Long-term potentiation in basal dendrites of stratum oriens and NMDA receptors in hippocampal slices

1988 ◽  
Vol 24 (2) ◽  
pp. 184 ◽  
Keyword(s):  
Nmda Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Stratum Oriens ◽  
Basal Dendrites ◽  
Term Potentiation

Mechanisms of selective long-term potentiation of excitatory synapses in stratum oriens/alveus interneurons of rat hippocampal slices

1995 ◽  
Vol 73 (2) ◽  
pp. 810-819 ◽  
Author(s):  
M. Ouardouz ◽  
J. C. Lacaille
Keyword(s):  
Receptor Antagonist ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Peak Amplitude ◽  
Excitatory Synapses ◽  
Metabotropic Glutamate ◽  
Stratum Oriens ◽  
Term Potentiation ◽  
The Mean

1. We investigated long-term potentiation (LTP) of synaptic transmission in different populations of interneurons in the CA1 region of rat hippocampal slices using whole cell recordings. We elicited excitatory postsynaptic currents (EPSCs) in interneurons located in stratum oriens near the alveus (O/A) or in stratum lacunosum-moleculare near the stratum radiatum border (L-M) by electrical stimulation of nearby axons in stratum oriens and radiatum, respectively. 2. High-frequency stimulation (100 Hz, 1 s) of axons in conjunction with postsynaptic depolarization (to -20 mV) increased the peak amplitude of test EPSCs elicited at -80 mV in O/A interneurons. The mean peak amplitude of EPSCs was significantly potentiated relative to the control period at 10 min (39 +/- 7% increase, mean +/- SE; n = 11 cells) and 30 min (30 +/- 1% increase; n = 5 cells) after tetanization. Similar stimulation did not produce potentiation of EPSCs in L-M interneurons (n = 7 cells). 3. This selective LTP in O/A interneurons was reversibly blocked by the N-methyl-D-aspartate receptor antagonist (+/-)2-amino-5-phosphonopentanoic acid (AP-5). Tetanization in the presence of 25 microM AP-5 did not increase the amplitude of EPSCs (8 cells). After washout of AP-5 (4 cells), a second tetanization resulted in long-term potentiation of EPSCs. 4. LTP was dependent on the activation of metabotropic glutamate receptors. The peak amplitude of EPSCs was not increased 5-10 or 15-20 min after tetanization during bath application of the metabotropic glutamate receptor antagonist (RS)-alpha-methyl-4-carboxyphenylglycine (500 microM) (n = 5 cells). 5. Inclusion of the Ca2+ chelator 1,2-bis(2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA; 25 mM) in the patch pipette blocked LTP in O/A interneurons. In five cells recorded with BAPTA-containing electrodes, the mean peak amplitude was not significantly increased after tetanization. Thus a rise in postsynaptic intracellular Ca2+ appeared necessary for the induction of LTP in these interneurons. 6. Incubation of slices with the inhibitor of nitric oxide synthase N omega-nitro-L-arginine methyl ester (100 microM) before and throughout the recording session also blocked the increase in EPSC amplitude at 5-10 min (5 cells) and 15-20 min (3 cells) after tetanization. NO synthesis may therefore be necessary for LTP in O/A interneurons. 7. These results suggest that LTP of excitatory synapses is selectively produced in O/A but not L-M interneurons, and that this LTP shares similar characteristics with LTP in hippocampal CA1 pyramidal cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Long-term potentiation in hippocampal slices induced by temporary suppression of glycolysis

1995 ◽  
Vol 74 (6) ◽  
pp. 2763-2766 ◽  
Author(s):  
S. Tekkok ◽  
K. Krnjevic
Keyword(s):  
Nmda Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Synaptic Function ◽  
Excitatory Postsynaptic Potentials ◽  
Postsynaptic Potentials ◽  
After Effects ◽  
Population Spikes ◽  
Term Potentiation

1. Temporary suppression of glycolysis by 2-deoxy-D-glucose (2-DG)-long enough to abolish CA1 population spikes (PSs) and reduce field excitatory postsynaptic potentials (EPSPs) by two-thirds-is followed by a sustained rebound of EPSPs and PSs (both up by 70-150%). 2. Post 2-DG long-term potentiation (2-DG-LTP) is prevented by block of N-methyl-D-aspartate (NMDA) receptors (NMDARs). Though 2-DG-LTP is normally expressed by other receptors, in presence of picrotoxin 2-DG causes similar LTP of NMDAR-mediated EPSPs. 3. Stimulation at 1 s-1 fully depotentiates 2-DG-LTP. 4. Unlike tetanic LTP, 2-DG-LTP is not pathway-specific, is not occluded by a preceding tetanic LTP (or vice versa) and is insensitive to block of NO synthesis. 5. Hypoglycemic states may have long-lasting after-effects on cerebral synaptic function.

