Associative Induction of Posttetanic and Long-Term Potentiation in CA1 Neurons of Rat Hippocampus

Sastry, B.R.; Goh, Joanne W.; Auyeung, Ariana

doi:10.1126/science.3010459

Cited by 213 publications

(84 citation statements)

References 21 publications

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“…The results of the previous experiment suggest that the processes responsible for the stabilization of LTP must be activated during LTP induction and cannot be accessed at later times. These processes must also be activated to a certain degree during STP since pairing low-frequency afferent stimulation with postsynaptic depolarization can generate robust, stable LTP (Gustafsson and Wigstrom, 1986;Kelso et al, 1986;Sastry et al, 1986). It was therefore of interest to determine the time interval tion(PPF, 200% mdicatesthat the EPSP slope of the second response was twice that of the first).…”

Section: Resultsmentioning

confidence: 99%

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Characterization of the integration time for the stabilization of long- term potentiation in area CA1 of the hippocampus

1992

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In area CA1 of the hippocampus, synaptic activation of NMDA receptors during postsynaptic depolarization can generate either a decremental synaptic potentiation termed short-term potentiation (STP) or stable, long-term potentiation (LTP). Examining the relationship between these two forms of synaptic enhancement should provide information about the intracellular processes responsible for the stabilization of LTP. Using the hippocampal slice preparation, initial experiments confirmed that STP can be generated either by a weak tetanus or by pairing a single EPSP with postsynaptic depolarization. Following the generation of submaximal LTP, application of a weak, STP-inducing tetanus resulted in STP (not LTP), suggesting that the processes responsible for stabilizing LTP must be activated during induction and cannot be accessed at later times. To determine the interval over which processes activated during STP can be integrated and result in stable LTP (the “integration time” for the stabilization of LTP), a fixed number of afferent stimuli were given at varying intervals (5–60 sec) during postsynaptic depolarization. Using either extracellular or whole-cell recording, LTP was rarely (11% of experiments) elicited at 1 min intervals and frequently (76% of experiments) elicited at 10 sec intervals. These results indicate that following a single EPSP during postsynaptic depolarization, the processes responsible for the stabilization of LTP decay significantly within approximately 1 min, although this value may depend on the level of activation of the requisite intracellular processes.

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Section: Resultsmentioning

confidence: 99%

“…lB), yet a number of such pairings result in stable LTP (Gustafsson and Wigstrom, 1986;Kelso et al, 1986;Sastry et al, 1986). This indicates that there must be some interval over which the processes activated by a single EPSP can be integrated.…”

Section: Discussionmentioning

confidence: 99%

Characterization of the integration time for the stabilization of long- term potentiation in area CA1 of the hippocampus

1992

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“…The differences in calcium levels in the dendrites could be responsible for producing EPSP potentiation in the case of orthodromic conditioning and not in the case of antidromic conditioning. Another type of conditioning that results in EPSP potentiation is pairing intracellular depolarization with low-frequency synaptic input (Sastry et al 1986;Gustafsson et al 1987;Bonhoeffer, Staiger & Aertsen, 1989). Intracellular depolarization differs from antidromic conditioning in two ways.…”

Section: Discussionmentioning

confidence: 99%

Associative EPSP‐‐spike potentiation induced by pairing orthodromic and antidromic stimulation in rat hippocampal slices.

Jester

Campbell

Sejnowski

1995

The Journal of Physiology

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1. Pairing low-frequency orthodromic stimulation with high-frequency antidromic conditioning of pyramidal cells in area CAI of the rat hippocampus resulted in long-lasting potentiation of the extracellular population spike of the cells, without an accompanying increase in the extracellular excitatory postsynaptic potential (EPSP), indicating an increase in EPSP-spike (E-S) coupling, also called E-8 potentiation. 2. The amplitude of the antidromically conditioned E-S potentiation took up to 60 min to reach its peak, much longer than synaptic long-term potentiation (LTP) induced by orthodromic tetanic stimulation. 3. The population spike amplitude of a control orthodromic input, which stimulated a separate set of fibres and which was inactive during the pairing, was also increased in over half the slices tested. That it can affect a silent pathway suggests that antidromically conditioned E-S potentiation is not generated locally at tetanized synapses. 4. Bath application of 50 AM D,L-2-amino-5-phosphonovaleric acid (AP5) blocked induction of antidromically conditioned E-S potentiation. After washing out the AP5, the same stimulation resulted in population spike increases. This suggests that activation of the NMDA subtype of glutamate receptor is necessary for the induction of this form of E-S potentiation.

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“…LTP is induced specifically in synapses that are stimulated repetitively (Andersen et al 1977;Lynch et al 1977;Levy and Steward 1979) and that are coactive with a sufficient postsynaptic activation (Levy and Steward 1979;Gustafsson and Wigstr6m 1986;Kelso and Brown 1986;Larson and Lynch 1986;Sastry et al 1986). These characteristics are believed to derive from Ca 2+ entry through synaptically activated voltage-dependent, N-methyl-n-aspartate (NMDA) receptor/channels (Bliss and Collingridge 1993).…”

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Long-term potentiation and evidence for novel synaptic association in CA1 stratum oriens of rat hippocampus.

Otani¹,

Connor²,

Levy³

1995

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IntroductionIn CA1 stratum oriens of hippocampal slices, a robust long-term potentiation (LTP) induced by tetanic stimulation (20 pulses at 100 Hz, 10 trains delivered at 0.1 Hz) was accompanied by a slowly developing potentiation in a second, untetanized pathway. N-methyl-D.aspartate (NMDA) receptor antagonist DL-2-amino-5-phosphonovaleric acid (D-APV, 50 or 100 p.M) reduced the homosynaptic LTP by 80% but failed to affect heterosynaptic LTP. The metabotropic receptor antagonist DL-2-amino-3-phosphonopropionic acid DI-AP3, 300 ttm) or (+)-(x-methyl-4-carboxyphenylglycine (MCPG, 500 ttM), applied with DL-APV, further reduced homosynaptic LTP and blocked heterosynaptic LTP. The inhibitor of Ca2+-induced Ca 2+ release dantrolene (20 ItM), also applied with DL-APV, blocked both components of LTP. Importantly, when low-frequency test stimulation (0.017 Hz) to the untetanized, heterosynaptic pathway was interrupted for 30 rain after homosynaptic tetanization, heterosynaptic LTP did not develop. These results demonstrate homosynaptic and heterosynaptic LTP inductions in stratum oriens of the area CA1 and suggest that the heterosynaptic LTP is induced by NMDA-independent, novel associative processes between tetanized and untetanized pathways.

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Associative Induction of Posttetanic and Long-Term Potentiation in CA1 Neurons of Rat Hippocampus

Cited by 213 publications

References 21 publications

Characterization of the integration time for the stabilization of long- term potentiation in area CA1 of the hippocampus

Characterization of the integration time for the stabilization of long- term potentiation in area CA1 of the hippocampus

Associative EPSP‐‐spike potentiation induced by pairing orthodromic and antidromic stimulation in rat hippocampal slices.

Long-term potentiation and evidence for novel synaptic association in CA1 stratum oriens of rat hippocampus.

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