Postsynaptic contribution to long-term potentiation revealed by the analysis of miniature synaptic currents

Manabe, Toshiya; Renner, P.; Nicoll, Roger A.

doi:10.1038/355050a0

Cited by 361 publications

(170 citation statements)

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“…Quanta1 analyses (Bekkers and Stevens, 1990;Malinow and Tsien, 1990;Larkman et al, 1992;Liao et al, 1992;Manabe et al, 1992;Voronin, 1993;Kullmann, 1994) have indicated that all of the statistical parameters of quanta1 transmission-quanta1 size, q; number of available release units, n; and probability of quanta1 release, P-may be altered in LTP Morphological changes in dendritic spines could in principle affect any of these parameters (Carlin and Siekevitz, 1983;Harris and Stevens, 1989;Calverley and Jones, 1990;Edwards, 1991;Lisman and Harris, 1993;McNaughton, 1993;Bailey and Kandel, 1993). Thus, for example, if quanta1 release saturates available receptors at central synapses (Redman, 1990;Korn and Faber, 1991;Tong and Jahr, 1994), spine growth incorporating more postsynaptic receptors could yield increased q.…”

Section: Discussionmentioning

confidence: 99%

Repeated confocal imaging of individual dendritic spines in the living hippocampal slice: evidence for changes in length and orientation associated with chemically induced LTP

et al. 1995

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Using confocal microscopy in conjunction with microdrop application of Dil, we have imaged and measured individual dendritic spines of living hippocampal CA1 pyramidal neurons in acute brain slices, before and approximately 3 hr after induction of long-term potentiation by chemical means. Statistical analysis of changes in the length of individual spines, and comparison with results of Monte Carlo simulations, suggests that two forms of structural change occur in chemically induced long-term potentiation: growth of a subpopulation of small spines, and angular displacement of spines. These changes could provide a structural basis for the expression of long-term potentiation.

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Section: Discussionmentioning

confidence: 99%

Repeated confocal imaging of individual dendritic spines in the living hippocampal slice: evidence for changes in length and orientation associated with chemically induced LTP

et al. 1995

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“…However, Manabe et al 119921 found that LTP produces a marked increase of spontaneous miniature postsynaptic potentials in CA1 neurons, which suggests a postsynaptic change, perhaps at the receptor level. Of course, the findings of Manabe et al [1992] do not rule out a simultaneous presynaptic change.…”

Section: Ltp Maintenancementioning

confidence: 99%

Long‐term potentiation and the mechanisms of memory

Izquierdo

1993

Drug Development Research

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Long-term potentiation (LIP) is a cellular model of the memory processes that occurs in many nerve cells, usually at glutamatergic synapses. For this reason, glutamatergic synapses being the most abundant in the brain, LTP has been widely proposed as a mechanism of memory. Recent findings support this proposal and indicate that, indeed, LTP and memory processes share many properties. The initial steps of LTP and of memory involve the activation of glutamatergic NMDA (N-methyl-D-asprtate) receptors, sensitive to AP5 (amino phosphono valerate), and are very sensitive to inhibition by GABA, (gamma amino butyric acid type A) receptor agonists. The phase that follows in the next 2 or 3 h depends on activation of protein kinase C (PKC) and is sensitive to inhibitors of this enzyme family. Like LTP, the underlying mechanism of memories persists for very long periods without the need of expression; and, like LTP, memories are readily expressed upon a reinstatement of the stimuli used in their induction, as i s the case in test sessions. The expression of LTP and the expression of memory rely on AMPA (D,L-alpha-amino hydroxy methyl isoxazolone propionate) receptors sensitive to CNQX (cyano nitro quinoxaline dione). LTP occurs in many places within the brain, including the hippocampus, amygala, medial septum, and entorhinal cortex. The drug effects on memory mentioned above are seen when the drugs are infused into these brain regions. The region(s) involved depend on the type of memory being processed. These findings support the idea that LTP underlies memory acquisition, retention, and retrieval (the latter, at least for many days after acquisition) and may provide some clues for the development of drugs to alleviate memory disorders. o 1993 Wiley-Liss, Inc.

