Increase in glutamate receptors following repetitive electrical stimulation in hippocampal slices

Life Sciences ◽  
1980 ◽  
Vol 27 (4) ◽  
pp. 325-330 ◽  
Author(s):  
M. Baudry ◽  
M. Oliver ◽  
R. Creager ◽  
A. Wieraszko ◽  
G. Lynch
Keyword(s):  
Electrical Stimulation ◽  
Glutamate Receptors ◽  
Hippocampal Slices ◽  
Repetitive Electrical Stimulation

scholarly journals Activity-dependent regulation of synaptic strength by PSD-95 in CA1 neurons

2012 ◽  
Vol 107 (4) ◽  
pp. 1058-1066 ◽  
Author(s):  
Peng Zhang ◽  
John E. Lisman
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Synaptic Strength ◽  
Ca1 Neurons ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Term Potentiation ◽  
Activity Dependent

CaMKII and PSD-95 are the two most abundant postsynaptic proteins in the postsynaptic density (PSD). Overexpression of either can dramatically increase synaptic strength and saturate long-term potentiation (LTP). To do so, CaMKII must be activated, but the same is not true for PSD-95; expressing wild-type PSD-95 is sufficient. This raises the question of whether PSD-95's effects are simply an equilibrium process [increasing the number of AMPA receptor (AMPAR) slots] or whether activity is somehow involved. To examine this question, we blocked activity in cultured hippocampal slices with TTX and found that the effects of PSD-95 overexpression were greatly reduced. We next studied the type of receptors involved. The effects of PSD-95 were prevented by antagonists of group I metabotropic glutamate receptors (mGluRs) but not by antagonists of ionotropic glutamate receptors. The inhibition of PSD-95-induced strengthening was not simply a result of inhibition of PSD-95 synthesis. To understand the mechanisms involved, we tested the role of CaMKII. Overexpression of a CaMKII inhibitor, CN19, greatly reduced the effect of PSD-95. We conclude that PSD-95 cannot itself increase synaptic strength simply by increasing the number of AMPAR slots; rather, PSD-95's effects on synaptic strength require an activity-dependent process involving mGluR and CaMKII.

scholarly journals Low-Intensity Ultrasound Decreases Ischemia-Induced Edema by Inhibiting N-Methyl-d-Aspartic Acid Receptors

2018 ◽  
Vol 45 (6) ◽  
pp. 675-681
Author(s):  
Binika Hada ◽  
Mrigendra Bir Karmacharya ◽  
So R. Park ◽  
Byung H. Choi
Keyword(s):  
Glutamate Receptors ◽  
Brain Edema ◽  
Aspartic Acid ◽  
Hippocampal Slices ◽  
Dependent Manner ◽  
Edema Formation ◽  
Mk 801 ◽  
Low Intensity ◽  
Low Intensity Ultrasound ◽  
Brain Edema Formation

AbstractBackground: We have previously shown that low-intensity ultrasound (LIUS), a noninvasive mechanical stimulus, inhibits brain edema formation induced by oxygen and glucose deprivation (OGD) or treatment with glutamate, a mediator of OGD-induced edema, in acute rat hippocampal slice model in vitro. Methods: In this study, we treated the rat hippocampal slices with N-methyl-d-aspartic acid (NMDA) or (S)-3,5-dihydroxyphenylglycine (DHPG) to determine whether these different glutamate receptor agonists induce edema. The hippocampal slices were then either sonicated with LIUS or treated with N-methyl-d-aspartic acid receptor (NMDAR) antagonists, namely, MK-801 and ketamine, and observed their effects on edema formation. Results: We observed that treatment with NMDA, an agonist of ionotropic glutamate receptors, induced brain edema at similar degrees compared with that induced by OGD. However, treatment with DHPG, an agonist of metabotropic glutamate receptors, did not significantly induce brain edema. Treatment with the NMDAR antagonists MK-801 or ketamine efficiently prevented brain edema formation by both OGD and NMDA in a concentration-dependent manner. N-Methyl-d-aspartic acid-induced brain edema was alleviated by LIUS in an intensity-dependent manner when ultrasound was administered at 30, 50, or 100 mW/cm2 for 20 minutes before the induction of the edema. Furthermore, LIUS reduced OGD- and NMDA-induced phosphorylation of NMDARs at Y1325. Conclusion: These results suggest that LIUS can inhibit OGD- or NMDA-induced NMDAR activation by preventing NMDAR phosphorylation, thereby reducing a subsequent brain edema formation. The mechanisms by which LIUS inhibits NMDAR phosphorylation need further investigation.

