Induction of hippocampal long‐term potentiation in the absence of extracellular Ca<sup>2+</sup>

May, P. B. Y.; Goh, Joanne W.; Sastry, B.R.

doi:10.1002/syn.890010309

Cited by 11 publications

(3 citation statements)

References 20 publications

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“…Recent evidence suggests voltage-dependent, calcium-independent transmitter release at retinal synapses (Schwartz, 1987). Until recently there has been no evidence for voltage-dependent induction of long-term synaptic plasticity; however, recent evidence suggests that calcium-independent, depolarization-dependent long-term potentiation can occur in certain neural circuits of the mammalian hippocampus (May et al, 1987). We report here evidence for voltage-dependent longterm enhancement of transmission at crayfish neuromuscular synapses.…”

Section: Synaptic Transmissionmentioning

confidence: 56%

“…LLP resembles in its magnitude and its duration the long-term potentiation phenomenon of the mammalian brain. The mechanisms responsible for the induction of long-term potentiation are still under investigation, with the bulk of evidence pointing to the role of calcium influx (Turner et al, 1982;Lynch and Baudry, 1984) into the postsynaptic neurons via voltage-dependent V-methyl-D-aspartate channels (Wigstrom and Gustafsson, 1985;Wigstrom et al, 1986) and other evidence arguing against a role for calcium in certain of the neural circuits which show long-term potentiation (May et al, 1987). The locus (or loci) of long-term potentiation is not known with certainty, although the experimental evidence obtained thus far suggests that it is at least partly presynaptic (Malenka et al, 1986;Errington, et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

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Presynaptic long-term facilitation at the crayfish neuromuscular junction: voltage-dependent and ion-dependent phases

Wojtowicz

Atwood

1988

J. Neurosci.

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Long-term facilitation (LTF) of synaptic transmission was investigated in the crayfish opener muscle to determine the factors necessary for its induction and expression. LTF was induced without action potentials by intracellular depolarization of presynaptic nerve terminals. Following induction, the synaptic transmission was enhanced by about 80% for a period of several hours. Intracellular recordings from pre- and postsynaptic cells, combined with ionic and pharmacological tests, permitted dissection of LTF into 2 phases: an initial tetanic phase that depended on the presence of both sodium and calcium ions and a subsequent long-lasting phase. This latter long-lasting enhancement of synaptic transmission was induced by repeated depolarizations of synaptic terminals but did not depend on the influx of sodium or calcium ions or on intracellular release of calcium ions. Both tetanic and long-lasting phases of LTF are attributable to activity of a single neuron, i.e., they are homosynaptic phenomena. Furthermore, LTF is associated with an increase of quantal release, whereas the size of quanta remains unchanged. During the long-lasting phase of LTF, the nerve terminal releases more transmitter for a given depolarization than before induction of LTF. Thus, the locus of LTF is presynaptic. Our findings suggest the presence of a voltage-dependent mechanism in the presynaptic membrane different from voltage-gating of Na or Ca channels. Such a mechanism may be important in the establishment of long-lasting synaptic changes at the crayfish neuromuscular junction and perhaps in other neural systems.

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Section: Synaptic Transmissionmentioning

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Presynaptic long-term facilitation at the crayfish neuromuscular junction: voltage-dependent and ion-dependent phases

Wojtowicz

Atwood

1988

J. Neurosci.

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“…In the case of LTF, the idea of a calcium-independent enhancement of transmitter release, while at first glance somewhat heretical, has been raised in other systems, particularly for certain types of long-term potentiation in the mammalian central nervous system (May, Goh, and Sastry, 1987). The nature of long-term potentiation in the mammalian central nervous system has been much investigated, and currently it is believed that both pre-and postsynaptic mechanisms play a role, although the postsynaptic mechanisms have been emphasized more in recent thinking (e.g., Wigstrom, Gustafsson, and Huang, 1988).…”

Section: Discussionmentioning

confidence: 99%

Rapid introduction of long‐lasting synaptic changes at crustacean neuromuscular junctions

1989

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In this review we present recent evidence implicating second-messenger systems in two forms of long-lasting synaptic change seen at crustacean neuromuscular junctions. Crustacean motor axons are endowed with numerous terminals, each possessing many individual synapses. Some synapses appear to be quiescent or impotent, but can be recruited in response to imposed functional demands. Supernormal impulse activity leads to long-term facilitation (LTF) which persists for many hours. During the persistent phase, additional synapses are physiologically effective, and morphological changes in synapses are seen at the ultrastructural level. Pulsatile application of serotonin, a neuromodulator, also enhances synaptic transmission, but this enhancement declines more rapidly than LTF. Elevation of intraterminal Ca2+ is neither necessary nor sufficient for long-lasting enhancement of transmission, but activation of A-kinase is necessary. LTF is set in motion by an unknown depolarization-dependent mechanism leading to A-kinase activation, whereas serotonin facilitation depends for its initiation on the phosphatidylinositol system. The initial phase of serotonin facilitation may be accounted for by production of inositol triphosphate, whereas the secondary long-lasting phase appears to require participation of both C kinase and A kinase. Neither LTF nor serotonin facilitation requires an intact neuron; both are presynaptic phenomena expressed by the nerve terminals. Brief comparison is made with long-lasting synaptic changes in other systems.

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Are Nerve Growth Factors Involved in Long-Term Synaptic Potentiation in the Hippocampus and Spatial Memory?

Sastry

Chirwa

May

et al. 1988

Synaptic Plasticity in the Hippocampus

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Induction of hippocampal long‐term potentiation in the absence of extracellular Ca²⁺

Cited by 11 publications

References 20 publications

Presynaptic long-term facilitation at the crayfish neuromuscular junction: voltage-dependent and ion-dependent phases

Presynaptic long-term facilitation at the crayfish neuromuscular junction: voltage-dependent and ion-dependent phases

Rapid introduction of long‐lasting synaptic changes at crustacean neuromuscular junctions

Are Nerve Growth Factors Involved in Long-Term Synaptic Potentiation in the Hippocampus and Spatial Memory?

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Induction of hippocampal long‐term potentiation in the absence of extracellular Ca2+

Cited by 11 publications

References 20 publications

Presynaptic long-term facilitation at the crayfish neuromuscular junction: voltage-dependent and ion-dependent phases

Presynaptic long-term facilitation at the crayfish neuromuscular junction: voltage-dependent and ion-dependent phases

Rapid introduction of long‐lasting synaptic changes at crustacean neuromuscular junctions

Are Nerve Growth Factors Involved in Long-Term Synaptic Potentiation in the Hippocampus and Spatial Memory?

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Induction of hippocampal long‐term potentiation in the absence of extracellular Ca²⁺