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“…(1) The amplitude of miniature EPSCs (mEPSCs) is increased (decreased) during LTP (LTD) (Manabe et al, 1992;Oliet et al, 1996). (2) Hippocampal LTP (LTD) is accompanied by a higher (lower) sensitivity of the postsynaptic membrane for exogenously applied agonists (Davies et al, 1989;Kandler et al, 1998).…”

Section: Abstract: Caged Compounds; Expression Site; Ltp; Ltd; Neocomentioning

confidence: 99%

Neocortical Long-Term Potentiation and Long-Term Depression: Site of Expression Investigated by Infrared-Guided Laser Stimulation

2002

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The synaptic site of expression of long-term potentiation (LTP) and long-term depression (LTD) is still a matter of debate. To address the question of presynaptic versus postsynaptic expression of neocortical LTP and LTD in a direct approach, we measured the glutamate sensitivity of apical dendrites of layer 5 pyramidal neurons during LTP and LTD. We used infraredguided laser stimulation to release glutamate from its "caged" form with high spatial and temporal resolution. Responses to photolytically released glutamate and synaptically evoked EPSPs were recorded with patch-clamp pipettes from the neuronal somata. LTP and LTD could be induced by electrical stimulation at the same synapses in succession. The NMDA receptor-dependent LTD was accompanied by a decrease in the dendritic glutamate sensitivity, suggesting a postsynaptic expression of neocortical LTD. In contrast, LTP was never accompanied by a change in the dendritic glutamate sensitivity. A possible explanation for this finding is a presynaptic expression of neocortical LTP. Another set of experiments corroborated these results: Photolytic application of glutamate with a frequency of 5 Hz caused a long-lasting Ca 2ϩ and NMDA receptor-dependent decrease in the dendritic glutamate sensitivity. In contrast, LTP of dendritic glutamate sensitivity was never induced by photostimulation, despite several experimental modifications to prevent washout of the induction mechanism and to induce a stronger postsynaptic Ca 2ϩ influx. In conclusion, our findings provide strong evidence for a postsynaptic expression of neocortical LTD and favor a primarily presynaptic locus of neocortical LTP. Key words: caged compounds; expression site; LTP; LTD; neocortex; photostimulationLong-term potentiation (LTP) and long-term depression (LTD) of glutamatergic synapses are considered cellular correlates for learning and memory. The molecular mechanisms that underlie the induction and expression of LTP and LTD have been investigated extensively, primarily in the hippocampus. Most of the available evidence speaks in favor of a postsynaptic induction of LTP and LTD by a rise in the intracellular Ca 2ϩ concentration. However, the synaptic site of expression of LTP and LTD is still a matter of debate.Evidence for a postsynaptic expression of LTP and LTD is provided by several observations. (1) The amplitude of miniature EPSCs (mEPSCs) is increased (decreased) during LTP (LTD) (Manabe et al., 1992;Oliet et al., 1996). (2) Hippocampal LTP (LTD) is accompanied by a higher (lower) sensitivity of the postsynaptic membrane for exogenously applied agonists (Davies et al., 1989;Kandler et al., 1998). (3) A synaptic insertion (redistribution) of AMPA receptors occurs after the induction of LTP (LTD) (Liao et al

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Postsynaptic contribution to long-term potentiation revealed by the analysis of miniature synaptic currents

Cited by 361 publications

References 32 publications

Repeated confocal imaging of individual dendritic spines in the living hippocampal slice: evidence for changes in length and orientation associated with chemically induced LTP

Repeated confocal imaging of individual dendritic spines in the living hippocampal slice: evidence for changes in length and orientation associated with chemically induced LTP

Long‐term potentiation and the mechanisms of memory

Neocortical Long-Term Potentiation and Long-Term Depression: Site of Expression Investigated by Infrared-Guided Laser Stimulation

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