NMDA Receptor-Dependent Long-Term Synaptic Depression in the Entorhinal Cortex In Vitro

2003 ◽  
Vol 89 (4) ◽  
pp. 2112-2119 ◽  
Author(s):  
Saı̈d Kourrich ◽  
C. Andrew Chapman
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Entorhinal Cortex ◽  
Low Frequency ◽  
Synaptic Depression ◽  
Paired Pulse ◽  
Pulse Stimulation

The entorhinal cortex receives a large projection from the piriform (primary olfactory) cortex and, in turn, provides the hippocampal formation with most of its cortical sensory input. Synaptic plasticity in this pathway may therefore affect the processing of olfactory information and memory encoding. We have recently found that long-term synaptic depression (LTD) can be induced in this pathway in vivo by repetitive paired-pulse stimulation but not by low-frequency (1 Hz) stimulation with single pulses. Here, we have used field potential recordings to investigate the stimulation parameters and transmitter receptors required for the induction of LTD in the rat entorhinal cortex in vitro. The effectiveness of low-frequency stimulation (900 pulses at 1 or 5 Hz) and repeated delivery of pairs of stimulation pulses (30-ms interpulse interval) was assessed. Only repeated paired-pulse stimulation resulted in lasting LTD, and a low-intensity paired-pulse stimulation protocol that induces LTD in vivo was only effective in the presence of the GABAA receptor antagonist bicuculline (50 μM). LTD could also be induced in normal ACSF, however, by increasing the number of pulse-pairs delivered and by increasing the stimulation intensity during LTD induction. The induction of LTD was blocked by constant bath application of the N-methyl-d-aspartate (NMDA) glutamate receptor antagonist d-2-amino-5-phosphonovalerate (50 μM), indicating that LTD is dependent on NMDA receptor activation. However, LTD was not blocked by the group I/II mGluR antagonist (RS)-α-ethyl-4-carboxyphenylglycine (500 μM) or by bicuculline (50 μM). The induction of LTD in the entorhinal cortex in vitro is therefore dependent on intense stimulation that recruits activation of NMDA receptors, but does not require concurrent activation of mGluRs or inhibitory synaptic inputs.

scholarly journals Low-frequency stimulation induces long-term depression and slow onset long-term potentiation at perforant path-dentate gyrus synapses in vivo

2014 ◽  
Vol 111 (6) ◽  
pp. 1259-1273 ◽  
Author(s):  
Jossina Gonzalez ◽  
Isaiah S. Morales ◽  
Desiree M. Villarreal ◽  
Brian E. Derrick
Keyword(s):  
Nmda Receptor ◽  
Low Frequency ◽  
Perforant Path ◽  
Paired Pulse ◽  
Anesthetized Rats ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Slow Onset

The expression of homosynaptic long-term depression (LTD) is thought to mediate a crucial role in sustaining memory function. Our in vivo investigations of LTD expression at lateral (LPP) and medial perforant path (MPP) synapses in the dentate gyrus (DG) corroborate prior demonstrations that PP-DG LTD is difficult to induce in intact animals. In freely moving animals, LTD expression occurred inconsistently among LPP-DG and MPP-DG responses. Interestingly, following acute electrode implantation in anesthetized rats, low-frequency stimulation (LFS; 900 pulses, 1 Hz) promotes slow-onset LTP at both MPP-DG and LPP-DG synapses that utilize distinct induction mechanisms. Systemic administration of the N-methyl-d-aspartate (NMDA) receptor antagonist (+/−)-cyclopiperidine-6-piperiperenzine (CPP; 10 mg/kg) 90 min before LFS selectively blocked MPP-DG but not LPP-DG slow onset LTP, suggesting MPP-DG synapses express a NMDA receptor-dependent slow onset LTP whereas LPP-DG slow onset LTP induction is NMDA receptor independent. In experiments where paired-pulse LFS (900 paired pulses, 200-ms paired-pulse interval) was used to induce LTD, paired-pulse LFS of the LPP resulted in rapid onset LTP of DG responses, whereas paired-pulse LFS of the MPP induced slow onset LTP of DG responses. Although LTD observations were very rare following acute electrode implantation in anesthetized rats, LPP-DG LTD was demonstrated in some anesthetized rats with previously implanted electrodes. Together, our data indicate in vivo PP-DG LTD expression is an inconsistent phenomenon that is primarily observed in recovered animals, suggesting perturbation of the dentate through surgery-related tissue trauma influences both LTD incidence and LTP induction at PP-DG synapses in vivo.

