scholarly journals Comparing the Seizure-Induced Impairment of Short-Term Plasticity in Dorsal and Ventral Hippocampus in Kindled Mice

2021 ◽  
Author(s):  
Nahid Roohi ◽  
◽  
Mahboubeh Ahmadi ◽  
Yaghoun Fathollahi ◽  
Amir Shojaei ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Dorsal Hippocampus ◽  
Hippocampal Slices ◽  
Ventral Hippocampus ◽  
Control Group ◽  
Short Term ◽  
Paired Pulse ◽  
Short Term Plasticity ◽  
Dorsal Hippocampal ◽  
Fepsp Slope

There are many differences among dorsal and ventral hippocampal neural circuits that affect the synaptic plasticity. In this study we compared the occurrence of short-term plasticity in the field excitatory post synaptic potentials (fEPSP) in dorsal and ventral hippocampal CA1 area following kindled seizures. Animals (male C57 B6/J mice, 12 weeks of age) were kindled by intraperitoneal injections of pentylenetetrazole (PTZ) and fEPSPs were recorded from dorsal and ventral hippocampal slices. Short-term plasticity was evaluated by measuring fEPSP-slope and fEPSP-area following paired-pulse stimulation delivered at three inter-pulse intervals (20, 80 and 160 ms). Obtained results showed that in control slices fEPSP-slope was greater in ventral- compared to dorsal hippocampus, but there was no difference in fEPSP-area among two regions. In hippocampal slices of kindled animals, fEPSP-slope was similar in dorsal and ventral regions, but fEPSP-area was greater in ventral- compared to dorsal hippocampus. In addition, fEPSP-area was greater in kindled compared to control group only in ventral hippocampus. PTZ kindled slices showed impaired short-term facilitation and the paired-pulse index was reduced only at dorsal hippocampal slices. Kindling had no significant effect on paired-pulse ratio in ventral hippocampal slices. Our findings indicated that the seizure occurrence affected the neural activity of hippocampus in a regional dependent manner. Although kindling increased fEPSP-area in ventral hippocampus, kindling-induced changes in short-term synaptic plasticity was significant only in dorsal hippocampal slices compared to control group. The difference in the responses of hippocampal dorsal and ventral poles has to be considered in the future researches.

Net Interaction Between Different Forms of Short-Term Synaptic Plasticity and Slow-IPSPs in the Hippocampus and Auditory Cortex

1998 ◽  
Vol 80 (4) ◽  
pp. 1765-1774 ◽  
Author(s):  
Dean V. Buonomano ◽  
Michael M. Merzenich
Keyword(s):  
Synaptic Plasticity ◽  
Auditory Cortex ◽  
Hippocampal Neurons ◽  
Time Dependent ◽  
Peak Amplitude ◽  
Short Term ◽  
Paired Pulse ◽  
Postsynaptic Potentials ◽  
Short Term Plasticity ◽  
Cgp 55845

Buonomano, Dean V. and Michael M. Merzenich. Net interaction between different forms of short-term synaptic plasticity and slow-IPSPs in the hippocampus and auditory cortex. J. Neurophysiol. 80: 1765–1774, 1998. Paired-pulse plasticity is typically used to study the mechanisms underlying synaptic transmission and modulation. An important question relates to whether, under physiological conditions in which various opposing synaptic properties are acting in parallel, the net effect is facilitatory or depressive, that is, whether cells further or closer to threshold. For example, does the net sum of paired-pulse facilitation (PPF) of excitatory postsynaptic potentials (EPSPs), paired-pulse depression (PPD) of inhibitory postsynaptic potentials (IPSPs), and the hyperpolarizing slow IPSP result in depression or facilitation? Here we examine how different time-dependent properties act in parallel and examine the contribution of γ-aminobutyric acid-B (GABAB) receptors that mediate two opposing processes, the slow IPSP and PPD of the fast IPSP. Using intracellular recordings from rat CA3 hippocampal neurons and L-II/III auditory cortex neurons, we examined the postsynaptic responses to paired-pulse stimulation (with intervals between 50 and 400 ms) of the Schaffer collaterals and white matter, respectively. Changes in the amplitude, time-to-peak (TTP), and slope of each EPSP were analyzed before and after application of the GABAB antagonist CGP-55845. In both CA3 and L-II/III neurons the peak amplitude of the second EPSP was generally depressed (further from threshold) compared with the first at the longer intervals; however, these EPSPs were generally broader and exhibited a longer TTP that could result in facilitation by enhancing temporal summation. At the short intervals CA3 neurons exhibited facilitation of the peak EPSP amplitude in the absence and presence of CGP-55845. In contrast, on average L-II/III cells did not exhibit facilitation at any interval, in the absence or presence of CGP-55845. CGP-55845 generally “erased” short-term plasticity, equalizing the peak amplitude and TTP of the first and second EPSPs at longer intervals in the hippocampus and auditory cortex. These results show that it is necessary to consider all time-dependent properties to determine whether facilitation or depression will dominate under intact pharmacological conditions. Furthermore our results suggest that GABAB-dependent properties may be the major contributor to short-term plasticity on the time scale of a few hundred milliseconds and are consistent with the hypothesis that the balance of different time-dependent processes can modulate the state of networks in a complex manner and could contribute to the generation of temporally sensitive neural responses.

