Repeated ECS induces GluR1 mRNA but not NMDAR1A-G mRNA in the rat hippocampus

Peter Naylor, Caroline A. Stewart, Simon R. Wright, R. Carl A. Pearson, Ian C. Reid

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    43 Citations (Scopus)

    Abstract

    The neural basis underlying the cognitive side effects of ECT is unknown. Recent studies suggest that the memory dysfunction may be caused by alterations in hippocampal synaptic efficacy [20]. In situ hybridisation was used to examine the possible receptor mechanisms responsible for this effect. Repeated ECS markedly increased mRNA expression for the GluR1 subunit of the AMPA receptor, but not the NMDAR1A-G subtypes of the NMDA receptor, relative to control treatments. This effect was present 24 h after the last seizure and may be responsible for the expression of the ECS-induced increase in synaptic efficacy.

    Original languageEnglish
    Pages (from-to)349-353
    Number of pages5
    JournalMolecular Brain Research
    Volume35
    Issue number1-2
    DOIs
    Publication statusPublished - Jan 1996

    Keywords

    • n sity hybridization
    • AMPA receptor
    • NMDA receptor
    • Electroconvulsive stimulation
    • Long-term potentiation
    • Memory

    Cite this

    Naylor, P., Stewart, C. A., Wright, S. R., Pearson, R. C. A., & Reid, I. C. (1996). Repeated ECS induces GluR1 mRNA but not NMDAR1A-G mRNA in the rat hippocampus. Molecular Brain Research, 35(1-2), 349-353. https://doi.org/10.1016/0169-328X(95)00264-S