Expression of EPSP/spike potentiation following low frequency and tetanic stimulation in the CA1 area of the rat hippocampus

Bernard, C; Wheal, H.V.

doi:10.1523/jneurosci.15-10-06542.1995

Cited by 32 publications

(21 citation statements)

References 34 publications

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“…1 A and B). These reported in non-lesioned slices following LFS (Bernard & Wheal, 1995d). Following LFS, the number of spikes in the burst had decreased from five to two, suggesting a reduction of the evoked epileptiform activity (Fig.…”

Section: Methodsmentioning

confidence: 54%

“…4D These results suggest that in the KA-lesioned slice synapses can be saturated either towards potentiation or depression. The fact that E-S potentiation occurs whatever the direction of synaptic modification and cannot be changed when this modification is reversed also suggests that E-S modification is independent of synaptic plasticity as reported in the control tissue (Bernard & Wheal, 1995d (46 % of control). HowN-ev-er, PSAs wvere further depressed (31 % of conitrol).…”

Section: Methodsmentioning

confidence: 61%

“…These curves were then used to draw? the E-S curves (Bernard & Wheal, 1995d). PSAs were displayed as a function of their respective popEPSP slope.…”

Section: Methodsmentioning

confidence: 99%

“…We have tested the effects of low-frequency stimulation (LFS; 1 Hz for 15 min) on the synaptic responses, the epileptiform activity and the firing probability of the neurons. LFS is a conditioning stimulus which has been shown to produce NMDA-dependent synaptic LTD (see Bear & Malenka, 1994) and an NMDA-independent E-S potentiation (Bernard & Wheal, 1995d) in the CAl area of non-lesioned hippocampus. Attention was focused on the possible role of LFS as a functional, efficient way to reduce epileptiform activity.…”

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confidence: 99%

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A role for synaptic and network plasticity in controlling epileptiform activity in CA1 in the kainic acid‐lesioned rat hippocampus in vitro.

Bernard

Wheal

1996

The Journal of Physiology

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1. Stimulation of the surviving afferents in the stratum radiatum of the CAl area in kainic acid-lesioned hippocampal slices produced graded epileptiform activity, part of which (> 20 %) involved the activation of N-methyl-D-aspartate (NMDA) receptors. There was also a failure of synaptic inhibition in this region. In this preparation, we have tested the effects of low-frequency stimulation (LFS; 1 Hz for 15 min) on synaptic responses and epileptiform activity.2. LFS resulted in long-term depression (LTD) of excitatory synaptic potentials (EPSPs), longterm decrease of population spike amplitudes (PSAs) and EPSP-spike (E-S) potentiation. Evoked epileptiform activity was reduced but neurons had a higher probability of discharge. LTD could be reversed by subsequent tetanic stimulation whereas E-S dissociation remained unchanged. Synaptic and network responses could be saturated towards either potentiation or depression. However, E-S potentiation was maximal following the first conditioning stimulus. 3. NMDA receptor-mediated responses were pharmacologically isolated. LFS resulted in LTD of synaptic responses, long-term decrease of PSAs and E-S depression. These depressions could not be reversed by subsequent tetanic stimulation. a-Amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) and NMDA receptor-mediated responses were then measured in isolation before and following conditioning stimuli. LFS was shown to simultaneously produce LTD of AMPA and NMDA receptor-mediated responses. E-S potentiation of the AMPA component and E-S depression of the NMDA component occurred coincidentally. 4. LTD of AMPA and NMDA receptor-mediated responses were shown to be NMDA dependent. In contrast, E-S potentiation and depression occurred even when NMDA receptors were pharmacologically blocked. 5. These findings indicate that synaptic responses could be modified bidirectionally in the CAI area of kainic acid-lesioned rat hippocampus in an NMDA receptor-dependent manner.However, E-S dissociations were independent of the activation of NMDA receptors, hinting at mechanisms different from those of synaptic LTD. We suggest that changes in E-S coupling were caused by a modification of the firing threshold of the CAl pyramidal neurons.Furthermore, the firing mechanisms controlling NMDA and AMPA receptor-mediated network activity appeared to be different. The possible use of LFS applied to the hippocampus as a clinical intervention to suppress epileptiform activity is discussed.The understanding of the plasticity of synaptic and network common mechanisms through the activation of N-methylresponses in the hippocampus may provide some insight D-aspartate (NMDA) receptors. As a consequence, the into mechanisms that can be used to control epileptiform manipulation of one phenomenon may also strongly affect activity and the generation of epileptiform discharges. the other. On the one hand, if long-term potentiation (LTP) However, epileptiform activity and synaptic plasticity share of synaptic responses is induced, it is likely that the

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Section: Methodsmentioning

confidence: 54%

Section: Methodsmentioning

confidence: 61%

“…These curves were then used to draw? the E-S curves (Bernard & Wheal, 1995d). PSAs were displayed as a function of their respective popEPSP slope.…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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A role for synaptic and network plasticity in controlling epileptiform activity in CA1 in the kainic acid‐lesioned rat hippocampus in vitro.

Bernard

Wheal

1996

The Journal of Physiology

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“…The reversal of LTP preserves a potential for network plasticity and appears essential for any model of memory (8). Long-term synaptic depotentiation has been reported in the area CA1 (9), but the reversal of E-S P has never been clearly established (10,11). We show here that E-S depression (E-S D) is expressed concomitantly with long-term depression (LTD).…”

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confidence: 64%

Bidirectional plasticity of excitatory postsynaptic potential (EPSP)-spike coupling in CA1 hippocampal pyramidal neurons

Daoudal

Hanada

Debanne

2002

Proc. Natl. Acad. Sci. U.S.A.

