scholarly journals Synaptically Released Glutamate Does Not Overwhelm Transporters on Hippocampal Astrocytes During High-Frequency Stimulation

2000 ◽  
Vol 83 (5) ◽  
pp. 2835-2843 ◽  
Author(s):  
Jeffrey S. Diamond ◽  
Craig E. Jahr
Keyword(s):  
Synaptic Transmission ◽  
High Frequency ◽  
Hippocampal Slices ◽  
Synaptic Cleft ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Direct Role ◽  
Ca1 Region ◽  
Frequency Stimulation ◽  
Hippocampal Astrocytes

In addition to maintaining the extracellular glutamate concentration at low ambient levels, high-affinity glutamate transporters play a direct role in synaptic transmission by speeding the clearance of glutamate from the synaptic cleft and limiting the extent to which transmitter spills over between synapses. Transporters are expressed in both neurons and glia, but glial transporters are likely to play the major role in removing synaptically released glutamate from the extracellular space. The role of transporters in synaptic transmission has been studied directly by measuring synaptically activated, transporter-mediated currents (STCs) in neurons and astrocytes. Here we record from astrocytes in the CA1 region of hippocampal slices and elicit STCs with high-frequency (100 Hz) stimulus trains of varying length to determine whether transporters are overwhelmed by stimuli that induce long-term potentiation. We show that, at near-physiological temperatures (34°C), high-frequency stimulation (HFS) does not affect the rate at which transporters clear glutamate from the extrasynaptic space. Thus, although spillover between synapses during “normal” stimulation may compromise the absolute synapse specificity of fast excitatory synaptic transmission, spillover is not exacerbated during HFS. Transporter capacity is diminished somewhat at room temperature (24°C), although transmitter released during brief, “theta burst” stimulation is still cleared as quickly as following a single stimulus, even when transport capacity is partially diminished by pharmacological means.

scholarly journals Low-frequency stimulation erases LTP through an NMDA receptor-mediated activation of protein phosphatases.

1994 ◽  
Vol 1 (2) ◽  
pp. 129-139
Author(s):  
T J O'Dell ◽  
E R Kandel
Keyword(s):  
Synaptic Transmission ◽  
Protein Phosphatases ◽  
Hippocampal Slices ◽  
Low Frequency ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Phosphatase Inhibitors ◽  
Ca1 Region ◽  
Protein Phosphatase Inhibitors ◽  
Frequency Stimulation

In the CA1 region of adult guinea pig hippocampal slices, long trains of theta frequency (5 Hz) stimulation produced a small enhancement of basal synaptic transmission but depressed the strength of synaptic transmission at synapses that had recently undergone long-term potentiation (LTP). Five hertz stimulation delivered immediately prior to high-frequency stimulation also inhibited the subsequent induction of LTP. The depression of potentiated synapses by 5 Hz stimulation (depotentiation) was blocked by 2-amino-5-phosphonovalerate and was observed only during the early phases of LTP. Furthermore, the protein phosphatase inhibitors okadaic acid and calyculin A blocked both depotentiation and the ability of 5 Hz stimulation to inhibit subsequent LTP, suggesting that protein phosphatases are involved in the ability of 5 Hz stimulation to modulate synaptic plasticity in the CA1 region of the hippocampus.

Medial amygdala enhances synaptic transmission and synaptic plasticity in the dentate gyrus of rats in vivo

1995 ◽  
Vol 74 (5) ◽  
pp. 2201-2203 ◽  
Author(s):  
Y. Ikegaya ◽  
K. Abe ◽  
H. Saito ◽  
N. Nishiyama
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Dentate Gyrus ◽  
High Frequency ◽  
Long Term Potentiation ◽  
Perforant Path ◽  
High Frequency Stimulation ◽  
Medial Amygdala ◽  
Frequency Stimulation ◽  
Stimulation Of

1. The present experiment was designed to test whether synaptic transmission and synaptic plasticity in the dentate gyrus were modulated by the medial amygdala (MeA). Field potentials in the dentate gyrus (DG) evoked by stimulations of the medial perforant path (PP) were extracellularly recorded in anesthetized rats. 2. Although single-pulse stimulation of the MeA augmented PP stimulation-evoked population spike amplitude in the DG transiently, high-frequency stimulation (100 Hz for 1 s) of the MeA induced long-lasting enhancement of synaptic transmission that was not occluded by PP tetanus-induced long-term potentiation (LTP). 3. When high-frequency stimulation of the MeA was applied concurrently with weak tetanus of the PP, which alone induced only marginal LTP, the magnitude of LTP increased considerably. 4. These results demonstrate that neuron activities in the MeA induce short- and long-lasting changes in the excitability of the PP-DG synapses and thereby enhance their synaptic plasticity.

