Gating of hippocampal output by β-adrenergic receptor activation in the pilocarpine model of epilepsy

Grosser, Sabine; Hollnagel, Jan‐Oliver; Gilling, Kate E.; Bartsch, Julia; Heinemann, Uwe; Behr, Jüergen

doi:10.1016/j.neuroscience.2014.11.055

Cited by 6 publications

(7 citation statements)

References 58 publications

(75 reference statements)

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“…Also, EPSP kinetics determined by rise and decay time constants and the transmembrane charge movement were not different between cell types or animal groups (not shown). As subicular tissue from pilocarpine-treated animals displays increased excitability (Grosser et al, 2015 ), we investigated EPSPs in both cell types at various stimulation intensities. We found that the input-output behavior for subthreshold EPSPs in single cell recordings was not changed in slices from pilocarpine-treated rats as compared to control preparations ( Figure 2D ), indicating that increased excitability in the subiculum from epileptic animals is rather due to network alterations than to an increased synaptic excitability at CA1-subiculum synapses.…”

Section: Resultsmentioning

confidence: 99%

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Loss of Long-Term Potentiation at Hippocampal Output Synapses in Experimental Temporal Lobe Epilepsy

Grosser

Buck

Braunewell

et al. 2020

Front. Mol. Neurosci.

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Patients suffering from temporal lobe epilepsy (TLE) show severe problems in hippocampus dependent memory consolidation. Memory consolidation strongly depends on an intact dialog between the hippocampus and neocortical structures. Deficits in hippocampal signal transmission are known to provoke disturbances in memory formation. In the present study, we investigate changes of synaptic plasticity at hippocampal output structures in an experimental animal model of TLE. In pilocarpine-treated rats, we found suppressed long-term potentiation (LTP) in hippocampal and parahippocampal regions such as the subiculum and the entorhinal cortex (EC). Subsequently we focused on the subiculum, serving as the major relay station between the hippocampus proper and downstream structures. In control animals, subicular pyramidal cells express different forms of LTP depending on their intrinsic firing pattern. In line with our extracellular recordings, we could show that LTP could only be induced in a minority of subicular pyramidal neurons. We demonstrate that a well-characterized cAMP-dependent signaling pathway involved in presynaptic forms of LTP is perturbed in pilocarpine-treated animals. Our findings suggest that in TLE, disturbances of synaptic plasticity may influence the information flow between the hippocampus and the neocortex.

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Section: Resultsmentioning

confidence: 99%

“…Multielectrode array (MEA) recordings were performed as reported earlier (Grosser et al, 2015 ). In brief, slices were placed on 8 × 8 electrode grids consisting of 59 titanium nitride electrodes (60MEA200/30iR-Ti, Multichannel Systems, Reutlingen, Germany) and perfused with aerated ACSF at a rate of 5–6 ml/min.…”

Section: Methodsmentioning

confidence: 99%

Loss of Long-Term Potentiation at Hippocampal Output Synapses in Experimental Temporal Lobe Epilepsy

Grosser

Buck

Braunewell

et al. 2020

Front. Mol. Neurosci.

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“…Extracellular recordings have shown that β-AR-activation modulates LTP at ventral CA1-subiculum synapses (Huang and Kandel, 2005). Chemical activation of AR by the β-adrenergic agonist isoprotenerol has been reported to induce LTP in burst-spiking but not regularspiking ventral subicular pyramidal cells (Wójtowicz et al, 2010;Grosser et al, 2015). Associated with stress, prenatal stress switched the LTP-enhancing effect of norepinephrine from dorsal to ventral hippocampus (Grigoryan and Segal, 2013).…”

Section: Discussionmentioning

confidence: 99%

Stress-Induced Enhanced Long-Term Potentiation and Reduced Threshold for N-Methyl-D-Aspartate Receptor- and β-Adrenergic Receptor-Mediated Synaptic Plasticity in Rodent Ventral Subiculum

Bartsch

Cramon

Gruber

et al. 2021

Front. Mol. Neurosci.