Activation of metabotropic glutamate receptors induces long-term depression of GABAergic inhibition in hippocampus

1993 ◽  
Vol 69 (3) ◽  
pp. 1000-1004 ◽  
Author(s):  
Y. B. Liu ◽  
J. F. Disterhoft ◽  
N. T. Slater
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Hippocampal Slices ◽  
Input Resistance ◽  
Nmda Receptor Antagonist ◽  
Metabotropic Glutamate ◽  
Epileptiform Discharges ◽  
Bath Application

1. The long-term enhancement of synaptic excitability in CA1 hippocampal pyramidal neurons produced by activation of metabotropic glutamate receptors (mGluRs) was studied in rabbit hippocampal slices in vitro. 2. Bath application of the mGluR agonist (1S,3R)-1-aminocyclopentane-1,3- dicarboxylic acid (1S,3R-ACPD) (5-20 microM) for 20 min produced a reversible depolarization of membrane potentiatil, blockade of spike accommodation, and increase in input resistance of CA1 neurons. However, a long-lasting increase in synaptic excitability was observed: single stimuli applied to the Schaffer collateral commisural fiber pathway evoked epileptiform discharges in the presence of 1S,3R-ACPD and after the washout of 1S,3R-ACPD, persistent paroxysmal depolarization shifts (PDSs) were evoked by afferent stimulation. A long-lasting enhancement of synaptic excitability was also observed in the presence of the NMDA receptor antagonist D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5), which blocked the stimulation-evoked PDS and associated afterdischarges. 3. When biphasic, monosynaptically evoked inhibitory post-synaptic potentials (IPSPs) were recorded in the presence of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10–15 microM) and D-AP5 (20 microM), the bath application of 1S,3R-ACPD produced a significant reduction (approximately 50%) of both components of the IPSP, which persisted after the washout of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Excitability of the motoneuron after repetitive electrical stimulation to the tibial nerve.

1990 ◽  
Vol 5 (2) ◽  
pp. 77-80
Author(s):  
Hirobumi KAWAMURA ◽  
Takamasa TSURUMI ◽  
Morihiro TSUJISHITA ◽  
Hiroshi YAMAMOTO ◽  
Tetsuro SADAHIRO ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Tibial Nerve ◽  
Repetitive Electrical Stimulation

scholarly journals Synaptically Activated Calcium Responses in Dendrites of Hippocampal Oriens-Alveus Interneurons

2001 ◽  
Vol 85 (4) ◽  
pp. 1603-1613 ◽  
Author(s):  
Christine E. Gee ◽  
Gavin Woodhall ◽  
Jean-Claude Lacaille
Keyword(s):  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Hippocampal Slices ◽  
Selective Vulnerability ◽  
Ionotropic Glutamate Receptors ◽  
Repetitive Firing ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Frequency Of Action Potentials ◽  
Mglur Antagonist

Activation of metabotropic glutamate receptors (mGluRs) by agonists increases intracellular calcium levels ([Ca2+]i) in interneurons of stratum oriens/alveus (OA) of the hippocampus. We examined the mechanisms that contribute to dendritic Ca2+ increases in these interneurons during agonist activation of mGluRs and during synaptically evoked burst discharges, using simultaneous whole cell recordings and confocal Ca2+ imaging in rat hippocampal slices. First, we found that the group I/II mGluR agonist 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD; 100 μM) increased dendritic [Ca2+]i and depolarized OA interneurons. Dendritic Ca2+ responses were correlated with membrane depolarizations, but Ca2+ responses induced by ACPD were larger in amplitude than those elicited by equivalent somatic depolarization. Next, we used linescans to measure changes in dendritic [Ca2+]i during synaptically evoked burst discharges and somatically elicited repetitive firing in disinhibited slices. Dendritic Ca2+ signals and electrophysiological responses were stable over repeated trials. Peak Ca2+responses were linearly related to number and frequency of action potentials in burst discharges for both synaptic and somatic stimulation, but the slope of the relationship was steeper for responses evoked somatically. Synaptically evoked [Ca2+]i rises and excitatory postsynaptic potentials were abolished by antagonists of ionotropic glutamate receptors. The group I/II mGluR antagonist S-α-methyl-4-carboxyphenylglycine (500 μM) produced a significant partial reduction of synaptically evoked dendritic Ca2+ responses. The mGluR antagonist did not affect synaptically evoked burst discharges and did not reduce either Ca2+ responses or burst discharges evoked somatically. Therefore ionotropic glutamate receptors appear necessary for synaptically evoked dendritic Ca2+ responses, and group I/II mGluRs may contribute partially to these responses. Dendritic [Ca2+]i rises mediated by both ionotropic and metabotropic glutamate receptors may be important for synaptic plasticity and the selective vulnerability to excitotoxicity of OA interneurons.

Polarity of effects of stimulation of Auerbach's plexus on longitudinal muscle.

1978 ◽  
Vol 235 (4) ◽  
pp. E345
Author(s):  
S Yokoyama ◽  
T Ozaki
Keyword(s):  
Electrical Stimulation ◽  
Longitudinal Muscle ◽  
Oral Side ◽  
Metal Microelectrode ◽  
Rabbit Intestine ◽  
Auerbach’S Plexus ◽  
Repetitive Electrical Stimulation ◽  
Auerbach's Plexus ◽  
Anal Side ◽  
Stimulation Of

The effects of repetitive electrical stimulation of nodes in Auerbach's plexus on the longitudinal muscle of rabbit intestine were investigated. Peeled longitudinal muscle strips, with adherent Auerbach's plexus, were obtained and placed under a stereodissecting microscope. Neural elements within nodes of Auerbach's plexus were stimulated repetitively using a metal microelectrode with tip diameter of 5 micrometer. Stimuli applied to a node generally caused excitation of the longitudinal muscle on the oral side and inhibition on the anal side of the point of stimulation. Excitation of the muscle was mainly cholinergic, and inhibition of the muscle was nonadrenergic. From the results of the present study the concept of the law of the intestine, excitation above and inhibition below the stimulated spot, was supported.

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