scholarly journals Long-Term Recording of LTP in Cultured Hippocampal Slices

2002 ◽  
Vol 9 (4) ◽  
pp. 249-254 ◽  
Author(s):  
Ken Shimono ◽  
Michel Baudry ◽  
Lam Ho ◽  
Makoto Taketani ◽  
Gary Lynch
Keyword(s):  
Nmda Receptor ◽  
High Frequency ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Electrode Arrays ◽  
Chronic Recording ◽  
Term Potentiation ◽  
Frequency Stimulation

Long-term potentiation (LTP) was elicited by high frequency stimulation in hippocampal slices cultured on multi-electrode arrays. LTP lasting more than 1 h was recorded in 75% of slices, and a significant number of slices exhibited a non-decaying LTP that lasted more than 48 h. LTP induction was completely and reversibly blocked by an antagonist of the NMDA receptor, APV. Our results suggest the possibility of using chronic recording in hippocampal slices cultured on multi-electrode arrays to study the mechanisms underlying LTP maintenance and stabilization.

Sevoflurane Blocks the Induction of Long-term Potentiation When Present during, but Not When Present Only before, the High-frequency Stimulation

2018 ◽  
Vol 128 (3) ◽  
pp. 555-563 ◽  
Author(s):  
Jinyang Liu ◽  
Lie Yang ◽  
Daisy Lin ◽  
James E. Cottrell ◽  
Ira S. Kass
Keyword(s):  
High Frequency ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Excitatory Postsynaptic Potential ◽  
Ca1 Region ◽  
Postsynaptic Potential ◽  
Artificial Cerebrospinal Fluid ◽  
Term Potentiation ◽  
Frequency Stimulation

Abstract Background This study tests the hypothesis that sevoflurane blocks long-term potentiation only if it is present during the high-frequency stimulation that induces long-term potentiation. Methods Long-term potentiation, an electrophysiologic correlate of memory, was induced by high-frequency stimulation and measured as a persistent increase in the field excitatory postsynaptic potential slope in the CA1 region. Results Long-term potentiation was induced in the no sevoflurane group (171 ± 58% vs. 96 ± 11%; n = 13, mean ± SD); when sevoflurane (4%) was present during the high-frequency stimulation, long-term potentiation was blocked (92 ± 22% vs. 99 ± 7%, n = 6). While sevoflurane reduced the size of the field excitatory postsynaptic potential to single test stimuli by 59 ± 17%, it did not significantly reduce the size of the field excitatory postsynaptic potentials during the 100 Hz high-frequency stimulation. If sevoflurane was removed from the artificial cerebrospinal fluid superfusing the slices 10 min before the high-frequency stimulation, then long-term potentiation was induced (185 ± 48%, n = 7); this was not different from long-term potentiation in the no sevoflurane slices (171 ± 58). Sevoflurane before, but not during, ⊖-burst stimulation, a physiologic stimulus, did not block the induction of long-term potentiation (151 ± 37% vs. 161 ± 34%, n = 7). Conclusions Sevoflurane blocks long-term potentiation formation if present during the high-frequency stimulation; this blockage of long-term potentiation does not persist if sevoflurane is discontinued before the high-frequency stimulation. These results may explain why short periods of insufficient sevoflurane anesthesia may lead to recall of painful or traumatic events during surgery.