137

152

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Integration of synaptic excitation to generate an action potential (excitatory postsynaptic potential-spike coupling or E-S coupling) determines the neuronal output. Bidirectional synaptic plasticity is well established in the hippocampus, but whether active synaptic integration can display potentiation and depression remains unclear. We show here that synaptic depression is associated with an N-methyl-D-aspartate receptor-dependent and long-lasting depression of E-S coupling. E-S depression is input-specific and is expressed in the presence of ␥-aminobutyric acid type A and B receptor antagonists. In single neurons, E-S depression is observed without modification of postsynaptic passive properties. We conclude that a decrease in intrinsic excitability underlies E-S depression and is synergic with glutamatergic long-term depression.I ntegration of synaptic inputs to produce an action potential at the axon hillock is a complex operation that depends on two critical factors: the distribution of voltage-gated ion channels in the dendrites and the passive electrical properties upon which these active channels are superimposed (1). Synaptic potentials have been shown to be shaped by intrinsic voltage-gated conductances located in the dendrites and the soma (2), but the dynamics of active synaptic integration remains poorly understood. We addressed here the question as to whether synaptic integration is modified after induction of long-term synaptic potentiation and depotentiation.In the area CA1, homosynaptic long-term potentiation (LTP) of excitatory synaptic transmission is induced by high-frequency stimulation (HFS, 100 Hz) of the afferent fibers (3). In parallel, the probability of discharge of the postsynaptic neurons in response to a given excitatory postsynaptic potential (EPSP) is enhanced (4-7). This second component has been called EPSPto-Spike potentiation (E-S potentiation, E-S P) which is complementary to LTP and functionally important. The reversal of LTP preserves a potential for network plasticity and appears essential for any model of memory (8). Long-term synaptic depotentiation has been reported in the area CA1 (9), but the reversal of E-S P has never been clearly established (10, 11). We show here that E-S depression (E-S D) is expressed concomitantly with long-term depression (LTD). E-S D is largely independent of synaptic inhibition but requires N-methyl-D-aspartate (NMDA) receptor (NMDAR) activation for its induction. We provide evidence for an activity-dependent decrease of the intrinsic excitability of CA1 pyramidal neurons that acts in synergy with LTD. MethodsSlice Preparation. Hippocampal slices (400 m) were obtained from 3-to 6-week-old rats according to institutional guidelines. Slices were cut in a solution (280 mM sucrose͞26 mM NaHCO 3 ͞10 mM D-glucose͞1.3 mM KCl͞1 mM CaCl 2 ͞10 mM MgCl 2 ), and were maintained for 1 h at room temperature in oxygenated (95% O 2 ͞5% CO 2 ) artificial cerebrospinal fluid (ACSF; 125 mM NaCl͞2.5 mM KCl͞0.8 mM NaH 2 PO 4 ͞26 mM NaHCO 3 ͞3 mM CaCl 2 ͞2 mM Mg...

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Matrix metalloprotease activity shapes the magnitude of EPSPs and spike plasticity within the hippocampal CA3 network

Wójtowicz

Mozrzymas

2013

Hippocampus

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Matrix metalloproteases (MMP) play a pivotal role in long-term synaptic plasticity, learning, and memory. The roles of different MMP subtypes are emerging, but the proteolytic activity of certain MMPs was shown to support these processes through the structural and functional modification of hippocampal Schaeffer collateral and mossy fiber (MF) synapses. However, certain patterns of synaptic activity are additionally associated with non-synaptic changes, such as the scaling of neuronal excitability. However, the extent to which MMPs affect this process remains unknown. We determined whether MMP activity interferes with excitatory post-synaptic potential EPSP-to-spike (E-S) coupling under conditions of varying synaptic activity. We evoked short- and long-term synaptic plasticity at associational/commissural (A/C) synapses of CA3 pyramidal neurons and simultaneously recorded population spikes (PSs) and EPSPs in acute rat (P30-60) brain slices in the presence of various MMP inhibitors. We found that MMP inhibition significantly reduced E-S coupling and shortened the PS latency associated with 4× 100 Hz stimulation or paired burst activity of MF-CA3 and A/C synapses. Moreover, MMP inhibition interfered with the scaling of amplitude of measured signals during high-frequency trains, thus affecting the induction of long-term potentiation (LTP). The inhibition of L-type voltage-gated calcium channels with 20 µM nifedipine or GABA-A receptors with 1-30 µM picrotoxin did not occlude the effects of MMP inhibitors. However, MMP inhibition significantly reduced the LTP of NMDA receptor-mediated EPSPs. Finally, the analysis of LTP saturation with multiple single (1× 100 Hz) or packed (4× 100 Hz) trains indicated that MMPs support E-S coupling evoked by selected synaptic activity patterns and set the ceiling for tetanically evoked E-S LTP. In conclusion, the activity of MMPs, particularly MMP-3, regulated the magnitude of EPSPs and spike plasticity in the CA3 network and may affect information processing. Our data provide a novel link between MMP activity and neural excitability. Therefore, by limiting the number of firing neurons, MMP may functionally act beyond the synapse.

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Expression of EPSP/spike potentiation following low frequency and tetanic stimulation in the CA1 area of the rat hippocampus

Cited by 32 publications

References 34 publications

A role for synaptic and network plasticity in controlling epileptiform activity in CA1 in the kainic acid‐lesioned rat hippocampus in vitro.

A role for synaptic and network plasticity in controlling epileptiform activity in CA1 in the kainic acid‐lesioned rat hippocampus in vitro.

Bidirectional plasticity of excitatory postsynaptic potential (EPSP)-spike coupling in CA1 hippocampal pyramidal neurons

Matrix metalloprotease activity shapes the magnitude of EPSPs and spike plasticity within the hippocampal CA3 network

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