scholarly journals A mechanism for synaptic copy between neural circuits

2018 ◽  
Author(s):  
Yuxiu Shao ◽  
Binxu Wang ◽  
Andrew T. Sornborger ◽  
Louis Tao
Keyword(s):  
Memory Consolidation ◽  
Information Transfer ◽  
Neural Circuits ◽  
Neural Circuit ◽  
Neural Systems ◽  
Long Term Memory ◽  
Cortical Oscillations ◽  
The Brain ◽  
Putative Mechanism

The brain has a central, short-term learning module, the hippocampus, which transfers what it has learned to long-term memory in cortex during non-REM sleep. The putative mechanism responsible for this type of memory consolidation invokes hierarchically nested hippocampal ripples (100-250 Hz), thalamo-cortical spindles (7-15 Hz), and cortical slow oscillations (< 1 Hz) to enable transfer. Suppression of, for instance, thalamic spindles has been shown to impair hippocampus-dependent memory consolidation. Cortical oscillations are central to information transfer in neural systems. Significant evidence supports the idea that coincident spike input can allow the neural threshold to be overcome, and spikes to be propagated downstream in a circuit. Thus, an observation of oscillations in neural circuits would be an indication that repeated synchronous spiking is enabling information transfer. However, for memory transfer, in which synaptic weights must be being transferred from one neural circuit (region) to another, what is the mechanism? Here, we present a synaptic transfer mechanism whose structure provides some understanding of the phenomena that have been implicated in memory transfer, including the nested oscillations at various frequencies. The circuit is based on the principle of pulse-gated, graded information transfer between neural populations.PACS numbers: 87.18.Sn,87.19.lj,87.19.lm,87.19.lq

scholarly journals A Mechanism for Synaptic Copy Between Neural Circuits

2019 ◽  
Vol 31 (10) ◽  
pp. 1964-1984
Author(s):  
Yuxiu Shao ◽  
Binxu Wang ◽  
Andrew T. Sornborger ◽  
Louis Tao
Keyword(s):  
Information Transfer ◽  
Neural Circuits ◽  
Neural Circuit ◽  
Transfer Mechanism ◽  
Neural Systems ◽  
Memory Transfer ◽  
Significant Evidence ◽  
Cortical Oscillations ◽  
Neural Populations

Cortical oscillations are central to information transfer in neural systems. Significant evidence supports the idea that coincident spike input can allow the neural threshold to be overcome and spikes to be propagated downstream in a circuit. Thus, an observation of oscillations in neural circuits would be an indication that repeated synchronous spiking may be enabling information transfer. However, for memory transfer, in which synaptic weights must be being transferred from one neural circuit (region) to another, what is the mechanism? Here, we present a synaptic transfer mechanism whose structure provides some understanding of the phenomena that have been implicated in memory transfer, including nested oscillations at various frequencies. The circuit is based on the principle of pulse-gated, graded information transfer between neural populations.

Impaired long term memory consolidation in transgenic mice overexpressing the human soluble form of IL-1ra in the brain

2009 ◽  
Vol 208 (1-2) ◽  
pp. 46-53 ◽  
Author(s):  
Stefan Spulber ◽  
Laura Mateos ◽  
Mircea Oprica ◽  
Angel Cedazo-Minguez ◽  
Tamas Bartfai ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Memory Consolidation ◽  
Soluble Form ◽  
Long Term Memory ◽  
Term Memory ◽  
The Brain

The Acute Effect of Alcohol on Various Memory Processes

2010 ◽  
Vol 24 (4) ◽  
pp. 249-252 ◽  
Author(s):  
Márk Molnár ◽  
Roland Boha ◽  
Balázs Czigler ◽  
Zsófia Anna Gaál
Keyword(s):  
Low Dose ◽  
Short Term Memory ◽  
Acute Effect ◽  
Long Term Memory ◽  
Term Memory ◽  
Memory Processes ◽  
Different Types ◽  
The Brain ◽  
Legal Consequences