Caffeine-Mediated Presynaptic Long-Term Potentiation in Hippocampal CA1 Pyramidal Neurons

2003 ◽  
Vol 89 (6) ◽  
pp. 3029-3038 ◽  
Author(s):  
Eduardo D. Martín ◽  
Washington Buño
Keyword(s):  
Nmda Receptors ◽  
Glutamate Release ◽  
Ryanodine Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Cellular Mechanisms ◽  
Pipette Solution ◽  
Term Potentiation

We report a new form of long-term potentiation (LTP) in Schaffer collateral (SC)-CA1 pyramidal neuron synapses that originates presynaptically and does not require N-methyl-d-aspartate (NMDA) receptor activation nor increases in postsynaptic-free Ca2+. Using rat hippocampal slices, application of a brief “pulse” of caffeine in the bath evoked a nondecremental LTP (CAFLTP) of SC excitatory postsynaptic currents. An increased probability of transmitter release paralleled the CAFLTP, suggesting that it originated presynaptically. The P1 adenosine receptor antagonist 8-cyclopentyltheophylline and the P2 purinoreceptor antagonists suramin and piridoxal-5′-phosphate-azophenyl 2′,4′-disulphonate blocked the CAFLTP. Inhibition of Ca2+ release from caffeine/ryanodine stores by bath-applied ryanodine inhibited the CAFLTP, but ryanodine in the pipette solution was ineffective, suggesting a presynaptic effect of ryanodine. Previous induction of the “classical” LTP did not prevent the CAFLTP, suggesting that the LTP and the CAFLTP have different underlying cellular mechanisms. The CAFLTP is insensitive to the block of NMDA receptors by 2-amino-5-phosphonopentanoic acid and to Ca2+ chelation with intracellular 1,2-bis (2-aminophenoxy) ethane- N,N,N′ ,N′-tetraacetic acid, indicating that neither postsynaptic NMDA receptors nor increases in cytosolic-free Ca2+ participate in the CAFLTP. We conclude that the CAFLTP requires the interaction of caffeine with presynaptic P1, P2 purinoreceptors, and ryanodine receptors and is caused by an increased probability of glutamate release at SC terminals.

scholarly journals Multiple roles of GluN2D-containing NMDA receptors in short-term potentiation and long-term potentiation in mouse hippocampal slices

2021 ◽  
Vol 201 ◽  
pp. 108833
Author(s):  
Alen V. Eapen ◽  
Diego Fernández-Fernández ◽  
John Georgiou ◽  
Zuner A. Bortolotto ◽  
Stafford Lightman ◽  
...  
Keyword(s):  
Nmda Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Multiple Roles ◽  
Short Term ◽  
Term Potentiation

Induction of long-term potentiation without participation of N-methyl-D-aspartate receptors in kitten visual cortex

1991 ◽  
Vol 65 (1) ◽  
pp. 20-32 ◽  
Author(s):  
Y. Komatsu ◽  
S. Nakajima ◽  
K. Toyama
Keyword(s):  
Nmda Receptors ◽  
Stimulus Frequency ◽  
Low Frequency ◽  
Nmda Antagonist ◽  
Long Term Potentiation ◽  
Conditioning Stimulation ◽  
Postsynaptic Potential ◽  
Term Potentiation ◽  
Stimulation Of

1. Intracellular recording was made from layer II-III cells in slice preparations of kitten (30-40 days old) visual cortex. Low-frequency (0.1 Hz) stimulation of white matter (WM) usually evoked an excitatory postsynaptic potential (EPSP) followed by an inhibitory postsynaptic potential (IPSP). The postsynaptic potentials (PSPs) showed strong dependence on stimulus frequency. Early component of EPSP and IPSP evoked by weak stimulation both decreased monotonically at frequencies greater than 0.5-1 Hz. Strong stimulation similarly depressed the early EPSP at higher frequencies (greater than 2 Hz) and replaced the IPSP with a late EPSP, which had a maximum amplitude in the stimulus frequency range of 2-5 Hz. 2. Very weak WM stimulation sometimes evoked EPSPs in isolation from IPSPs. The falling phase of the EPSP revealed voltage dependence characteristic to the responses mediated by N-methyl-D-aspartate (NMDA) receptors and was depressed by application of an NMDA antagonist DL-2-amino-5-phosphonovalerate (APV), whereas the rising phase of the EPSP was insensitive to APV. 3. The early EPSPs followed by IPSPs were insensitive to APV but were replaced with a slow depolarizing potential by application of a non-NMDA antagonist 6,7-dinitro-quinoxaline-2,3-dione (DNQX), indicating that the early EPSP is mediated by non-NMDA receptors. The slow depolarization was mediated by NMDA receptors because it was depressed by membrane hyperpolarization or addition of APV. 4. The late EPSP evoked by higher-frequency stimulation was abolished by APV, indicating that it is mediated by NMDA receptors, which are located either on the recorded cell or on presynaptic cells to the recorded cells. 5. Long-term potentiation (LTP) of EPSPs was examined in cells perfused with solutions containing 1 microM bicuculline methiodide (BIM), a gamma-aminobutyric acid (GABA) antagonist. WM was stimulated at 2 Hz for 15 min as a conditioning stimulus to induce LTP, and the resultant changes were tested by low-frequency (0.1 Hz) stimulation of WM. 6. LTP of early EPSPs occurred in more than one-half of the cells (8/13) after strong conditioning stimulation. The rising slope of the EPSP was increased 1.6 times on average. 7. To test involvement of NMDA receptors in the induction of LTP in the early EPSP, the effect of conditioning stimulation was studied in a solution containing 100 microM APV, which was sufficient to block completely synaptic transmission mediated by NMDA receptors. LTP occurred in the same frequency and magnitude as in control solution.

Sign in / Sign up

Export Citation Format

Share Document