Evidence map›Paper›PMID 16339032›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Modulation of NMDA receptors by pituitary adenylate cyclase activating peptide in CA1 neurons requires G alpha q, protein kinase C, and activation of Src.

D S Macdonald, M Weerapura, M A Beazely, L Martin, W Czerwinski, J C Roder, B A Orser, J F MacDonald

Erratum issuedOpen access · bronzeAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

57 citing papers in PubMed, 112 citations in OpenAlex.

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  20. Long-Term Depression Induced by Optogenetically Driven Nociceptive Inputs to Trigeminal Nucleus Caudalis or Headache Triggers.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

D S MacdonaldDepartment of Pharmacology, Faculty of Medicine, University of Toronto, Mount Sinai Hospital, Toronto, Ontario, M5S 1A8, Canada.
M Weerapura
M A Beazely
L Martin
W Czerwinski
J C Roder
B A Orser
J F MacDonald
Canada Research Chairs · CAMount Sinai Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

At CA1 synapses, activation of NMDA receptors (NMDARs) is required for the induction of both long-term potentiation and depression. The basal level of activity of these receptors is controlled by converging cell signals from G-protein-coupled receptors and receptor tyrosine kinases. Pituitary adenylate cyclase activating peptide (PACAP) is implicated in the regulation of synaptic plasticity because it enhances NMDAR responses by stimulating Galphas-coupled receptors and protein kinase A (Yaka et al., 2003). However, the major hippocampal PACAP1 receptor (PAC1R) also signals via Galphaq subunits and protein kinase C (PKC). In CA1 neurons, we showed that PACAP38 (1 nM) enhanced synaptic NMDA, and evoked NMDAR, currents in isolated CA1 neurons via activation of the PAC1R, Galphaq, and PKC. The signaling was blocked by intracellular applications of the Src inhibitory peptide Src(40-58). Immunoblots confirmed that PACAP38 biochemically activates Src. A Galphaq pathway is responsible for this Src-dependent PACAP enhancement because it was attenuated in mice lacking expression of phospholipase C beta1, it was blocked by preventing elevations in intracellular Ca2+, and it was eliminated by inhibiting either PKC or cell adhesion kinase beta [CAKbeta or Pyk2 (proline rich tyrosine kinase 2)]. Peptides that mimic the binding sites for either Fyn or Src on receptor for activated C kinase-1 (RACK1) also enhanced NMDAR in CA1 neurons, but their effects were blocked by Src(40-58), implying that Src is the ultimate regulator of NMDARs. RACK1 serves as a hub for PKC, Fyn, and Src and facilitates the regulation of basal NMDAR activity in CA1 hippocampal neurons.

Indexed as

Amino Acid SequenceAnimalsEnzyme ActivationGTP-Binding Protein alpha Subunits, Gq-G11HippocampusIn Vitro TechniquesMiceMice, KnockoutMolecular Sequence DataNeuronsPituitary Adenylate Cyclase-Activating PolypeptideProtein Kinase CRatsRats, WistarReceptors, N-Methyl-D-Aspartatesrc-Family KinasesGTP-Binding Protein alpha Subunits, Gq-G11Pituitary Adenylate Cyclase-Activating PolypeptideProtein Kinase CReceptors, N-Methyl-D-Aspartatesrc-Family Kinases

Identifiers

PMID16339032
PMCPMC6725893
OpenAlexW2073831388

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.