A Simple Depletion Model of the Readily Releasable Pool of Synaptic Vesicles Cannot Account for Paired-Pulse Depression

2007 ◽  
Vol 97 (1) ◽  
pp. 948-950 ◽  
Author(s):  
Jane M. Sullivan
Keyword(s):  
Synaptic Vesicles ◽  
Hippocampal Neurons ◽  
Synaptic Activity ◽  
Excitatory Synapses ◽  
Short Term ◽  
Paired Pulse ◽  
Short Term Plasticity ◽  
Releasable Pool ◽  
Readily Releasable Pool ◽  
Paired Pulse Depression

Paired-pulse depression (PPD) is a form of short-term plasticity that plays a central role in processing of synaptic activity and is manifest as a decrease in the size of the response to the second of two closely timed stimuli. Despite mounting evidence to the contrary, PPD is still commonly thought to reflect depletion of the pool of synaptic vesicles available for release in response to the second stimulus. Here it is shown that PPD cannot be accounted for by depletion at excitatory synapses made by hippocampal neurons because PPD is unaffected by changes in the fraction of the readily releasable pool (RRP) released by the first of a pair of pulses.

Muscarinic presynaptic modulation in GABAergic pallidal synapses of the rat

2015 ◽  
Vol 113 (3) ◽  
pp. 796-807 ◽  
Author(s):  
Ricardo Hernández-Martínez ◽  
José J. Aceves ◽  
Pavel E. Rueda-Orozco ◽  
Teresa Hernández-Flores ◽  
Omar Hernández-González ◽  
...  
Keyword(s):  
Receptor Agonist ◽  
Projection Neurons ◽  
Quantal Content ◽  
Short Term ◽  
Paired Pulse ◽  
Short Term Plasticity ◽  
Striatal Projection Neurons ◽  
Muscarinic Cholinergic ◽  
Muscarinic Modulation

The external globus pallidus (GPe) is central for basal ganglia processing. It expresses muscarinic cholinergic receptors and receives cholinergic afferents from the pedunculopontine nuclei (PPN) and other regions. The role of these receptors and afferents is unknown. Muscarinic M1-type receptors are expressed by synapses from striatal projection neurons (SPNs). Because axons from SPNs project to the GPe, one hypothesis is that striatopallidal GABAergic terminals may be modulated by M1 receptors. Alternatively, some M1 receptors may be postsynaptic in some pallidal neurons. Evidence of muscarinic modulation in any of these elements would suggest that cholinergic afferents from the PPN, or other sources, could modulate the function of the GPe. In this study, we show this evidence using striatopallidal slice preparations: after field stimulation in the striatum, the cholinergic muscarinic receptor agonist muscarine significantly reduced the amplitude of inhibitory postsynaptic currents (IPSCs) from synapses that exhibited short-term synaptic facilitation. This inhibition was associated with significant increases in paired-pulse facilitation, and quantal content was proportional to IPSC amplitude. These actions were blocked by atropine, pirenzepine, and mamba toxin-7, suggesting that receptors involved were M1. In addition, we found that some pallidal neurons have functional postsynaptic M1 receptors. Moreover, some evoked IPSCs exhibited short-term depression and a different kind of modulation: they were indirectly modulated by muscarine via the activation of presynaptic cannabinoid CB1 receptors. Thus pallidal synapses presenting distinct forms of short-term plasticity were modulated differently.

