Evidence map›Paper›PMID 11222663›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Contribution of postsynaptic Ca2+ to the induction of post-tetanic potentiation in the neural circuit for siphon withdrawal in Aplysia.

J H Schaffhausen, T M Fischer, T J Carew

Open access · bronzeAbstract read
PubMed Full text at PMC
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Persistent long-term facilitation at an identified synapse becomes labile with activation of short-term heterosynaptic plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  3. A novel postsynaptic mechanism for heterosynaptic sharing of short-term plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  4. Multiple forms of long-term potentiation and long-term depression converge on a single interneuron in the leech CNS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004
    Article
  5. Article
  6. Presynaptic and postsynaptic mechanisms of a novel form of homosynaptic potentiation at aplysia sensory-motor neuron synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  7. Contribution of postsynaptic Ca2+ to the induction of post-tetanic potentiation in the neural circuit for siphon withdrawal in Aplysia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

J H SchaffhausenDepartment of Psychology, Yale University, New Haven, Connecticut 06520, USA.
T M Fischer
T J Carew
University of California, Irvine · USWayne State University · USYale University · US

Funding

NEUROCOMPUTATIONAL ANALYSIS OF LEARNINGR01MH048672 · NIMH · YALE UNIVERSITY · PI CAREW, THOMAS J · 1994 to 2001
$443k
NIMH NIH HHS 5R01 MH 48672-04-06
6 · The paper itself

Abstract

Recent studies in Aplysia have revealed a novel postsynaptic Ca(2+) component to posttetanic potentiation (PTP) at the siphon sensory to motor neuron (SN-MN) synapse. Here we asked whether the postsynaptic Ca(2+) component of PTP was a special feature of the SN-MN synapse, and if so, whether it reflected a unique property of the SN or the MN. We examined whether postsynaptic injection of BAPTA reduced PTP at SN synapses onto different postsynaptic targets by comparing PTP at SN-MN and SN-interneuron (L29) synapses. We also examined PTP at L29-MN synapses. Postsynaptic BAPTA reduced PTP only at the SN-MN synapse; it did not affect PTP at either the SN-L29 or the L29-MN synapse, indicating that the SN and the MN do not require postsynaptic Ca(2+) for PTP with all other synaptic partners. The postsynaptic Ca(2+) component of PTP is present at other Aplysia SN-MN synapses; tail SN-MN synapses also showed reduced PTP when the MN was injected with BAPTA. Surprisingly, in both tail and siphon SN-MN synapses, there was an inverse relationship between the initial size of the EPSP and the postsynaptic component to PTP; only the initially weak SN-MN synapses showed a BAPTA-sensitive component. Homosynaptic depression of initially strong SN-MN synapses into the size range of initially weak synapses did not confer postsynaptic Ca(2+) sensitivity to PTP. Finally, the postsynaptic Ca(2+) component of PTP could be induced in the presence of APV, indicating that it is not mediated by NMDA receptors. These results suggest a dual model for PTP at the SN-MN synapse, in which a postsynaptic Ca(2+) contribution summates with the conventional presynaptic mechanisms to yield an enhanced form of PTP.

Indexed as

2-Amino-5-phosphonovalerateAnimalsAplysiaCalciumChelating AgentsDose-Response Relationship, DrugEgtazic AcidExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsLong-Term PotentiationMicroinjectionsNerve NetNeuronal PlasticityNeurons, AfferentPerfusionReceptors, N-Methyl-D-Aspartate1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid2-Amino-5-phosphonovalerateCalciumChelating AgentsEgtazic AcidExcitatory Amino Acid AntagonistsReceptors, N-Methyl-D-Aspartate

Identifiers

PMID11222663
PMCPMC6762945
OpenAlexW1926244495

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.