Excitatory stimulation during postsynaptic inhibition induces long-term depression in hippocampus in vivo

1994 ◽  
Vol 72 (6) ◽  
pp. 3009-3016 ◽  
Author(s):  
E. Thiels ◽  
G. Barrionuevo ◽  
T. W. Berger
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Pyramidal Cell ◽  
Pyramidal Cells ◽  
Recording Site ◽  
Long Term Depression ◽  
Paired Pulse ◽  
Gabaa Receptor Antagonist ◽  
Pulse Stimulation

1. As part of an effort to evaluate the biological plausibility of theoretically derived principles of synaptic modification, we studied activity-dependent long-term depression (LTD) of glutamatergic transmission in the hippocampus of anesthetized adult rats. Field potentials of CA1 pyramidal cells evoked by single-pulse stimulation (0.1 Hz) of the commissural afferents were recorded before and after paired-pulse stimulation (0.5 Hz) of the same pathway. A train of 150 or 200 paired pulses produced robust LTD of the commissural input to the CA1 pyramidal neurons when the interstimulus interval (ISI) of the pairs was short (25 ms) but not when the ISI was long (1,000 ms). 2. Paired-pulse stimulation with the short but not with the long ISI also was associated with pronounced inhibition of pyramidal cell firing upon the second pulse of a pair, despite the fact that the excitatory input was facilitated with the short-ISI paradigm. The inhibition of pyramidal cell activity was mediated by input to the pyramidal cells from local gamma-aminobutyric acid (GABA)-releasing interneurons activated by commissural fibers and/or CA1 recurrent collaterals, because the inhibition was eliminated by local administration of the selective GABAA receptor antagonist, bicuculline (50 microM), near the recording site. 3. Postsynaptic input from GABAergic interneurons was necessary for the induction of LTD, because short-ISI paired-pulse stimulation failed to produce LTD in the presence of bicuculline. 4. N-methyl-D-aspartate (NMDA) receptor-mediated excitation also was necessary for the induction of LTD, because administration of the selective NMDA receptor antagonist, D-2-amino-5-phosphonvaleric acid (100 microM), near the recording site prevented the development of LTD.(ABSTRACT TRUNCATED AT 250 WORDS)

Novel Form of Long-Term Synaptic Depression in Rat Hippocampus Induced By Activation of α1 Adrenergic Receptors

2004 ◽  
Vol 91 (2) ◽  
pp. 1071-1077 ◽  
Author(s):  
Cary L. Scheiderer ◽  
Lynn E. Dobrunz ◽  
Lori L. McMahon
Keyword(s):  
Synaptic Transmission ◽  
Receptor Antagonist ◽  
Adrenergic Receptors ◽  
Hippocampal Slices ◽  
Low Frequency ◽  
Adrenergic System ◽  
Normal Cognitive Function ◽  
Dependent Learning

Neurons located in the locus coeruleus project to hippocampus and provide noradrenergic innervation necessary for hippocampal-dependent learning and memory. The mechanisms underlying the function of norepinephrine (NE) in memory processing are unknown but likely reside in the ability of NE to modulate the efficacy of glutamate synaptic transmission via activation of G-protein-coupled adrenergic receptors. Here we show that application of NE to rat hippocampal slices in vitro induces a long-term depression (LTD) of synaptic transmission at excitatory CA3–CA1 synapses that persists for ≥40 min after agonist washout. This LTD, which we refer to as NE LTD, is mediated by activation of α1 adrenergic receptors because the α1 agonist methoxamine can induce LTD at the same magnitude as that induced with the nonselective adrenergic agonist NE. Furthermore, NE LTD induced by either NE or methoxamine is blocked with the α1 receptor antagonist, prazosin, but is unaffected by antagonists of α2 and β receptors. This plasticity persists in the presence of the GABAA receptor antagonist bicuculline, indicating that adrenergic modulation of GABAA receptor-mediated transmission does not underlie NE LTD. Induction of NE LTD requires presynaptic activity during agonist application and postsynaptic activation of N-methyl-d-aspartate receptors, fulfilling Hebbian criteria of coincident pre- and postsynaptic activity. The expression of NE LTD is likely to be postsynaptic because paired-pulse facilitation ratios during NE LTD expression are not different from baseline, similar to LTD induced by low-frequency stimulation. Thus we report the identification and characterization of a novel Hebbian form of LTD in hippocampus that is induced after activation of α1 adrenergic receptors. This plasticity may be a mechanism by which the adrenergic system participates in normal cognitive function.

