hypotheses about the structural basis of long-term potentiation (LTP) are evaluated in light of new findings from immature rat hippocampal slices. First, it is shown why dendritic spines do not split during LTP. Instead a small number of spine-like dendritic protrusions may emerge to enhance connectivity with potentiated axons. These ‘same dendrite multiple synapse boutons’ provide less than a 3% increase in connectivity and do not account for all of LTP or memory, as they do not accumulate during maturation. Second, polyribosomes in dendritic spines served to identify which of the existing synapses enlarged to sustain more than a 30% increase in synaptic strength. Thus, both enhanced connectivity and enlarged synapses result during LTP, with synapse enlargement being the greater effect.

scholarly journals The biophysical basis underlying the maintenance of early phase long-term potentiation

2021 ◽  
Vol 17 (3) ◽  
pp. e1008813
Author(s):  
Moritz F. P. Becker ◽  
Christian Tetzlaff
Keyword(s):  
Early Phase ◽  
Structural Changes ◽  
Long Term Potentiation ◽  
Biophysical Model ◽  
Term Potentiation ◽  
Wide Range ◽  
Long Time ◽  
Synaptic Changes ◽  
Experimental Findings

The maintenance of synaptic changes resulting from long-term potentiation (LTP) is essential for brain function such as memory and learning. Different LTP phases have been associated with diverse molecular processes and pathways, and the molecular underpinnings of LTP on the short, as well as long time scales, are well established. However, the principles on the intermediate time scale of 1-6 hours that mediate the early phase of LTP (E-LTP) remain elusive. We hypothesize that the interplay between specific features of postsynaptic receptor trafficking is responsible for sustaining synaptic changes during this LTP phase. We test this hypothesis by formalizing a biophysical model that integrates several experimentally-motivated mechanisms. The model captures a wide range of experimental findings and predicts that synaptic changes are preserved for hours when the receptor dynamics are shaped by the interplay of structural changes of the spine in conjunction with increased trafficking from recycling endosomes and the cooperative binding of receptors. Furthermore, our model provides several predictions to verify our findings experimentally.

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