This review surveys relevant and recent data of the pertinent literature regarding the acute effect of alcohol on various kinds of memory processes with special emphasis on working memory. The characteristics of different types of long-term memory (LTM) and short-term memory (STM) processes are summarized with an attempt to relate these to various structures in the brain. LTM is typically impaired by chronic alcohol intake but according to some data a single dose of ethanol may have long lasting effects if administered at a critically important age. The most commonly seen deleterious acute effect of alcohol to STM appears following large doses of ethanol in conditions of “binge drinking” causing the “blackout” phenomenon. However, with the application of various techniques and well-structured behavioral paradigms it is possible to detect, albeit occasionally, subtle changes of cognitive processes even as a result of a low dose of alcohol. These data may be important for the consideration of legal consequences of low-dose ethanol intake in conditions such as driving, etc.

scholarly journals Sotalol does not interfere with the antielectroshock action of selected second-generation antiepileptic drugs in mice

2021 ◽  
Author(s):  
Kinga K. Borowicz-Reutt ◽  
Monika Banach ◽  
Monika Rudkowska ◽  
Anna Stachniuk
Keyword(s):  
Antiepileptic Drugs ◽  
Second Generation ◽  
Antidepressant Drug ◽  
Experimental Models ◽  
Long Term Memory ◽  
Avoidance Task ◽  
Maximal Electroshock ◽  
Term Memory ◽  
The Brain

Abstract Background Due to blocking β-receptors, and potassium KCNH2 channels, sotalol may influence seizure phenomena. In the previous study, we have shown that sotalol potentiated the antielectroshock action of phenytoin and valproate in mice. Materials and methods As a continuation of previous experiments, we examined the effect of sotalol on the action of four chosen second-generation antiepileptic drugs (oxcarbazepine, lamotrigine, pregabalin, and topiramate) against the maximal electroshock in mice. Undesired effects were evaluated in the chimney test (motor impairment) and step-through passive-avoidance task (long-term memory deficits). Finally, brain concentrations of antiepileptics were determined by fluorescence polarization immunoassay, while those of sotalol by liquid chromatography–mass spectrometry. Results Sotalol at doses of up to 100 mg/kg did not affect the electroconvulsive threshold. Applied at doses of 80–100 mg/kg, sotalol did not affect the antielectroshock action of oxcarbazepine, lamotrigine, pregabalin, or topiramate. Sotalol alone and in combinations with antiepileptics impaired neither motor performance nor long-term memory. Finally, sotalol significantly decreased the brain concentrations of lamotrigine and increased those of oxcarbazepine and topiramate. Pharmacokinetic interactions, however, did not influence the final antielectroshock effects of above-mentioned drug combinations. On the other hand, the brain concentrations of sotalol were not changed by second-generation antiepileptics used in this study. Conclusion Sotalol did not reduce the antielectroshock action of four second-generation antiepileptic drugs examined in this study. Therefore, this antidepressant drug should not interfere with antiseizure effects of lamotrigine, oxcarbazepine, pregabalin, and topiramate in patients with epilepsy. To draw final conclusions, our preclinical data should still be confirmed in other experimental models and clinical conditions.

Notch signalling becomes transiently attenuated during long-term memory consolidation in adult Wistar rats

2007 ◽  
Vol 88 (3) ◽  
pp. 342-351 ◽  
Author(s):  
Lisa Conboy ◽  
Claire M. Seymour ◽  
Marco P. Monopoli ◽  
Niamh C. O’Sullivan ◽  
Keith J. Murphy ◽  
...  
Keyword(s):  
Memory Consolidation ◽  
Wistar Rats ◽  
Notch Signalling ◽  
Long Term Memory ◽  
Term Memory

scholarly journals The amnestic agent anisomycin disrupts intrinsic membrane properties of hippocampal neurons via a loss of cellular energetics

