Post-synaptic depolarization in induction of long-term potentiation in the CA1 hippocampus

Yoshioka, Noboru; Sakurai, Masaki

doi:10.1097/00001756-199501000-00027

Cited by 5 publications

(6 citation statements)

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“…We showed that in the absence of Mg 2+ , low‐frequency stimulation induced LTP (Fig. 2) (Yoshioka & Sakurai, 1995) which occluded with LTP induced by tetanic stimulation. In the absence of Mg 2+ , single pulses evoked NMDA currents in whole‐cell recordings without postsynaptic depolarization (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…It is possible to adjust the amplitudes of the elevations of Ca 2+ by the use of different glutamate receptor antagonists and to vary its duration by changing the number of conditioning pulses. For these reasons, we used low‐frequency (1 Hz) stimulation in the absence of Mg 2+ for conditioning (Yoshioka & Sakurai, 1995) and investigated the conditions for determining the direction of synaptic plasticity. A preliminary report of this work has been presented previously in an abstract form (Mizuno & Sakurai, 1999).…”

Section: Introductionmentioning

confidence: 99%

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Differential induction of LTP and LTD is not determined solely by instantaneous calcium concentration: an essential involvement of a temporal factor

Mizuno

Kanazawa

Sakurai

2001

Eur J of Neuroscience

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Two opposite types of synaptic plasticity in the CA1 hippocampus, long-term potentiation (LTP) and long-term depression (LTD), require postsynaptic Ca2+ elevation. To explain these apparently contradictory phenomena, the current view assumes that a moderate postsynaptic increase in Ca2+ leads to LTD, whereas a large increase leads to LTP. No detailed study has so far been attempted to investigate whether the instantaneous Ca2+ elevation level differentially induces LTP or LTD. We therefore used low-frequency (1 Hz) stimulation of Schaffer collateral/commissural fibers in rat hippocampal slices, during a Mg2+-free period, as the conditioning stimulus to investigate this. This allowed low-frequency afferent stimulation to cause a postsynaptic Ca2+ influx because the voltage-dependent block of N-methyl-D-aspartate (NMDA) receptor-channels by Mg2+ was removed. When delivered during the Mg2+-free period, a single pulse, as well as 2-600 pulses, induced LTP that was occluded with tetanus-induced LTP. To decrease the Ca2+ influx, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors were completely blocked by the addition of 10 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) to the conditioning medium, in which 1 Hz afferent stimuli (1-600 pulses) induced less LTP and never induced LTD. To further reduce the Ca2+ influx, NMDA receptors were partially blocked with D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5). A small number of 1 Hz stimuli, however, never induced LTD. Only when the conditioning stimuli exceeded 200 pulses was LTD induced. The present findings provide definitive evidence that protracted conditioning is a prerequisite for the induction of LTD. Thus, not only the amplitude but also the duration of postsynaptic Ca2+ elevation could be essential factors for differentially inducing LTP or LTD.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Differential induction of LTP and LTD is not determined solely by instantaneous calcium concentration: an essential involvement of a temporal factor

Mizuno

Kanazawa

Sakurai

2001

Eur J of Neuroscience

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“…There are at least three potential causes of the deficit: 1) an intrinsic deficit in the LTP-induction cascade (i.e., the chain of events that begins with the influx of Ca 2ϩ through the N-methyl-D-aspartate (NMDA) receptor; for review, see Bliss and Collingridge, 1993); 2) a change in the synapses or dendrites of old rats that makes their neurons less susceptible to LTP; 3) a change in neurons of aged rats that reduces the postsynaptic depolarization elicited by a given stimulus. This last possibility would reduce the Ca 2ϩ influx during LTP-inducing stimulation, which would theoretically reduce the magnitude of the resultant LTP (McNaughton et al, 1978;Lynch et al, 1983;Gustafsson and Wigström, 1988;Malenka et al, 1988;Wigström et al, 1988;Malenka, 1991;Yoshioka and Sakurai, 1995).…”

Section: Introductionmentioning

confidence: 99%

Role of temporal summation in age-related long-term potentiation-induction deficits

et al. 1997

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“…On the other hand, it is possible that the NMDA receptor-mediated events leading to the induction of LTP are intact in old animals but that changes in the number or efficacy of individual synapses may result in less effective depolarization and hence less NMDA receptor activation for a given stimulus in the old rats (Gustafsson and Wigstr6m 1986;Gustafsson et al 1987;Malenka 1991;Yoshioka and Sakurai 1995). Such an effect would be nonlinear, affecting the apparent threshold for induction more than the asymptotic level of LTP obtained with strong stimulation.…”

Section: Introductionmentioning

confidence: 99%

Functional integrity of NMDA-dependent LTP induction mechanisms across the lifespan of F-344 rats.

1996

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Previous studies have reported a lack of an age effect in the induction of long-term potentiation (LTP) at CA1 synapses, using robust (supmmaxim~) stimulation parameters, but an apparent age effect on the induction threshold of LTP using less robust stimulation, in the perithreshold region. These findings have led to the suggestion that old animals may experience an alteration either in the efficacy of activation ofN-methyl-n-aspartate (NMDA) receptors or in the metabolic processes subsequent to NMDA receptor activation that lead to LTP expression. An alternative explanation for the apparent threshold change in old animals is that, because of the known reduction of the intracellularly recorded, compound EPSP magnitude in old rats, equivalent electrical stimulation results in a smaller effective depolarization of the postsynaptic cells and a consequently less effective activation of NMDA receptors, which are otherwise functionally normal. To distinguish between these two hypotheses, weak orthodromic stimulation was paired with intracellularly applied current pulses, thus holding constant the degree of postsynaptic depolarization. No differences in LTP induction threshold or magnitude were observed in a large sample of rats from three age groups. It is concluded that the NMDA receptor mechanisms and associated biochemical processes leading to LTP induction are not SCorresponding author. altered in aged F-344 rats. The reduced compound EPSP in old animals was reconfirmed in the present study, and a significant correlation was found in old rats between the magnitude of the EPSP at a fixed stimulus level and their performance on a spatial memory task.

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Post-synaptic depolarization in induction of long-term potentiation in the CA1 hippocampus

Cited by 5 publications

References 0 publications

Differential induction of LTP and LTD is not determined solely by instantaneous calcium concentration: an essential involvement of a temporal factor

Differential induction of LTP and LTD is not determined solely by instantaneous calcium concentration: an essential involvement of a temporal factor

Role of temporal summation in age-related long-term potentiation-induction deficits

Functional integrity of NMDA-dependent LTP induction mechanisms across the lifespan of F-344 rats.

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