scholarly journals A model of order-selectivity based on dynamic changes in the balance of excitation and inhibition produced by short-term synaptic plasticity

2015 ◽  
Vol 113 (2) ◽  
pp. 509-523 ◽  
Author(s):  
Vishwa Goudar ◽  
Dean V. Buonomano
Keyword(s):  
Synaptic Plasticity ◽  
Computational Models ◽  
Experimental Studies ◽  
Inhibitory Synapses ◽  
Speech Discrimination ◽  
Short Term ◽  
Dynamic Changes ◽  
Short Term Plasticity ◽  
Underlying Mechanisms ◽  
Parametric Analyses

Determining the order of sensory events separated by a few hundred milliseconds is critical to many forms of sensory processing, including vocalization and speech discrimination. Although many experimental studies have recorded from auditory order-sensitive and order-selective neurons, the underlying mechanisms are poorly understood. Here we demonstrate that universal properties of cortical synapses—short-term synaptic plasticity of excitatory and inhibitory synapses—are well suited for the generation of order-selective neural responses. Using computational models of canonical disynaptic circuits, we show that the dynamic changes in the balance of excitation and inhibition imposed by short-term plasticity lead to the generation of order-selective responses. Parametric analyses predict that among the forms of short-term plasticity expressed at excitatory-to-excitatory, excitatory-to-inhibitory, and inhibitory-to-excitatory synapses, the single most important contributor to order-selectivity is the paired-pulse depression of inhibitory postsynaptic potentials (IPSPs). A topographic model of the auditory cortex that incorporates short-term plasticity accounts for both context-dependent suppression and enhancement in response to paired tones. Together these results provide a framework to account for an important computational problem based on ubiquitous synaptic properties that did not yet have a clearly established computational function. Additionally, these studies suggest that disynaptic circuits represent a fundamental computational unit that is capable of processing both spatial and temporal information.

scholarly journals Short-term environmental enrichment enhances synaptic plasticity in hippocampal slices from aged rats

Neuroscience ◽  
2016 ◽  
Vol 329 ◽  
pp. 294-305 ◽  
Author(s):  
Liana R. Stein ◽  
Kazuko A. O’Dell ◽  
Michiyo Funatsu ◽  
Charles F. Zorumski ◽  
Yukitoshi Izumi
Keyword(s):  
Synaptic Plasticity ◽  
Environmental Enrichment ◽  
Hippocampal Slices ◽  
Aged Rats ◽  
Short Term

Implementation of Synaptic Device Using Various High-k Gate Dielectric Stacks

2020 ◽  
Vol 20 (7) ◽  
pp. 4292-4297
Author(s):  
Young-Tak Seo ◽  
Min-Kyu Park ◽  
Jong-Ho Bae ◽  
Byung-Gook Park ◽  
Jong-Ho Lee
Keyword(s):  
Synaptic Plasticity ◽  
Gate Dielectric ◽  
Memory Device ◽  
Control Device ◽  
Short Term ◽  
Paired Pulse ◽  
Retention Characteristic ◽  
High K ◽  
Neuromorphic Systems

We investigate the characteristics of short-term and long-term synaptic plasticity in a Si-based fieldeffect transistor (FET)-type memory device. An Al2O3/HfO2/Si3N4/SiO2 gate dielectric stack is used to realize short-term and long-term plasticity (STP/LTP). Si3N4 and HfO2 layers are designed to charge trap layer for synaptic device. The mechanism of STP and LTP operation is analyzed by considering the device response to the potentiation and depression pulses and retention measurement of the memory functionality. To investigate the STP operation, paired pulse facilitation (PPF) measurement is performed. The retention characteristic is also studied to validate the LTP property of the device. By investigating a device with an Al2O3/HfO2/Si3N4 stack as a control device, it is shown that the Al2O3/HfO2/Si3N4/SiO2 stack device is suitable for a synaptic device in neuromorphic systems.