2019 ◽  
Vol 122 (3) ◽  
pp. 1123-1135 ◽  
Author(s):  
C. J. Scavuzzo ◽  
M. J. LeBlancq ◽  
F. Nargang ◽  
H. Lemieux ◽  
T. J. Hamilton ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Mitochondrial Function ◽  
Neural Activity ◽  
Memory Consolidation ◽  
Hippocampal Neurons ◽  
Membrane Properties ◽  
Long Term Memory ◽  
Term Memory ◽  
Cellular Energetics

The nearly axiomatic idea that de novo protein synthesis is necessary for long-term memory consolidation is based heavily on behavioral studies using translational inhibitors such as anisomycin. Although inhibiting protein synthesis has been shown to disrupt the expression of memory, translational inhibitors also have been found to profoundly disrupt basic neurobiological functions, including the suppression of ongoing neural activity in vivo. In the present study, using transverse hippocampal brain slices, we monitored the passive and active membrane properties of hippocampal CA1 pyramidal neurons using intracellular whole cell recordings during a brief ~30-min exposure to fast-bath-perfused anisomycin. Anisomycin suppressed protein synthesis to 46% of control levels as measured using incorporation of radiolabeled amino acids and autoradiography. During its application, anisomycin caused a significant depolarization of the membrane potential, without any changes in apparent input resistance or membrane time constant. Anisomycin-treated neurons also showed significant decreases in firing frequencies and spike amplitudes, and showed increases in spike width across spike trains, without changes in spike threshold. Because these changes indicated a loss of cellular energetics contributing to maintenance of ionic gradients across the membrane, we confirmed that anisomycin impaired mitochondrial function by reduced staining with 2,3,5-triphenyltetrazolium chloride and also impaired cytochrome c oxidase (complex IV) activity as indicated through high-resolution respirometry. These findings emphasize that anisomycin-induced alterations in neural activity and metabolism are a likely consequence of cell-wide translational inhibition. Critical reevaluation of studies using translational inhibitors to promote the protein synthesis dependent idea of long-term memory is absolutely necessary. NEW & NOTEWORTHY Memory consolidation is thought to be dependent on the synthesis of new proteins because translational inhibitors produce amnesia when administered just after learning. However, these agents also disrupt basic neurobiological functions. We show that blocking protein synthesis disrupts basic membrane properties of hippocampal neurons that correspond to induced disruptions of mitochondrial function. It is likely that translational inhibitors cause amnesia through their disruption of neural activity as a result of dysfunction of intracellular energetics.

Impairments to Consolidation, Reconsolidation, and Long-Term Memory Maintenance Lead to Memory Erasure

2020 ◽  
Vol 43 (1) ◽  
pp. 297-314 ◽  
Author(s):  
Josué Haubrich ◽  
Matteo Bernabo ◽  
Andrew G. Baker ◽  
Karim Nader
Keyword(s):  
Memory Trace ◽  
Direct Approach ◽  
Long Term Memory ◽  
Retrieval Failure ◽  
Term Memory ◽  
The Brain

An enduring problem in neuroscience is determining whether cases of amnesia result from eradication of the memory trace (storage impairment) or if the trace is present but inaccessible (retrieval impairment). The most direct approach to resolving this question is to quantify changes in the brain mechanisms of long-term memory (BM-LTM). This approach argues that if the amnesia is due to a retrieval failure, BM-LTM should remain at levels comparable to trained, unimpaired animals. Conversely, if memories are erased, BM-LTM should be reduced to resemble untrained levels. Here we review the use of BM-LTM in a number of studies that induced amnesia by targeting memory maintenance or reconsolidation. The literature strongly suggests that such amnesia is due to storage rather than retrieval impairments. We also describe the shortcomings of the purely behavioral protocol that purports to show recovery from amnesia as a method of understanding the nature of amnesia.

Evidence for two distinct sleep-related long-term memory consolidation processes

Cortex ◽  
2015 ◽  
Vol 63 ◽  
pp. 68-78 ◽  
Author(s):  
Monika Schönauer ◽  
Melanie Grätsch ◽  
Steffen Gais
Keyword(s):  
Memory Consolidation ◽  
Long Term Memory ◽  
Term Memory
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