DHA supplementation enhances high-frequency, stimulation-induced synaptic transmission in mouse hippocampus

2012 ◽  
Vol 37 (5) ◽  
pp. 880-887 ◽  
Author(s):  
Steve Connor ◽  
Gustavo Tenorio ◽  
Michael Tom Clandinin ◽  
Yves Sauvé
Keyword(s):  
Synaptic Transmission ◽  
High Frequency ◽  
Control Group ◽  
High Frequency Stimulation ◽  
Spatial Learning And Memory ◽  
Mouse Hippocampus ◽  
Spatial Memories ◽  
Frequency Stimulation ◽  
Activity Dependent ◽  
Synaptic Responses

While some studies on dietary supplementation with docosahexaenoic acid (DHA, 22:6n-3) have reported a beneficial effect on memory as a function of age, others have failed to find any effect. To clarify this issue, we sought to determine whether supplementing mice with a DHA-enriched diet could alter the ability of synapses to undergo activity-dependent changes in the hippocampus, a brain structure involved in forming new spatial memories. We found that DHA was increased by 29% ± 5% (mean ± SE) in the hippocampus for the supplemented (DHA+) versus nonsupplemented (control) group (n = 5 mice per group; p < 0.05). Such DHA elevation was associated with enhanced synaptic transmission (p < 0.05) as assessed by application of a high-frequency electrical stimulation protocol (100 Hz stimulation, which induced transient (<2 h) increases in synaptic strength) to slices from DHA+ (n = 4 mice) hippocampi when compared with controls (n = 4 mice). Increased synaptic responses were evident 60 min poststimulation. These results suggest that dietary DHA supplementation facilitates synaptic plasticity following brief high-frequency stimulation. This increase in synaptic transmission might provide a physiological correlation for the improved spatial learning and memory observed following DHA supplementation.

scholarly journals Tau- but not Aß -pathology enhances NMDAR-dependent depotentiation in AD-mouse models

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Enrico Faldini ◽  
Tariq Ahmed ◽  
Luc Bueé ◽  
David Blum ◽  
Detlef Balschun
Keyword(s):  
Synaptic Plasticity ◽  
Transgenic Mice ◽  
Mouse Models ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Synaptic Loss ◽  
Ca1 Region ◽  
Term Potentiation ◽  
Frequency Stimulation

AbstractMany mouse models of Alzheimer’s disease (AD) exhibit impairments in hippocampal long-term-potentiation (LTP), seemingly corroborating the strong correlation between synaptic loss and cognitive decline reported in human studies. In other AD mouse models LTP is unaffected, but other defects in synaptic plasticity may still be present. We recently reported that THY-Tau22 transgenic mice, that overexpress human Tau protein carrying P301S and G272 V mutations and show normal LTP upon high-frequency-stimulation (HFS), develop severe changes in NMDAR mediated long-term-depression (LTD), the physiological counterpart of LTP. In the present study, we focused on putative effects of AD-related pathologies on depotentiation (DP), another form of synaptic plasticity. Using a novel protocol to induce DP in the CA1-region, we found in 11–15 months old male THY-Tau22 and APPPS1–21 transgenic mice that DP was not deteriorated by Aß pathology while significantly compromised by Tau pathology. Our findings advocate DP as a complementary form of synaptic plasticity that may help in elucidating synaptic pathomechanisms associated with different types of dementia.

scholarly journals Cholecystokinin release triggered by NMDA receptors produces LTP and sound–sound associative memory

2019 ◽  
Vol 116 (13) ◽  
pp. 6397-6406 ◽  
Author(s):  
Xi Chen ◽  
Xiao Li ◽  
Yin Ting Wong ◽  
Xuejiao Zheng ◽  
Haitao Wang ◽  
...  
Keyword(s):  
Associative Learning ◽  
Associative Memory ◽  
High Frequency ◽  
Low Frequency ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Low Frequency Stimulation ◽  
Term Potentiation ◽  
Frequency Stimulation

Memory is stored in neural networks via changes in synaptic strength mediated in part by NMDA receptor (NMDAR)-dependent long-term potentiation (LTP). Here we show that a cholecystokinin (CCK)-B receptor (CCKBR) antagonist blocks high-frequency stimulation-induced neocortical LTP, whereas local infusion of CCK induces LTP. CCK−/−mice lacked neocortical LTP and showed deficits in a cue–cue associative learning paradigm; and administration of CCK rescued associative learning deficits. High-frequency stimulation-induced neocortical LTP was completely blocked by either the NMDAR antagonist or the CCKBR antagonist, while application of either NMDA or CCK induced LTP after low-frequency stimulation. In the presence of CCK, LTP was still induced even after blockade of NMDARs. Local application of NMDA induced the release of CCK in the neocortex. These findings suggest that NMDARs control the release of CCK, which enables neocortical LTP and the formation of cue–cue associative memory.

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