Characterization of 3-carboxy-5-phosphono-1,2,3,4-tetrahydroisoquinoline (SC-48981), a potent competitive (NMDA) receptor antagonist, in vitro and in vivo

1992 ◽  
Vol 135 (2) ◽  
pp. 149-152 ◽  
Author(s):  
Michael L. Vazquez ◽  
Danny J. Garland ◽  
Eric T. Sun ◽  
Julie A. Cler ◽  
Steve J. Mick ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Nmda Receptor Antagonist

Mechanisms underlying induction of long-term potentiation in rat medial and lateral perforant paths in vitro

1993 ◽  
Vol 69 (4) ◽  
pp. 1150-1159 ◽  
Author(s):  
A. Colino ◽  
R. C. Malenka
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Intracellular Calcium ◽  
Granule Cells ◽  
Long Term Potentiation ◽  
Nmda Receptor Antagonist ◽  
Perforant Path ◽  
Term Potentiation

1. The mechanisms underlying the induction of long-term potentiation (LTP) in the medial and lateral perforant paths were studied by recording excitatory postsynaptic potentials (EPSPs) from rat dentate granule cells in vitro using extracellular and whole-cell recording techniques. 2. Paired stimuli (interstimulus interval, 50-1,000 ms) resulted in facilitation of the lateral and depression of the medial perforant path-evoked EPSPs, respectively. This physiological difference was used to isolate responses evoked by stimulation of a single path. 3. Tetanic stimulation induced LTP in both pathways, although the magnitude of LTP in the lateral perforant path was significantly less than that in the medial perforant path. Both forms of LTP were blocked by the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovaleric acid (D-APV). 4. Buffering intracellular calcium by loading granule cells with the calcium chelator bis (O-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid prevented LTP in both pathways. 5. Pairing of low-frequency (0.25 Hz) afferent stimulation with postsynaptic depolarization induced LTP in the medial but not the lateral perforant path. However, pairing of higher-frequency stimulation (1-4 Hz) with postsynaptic depolarization did potentiate the lateral perforant path-evoked EPSP in some cells. 6. Both the medial and lateral perforant path-evoked EPSPs had two components; a fast component blocked by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and a slower, voltage-dependent component blocked by D-APV. 7. The results indicate that the induction of LTP in both the medial and lateral perforant paths requires activation of postsynaptic NMDA receptors and a rise in intracellular calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Postsynaptic Signals Mediating Induction of Long-Term Synaptic Depression in the Entorhinal Cortex

2008 ◽  
Vol 2008 ◽  
pp. 1-9 ◽  
Author(s):  
Saïd Kourrich ◽  
Stephen D. Glasgow ◽  
Douglas A. Caruana ◽  
C. Andrew Chapman
Keyword(s):  
Entorhinal Cortex ◽  
Calcium Influx ◽  
Protein Phosphatases ◽  
Piriform Cortex ◽  
Synaptic Depression ◽  
Nmda Receptor Antagonist ◽  
Large Projection ◽  
Whole Cell Recordings

The entorhinal cortex receives a large projection from the piriform cortex, and synaptic plasticity in this pathway may affect olfactory processing. In vitro whole cell recordings have been used here to investigate postsynaptic signalling mechanisms that mediate the induction of long-term synaptic depression (LTD) in layer II entorhinal cortex cells. To induce LTD, pairs of pulses, using a 30-millisecond interval, were delivered at 1 Hz for 15 minutes. Induction of LTD was blocked by the NMDA receptor antagonist APV and by the calcium chelator BAPTA, consistent with a requirement for calcium influx via NMDA receptors. Induction of LTD was blocked when the FK506 was included in the intracellular solution to block the phosphatase calcineurin. Okadaic acid, which blocks activation of protein phosphatases 1 and 2a, also prevented LTD. Activation of protein phosphatases following calcium influx therefore contributes to induction of LTD in layer II of the entorhinal cortex.

Long-Term Synaptic Plasticity in the Honeybee

1997 ◽  
Vol 78 (1) ◽  
pp. 528-532 ◽  
Author(s):  
S. Oleskevich ◽  
J. D. Clements ◽  
M. V. Srinivasan
Keyword(s):  
Synaptic Plasticity ◽  
Field Potential ◽  
Low Frequency ◽  
Fold Increase ◽  
Afferent Input ◽  
Insect Brain ◽  
Paired Pulse ◽  
Frequency Stimulation

Oleskevich, S., J. D. Clements, and M. V. Srinivasan. Long-term synaptic plasticity in the honeybee. J. Neurophysiol. 78: 528–532, 1997. A monosynaptic response was recorded in vivo in the mushroom body of the bee brain, an important site for memory consolidation. Focal electrical stimulation of a major afferent input evoked an extracellular field potential that consisted of a presynaptic fiber volley and a postsynaptic response. We report a long-lasting potentiation of the synaptic response (2.6-fold increase; ≤3.5 h). Potentiation of the response was induced by low-frequency stimulation (0.02–1.0 Hz), was input specific, and was maintained in the absence of stimulation. Paired-pulse facilitation of the response was converted to paired-pulse depression after potentiation, suggesting a presynaptic mechanism. This is the first demonstration of long-term synaptic plasticity in the insect brain.

Sign in / Sign up

Export Citation Format

Share Document