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Stress is a biologically relevant signal and can modulate hippocampal synaptic plasticity. The subiculum is the major output station of the hippocampus and serves as a critical hub in the stress response network. However, stress-associated synaptic plasticity in the ventral subiculum has not been adequately addressed. Therefore, we investigated the impact of a single exposure to an inherently stressful two-way active avoidance conditioning on the induction of long-term potentiation (LTP) at CA1—subiculum synapses in ventral hippocampal slices from young adult rats 1 day after stressor exposure. We found that acute stress enhanced LTP and lowered the induction threshold for a late-onset LTP at excitatory CA1 to subicular burst-spiking neuron synapses. This late-onset LTP was dependent on the activation of β-adrenergic and glutamatergic N-methyl-D-aspartate receptors and independent of D1/D5 dopamine receptor activation. Thereby, we present a cellular mechanism that might contribute to behavioral stress adaptation after acute stressor exposure.

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“…The subiculum, located between the hippocampus proper and the entorhinal cortex, acts as an important output station, critically involved in hippocampal learning and memory consolidation ( Deadwyler and Hampson, 2004 ; O’Mara, 2006 ; Wozny et al, 2008a , b ; Behr et al, 2009 ; Fidzinski et al, 2012 ), as well as in pathological processes, such as epilepsy ( Miles et al, 2012 ; Grosser et al, 2015 ; Buchin et al, 2016 ; Grosser et al, 2020 ). It comprises two functional types of excitatory principal neurons: BS and RS PCs ( Jung et al, 2001 ; Menendez de la Prida et al, 2003 ).…”

Section: Introductionmentioning

confidence: 99%

Cell-type specific inhibitory plasticity in subicular pyramidal cells

Guinet,

Grosser,

Özbay

et al. 2024

Front. Cell. Neurosci.

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The balance between excitation and inhibition is essential to the proper function of cortical circuits. To maintain this balance during dynamic network activity, modulation of the strength of inhibitory synapses is a central requirement. In this study, we aimed to characterize perisomatic inhibition and its plasticity onto pyramidal cells (PCs) in the subiculum, the main output region of the hippocampus. We performed whole-cell patch-clamp recordings from the two main functional PC types, burst (BS) and regular spiking (RS) neurons in acute rat hippocampal slices and applied two different extracellular high-frequency stimulation paradigms: non-associative (presynaptic stimulation only) and associative stimulation (concurrent pre-and postsynaptic stimulation) to induce plasticity. Our results revealed cell type-specific differences in the expression of inhibitory plasticity depending on the induction paradigm: While associative stimulation caused robust inhibitory plasticity in both cell types, non-associative stimulation produced long-term potentiation in RS, but not in BS PCs. Analysis of paired-pulse ratio, variance of IPSPs, and postsynaptic Ca2+ buffering indicated a dominant postsynaptic calcium-dependent signaling and expression of inhibitory plasticity in both PC types. This divergence in inhibitory plasticity complements a stronger inhibition and a higher intrinsic excitability in RS as compared to BS neurons, suggesting differential involvement of the two PC types during network activation and information processing in the subiculum.

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Gating of hippocampal output by β-adrenergic receptor activation in the pilocarpine model of epilepsy

Cited by 6 publications

References 58 publications

Loss of Long-Term Potentiation at Hippocampal Output Synapses in Experimental Temporal Lobe Epilepsy

Loss of Long-Term Potentiation at Hippocampal Output Synapses in Experimental Temporal Lobe Epilepsy

Stress-Induced Enhanced Long-Term Potentiation and Reduced Threshold for N-Methyl-D-Aspartate Receptor- and β-Adrenergic Receptor-Mediated Synaptic Plasticity in Rodent Ventral Subiculum

Cell-type specific inhibitory plasticity in subicular pyramidal cells

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