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Cited by 157Neuroscience and Neuropharmacology ResearchMemory and Neural MechanismsTreatment of Major Depression

Common Molecular Pathways Mediate Long-Term Potentiation of Synaptic Excitation and Slow Synaptic Inhibition

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Huang, Cindy Shen, Shi, Song-Hai, Ule, Jernej, Ruggiu, Matteo, Barker, Laura A., Darnell, Robert B., Jan, Yuh Nung, Jan, Lily Yeh·2005·Cell
DOI 10.1016/j.cell.2005.07.033
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Abstract

Synaptic plasticity, the cellular correlate for learning and memory, involves signaling cascades in the dendritic spine. Extensive studies have shown that long-term potentiation (LTP) of the excitatory postsynaptic current (EPSC) through glutamate receptors is induced by activation of N-methyl-D-asparate receptor (NMDA-R)--the coincidence detector--and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). Here we report that the same signaling pathway in the postsynaptic CA1 pyramidal neuron also causes LTP of the slow inhibitory postsynaptic current (sIPSC) mediated by metabotropic GABA(B) receptors (GABA(B)-Rs) and G protein-activated inwardly rectifying K(+) (GIRK) channels, both residing in dendritic spines as well as shafts. Indicative of intriguing differences in the regulatory mechanisms for excitatory and inhibitory synaptic plasticity, LTP of sIPSC but not EPSC was abolished in mice lacking Nova-2, a neuronal-specific RNA binding protein that is an autoimmune target in paraneoplastic opsoclonus myoclonus ataxia (POMA) patients with latent cancer, reduced inhibitory control of movements, and dementia.

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Crossref · 10.1016/j.cell.2005.07.033

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  • The slow GABA B receptor-mediated IPSP can be potentiated if the postsynaptic neuron is strongly depolarized.

    “The slow GABA B receptor-mediated inhibitory postsynaptic potential (IPSP) can also be potentiated if the postsynaptic neuron is strongly depolarized (Huang et al. 2005).”

    From NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD). (2012) · cites this paper as Huang et al. 2005

  • The increase of this IPSP depends on NMDAR activation and CaMKII, sharing two key properties with hippocampal LTP of AMPARs.

    “The increase of this IPSP also depends on NMDAR activation and CaMKII, thus sharing two key properties with hippocampal LTP of AMPARs.”

    From NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD). (2012) · cites this paper as Huang et al. 2005

  • Long-term potentiation of excitatory post-synaptic currents is unchanged in Nova2-null hippocampus, as are basal excitatory and inhibitory synaptic transmission.

    “By contrast, long-term potentiation of excitatory post-synaptic currents is unchanged, as are basal excitatory and inhibitory synaptic transmission.”

    From The neurogenetics of alternative splicing (2016) · cites this paper as [100]

  • Mis-splicing of GABAB receptors and GIRK channels probably leads to deficient long-term potentiation of the slow inhibitory current seen in the Nova2-null hippocampus.

    “Mis-splicing of GABAB receptors and GIRK channels probably leads to deficient long-term potentiation of the slow inhibitory current seen in the Nova2-null hippocampus100.”

    From The neurogenetics of alternative splicing (2016) · cites this paper as [100]

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Authors
Huang, C. S., Shi, S.-H., Ule, J., Ruggiu, M., Barker, L. A., Darnell, R. B., Jan, Y. N., & Jan, L. Y.
Affiliations
  • Howard Hughes Medical Institute (US)
  • University of California, San Francisco (US)
Corresponding author
Jan, Lily Yeh
ORCID
Venue
Cell
Publisher
Elsevier BV
Published
2005-10
Volume
123
Issue
1
Pages
105-118
ISSN
0092-8674 (ISSN-L)
DOI
10.1016/j.cell.2005.07.033
OpenAlex
W2113596954
Cited by
157
References
78
Citations by year
2026: 1 · 2025: 7 · 2024: 7 · 2023: 3 · 2022: 5 · 2021: 3 · 2020: 13 · 2019: 5 · 2018: 5 · 2017: 7 · 2016: 9 · 2015: 5 · 2014: 5 · 2013: 8 · 2012: 10
FWCI
3.45
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
Funders
  • National Institutes of Health
  • National Institute of Mental Health (MH63981, P50MH063981)
  • National Institute of Neurological Disorders and Stroke (R01NS040955, R01NS047200, NS047200)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
Keywords
long-term potentiation, synaptic plasticity, dendritic spines, NMDA receptor, CaMKII, GABAB receptors, GIRK channels, excitatory postsynaptic currents, CA1 pyramidal neurons, RNA-binding proteins, glutamate signaling
MeSH terms
Neuro-Oncological Ventral Antigen, Animals, Cells, Cultured, Electric Stimulation, Hippocampus, Nerve Tissue Proteins, Neural Inhibition, Synaptic Transmission, Organ Culture Techniques, Synapses, Signal Transduction, RNA-Binding Proteins, Rats, Sprague-Dawley, Long-Term Potentiation, Calcium-Calmodulin-Dependent Protein Kinases, Pyramidal Cells, Receptors, GABA-B, Mice, Knockout, GABA Antagonists, Excitatory Postsynaptic Potentials, Dendritic Spines, Mice, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2, GABA-B Receptor Antagonists

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