Augmentation Controls the Fast Rebound From Depression at Excitatory Hippocampal Synapses

2008 ◽  
Vol 99 (4) ◽  
pp. 1770-1786 ◽  
Author(s):  
Elizabeth Garcia-Perez ◽  
John F. Wesseling
Keyword(s):  
Neurotransmitter Release ◽  
Single Pulse ◽  
Maximal Level ◽  
Short Term ◽  
Paired Pulse ◽  
Short Term Plasticity ◽  
Readily Releasable Pool ◽  
Hippocampal Synapses ◽  
Low Probability ◽  
Chemical Synapses

Short-term plasticity occurs at most central chemical synapses and includes both positive and negative components, but the principles governing interaction between components are largely unknown. The residual Ca2+ that persists in presynaptic terminals for several seconds after repetitive use is known to enhance neurotransmitter release under artificial, low probability of release conditions where depression is absent; this is termed augmentation. However, the full impact of augmentation under standard conditions at synapses where depression dominates is not known because of possibly complicated convolution with a variety of potential depression mechanisms. This report shows that residual Ca2+ continues to have a large enhancing impact on release at excitatory hippocampal synapses recovering from depression, including when only recently recruited vesicles are available for release. No evidence was found for gradual vesicle priming or for fast refilling of a highly releasable subdivision of the readily releasable pool (RRP). And decay of enhancement matched the clearance of residual Ca2+, thus matching the behavior of augmentation when studied in isolation. Because of incomplete RRP replenishment, synaptic strength was not typically increased above baseline when residual Ca2+ levels were highest. Instead residual Ca2+ caused single pulse release probability to rebound quickly from depression and then depress quickly during subsequent bursts of activity. Together, these observations can help resolve discrepancies in recent timing estimates of recovery from depression. Additionally, in contrast to results obtained under reduced release conditions, augmentation could be driven to a maximal level, occluding paired-pulse facilitation and other mechanisms that increase release efficiency.

scholarly journals Self-Tuning of Neural Circuits Through Short-Term Synaptic Plasticity

2007 ◽  
Vol 97 (6) ◽  
pp. 4079-4095 ◽  
Author(s):  
David Sussillo ◽  
Taro Toyoizumi ◽  
Wolfgang Maass
Keyword(s):  
Synaptic Plasticity ◽  
Activity Level ◽  
Cortical Circuits ◽  
Short Term ◽  
Cortical Networks ◽  
Short Term Plasticity ◽  
Numerous Experimental Data ◽  
Self Tuning ◽  
Synaptic Dynamics ◽  
Low Activity

Numerous experimental data show that cortical networks of neurons are not silent in the absence of external inputs, but rather maintain a low spontaneous firing activity. This aspect of cortical networks is likely to be important for their computational function, but is hard to reproduce in models of cortical circuits of neurons because the low-activity regime is inherently unstable. Here we show—through theoretical analysis and extensive computer simulations—that short-term synaptic plasticity endows models of cortical circuits with a remarkable stability in the low-activity regime. This short-term plasticity works as a homeostatic mechanism that stabilizes the overall activity level in spite of drastic changes in external inputs and internal circuit properties, while preserving reliable transient responses to signals. The contribution of synaptic dynamics to this stability can be predicted on the basis of general principles from control theory.

Structural Contributions to Short-Term Synaptic Plasticity

2004 ◽  
Vol 84 (1) ◽  
pp. 69-85 ◽  
Author(s):  
MATTHEW A. XU-FRIEDMAN ◽  
WADE G. REGEHR
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Synaptic Strength ◽  
Short Term ◽  
Ongoing Activity ◽  
Short Term Plasticity ◽  
Synaptic Ultrastructure

Xu-Friedman, Matthew A., and Wade G. Regehr. Structural Contributions to Short-Term Synaptic Plasticity. Physiol Rev 84: 69–85, 2004; 10.1152/physrev.00016.2003.—Synaptic ultrastructure is critical to many basic hypotheses about synaptic transmission. Various aspects of synaptic ultrastructure have also been implicated in the mechanisms of short-term plasticity. These forms of plasticity can greatly affect synaptic strength during ongoing activity. We review the evidence for how synaptic ultrastructure may contribute to facilitation, depletion, saturation, and desensitization.

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