These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: N-methyl-D-aspartate transmission modulates GABAB-mediated inhibition of rat hippocampal pyramidal neurons in vitro.
    Author: Benardo LS.
    Journal: Neuroscience; 1995 Oct; 68(3):637-43. PubMed ID: 8577364.
    Abstract:
    Slow inhibition was investigated by stimulating inhibitory neurons at the border of stratum radiatum and lacunosum-moleculare with focal microapplications of glutamate, while recording resultant slow inhibitory postsynaptic potentials in CA1 pyramidal neurons in rat hippocampal slices. The slow inhibitory postsynaptic potentials evoked had an average peak amplitude of -2.2 mV, measured at -60 mV. Their peak conductance was 2.5 nS. These events were characterized as slow GABAB inhibitory postsynaptic potentials because they reversed at -90 mV, and were blocked by CGP 35348 (500 microM). Exposure to magnesium-free solutions augmented glutamate-evoked slow inhibitory postsynaptic potentials. Mean peak amplitude and conductance were -3.1 mV and 4.0 nS. Exposure to the N-methyl-D-aspartate antagonist MK-801 (20 microM) allowed separation of the glutamate-triggered slow inhibitory postsynaptic potential into components induced by non-N-methyl-D-aspartate and N-methyl-D-aspartate receptor activation. The N-methyl-D-aspartate component dominated, even under control conditions, and could account for up to 60% of the control slow inhibitory postsynaptic potential. Thus, the activation and recruitment of GABAB-mediated inhibition depend on both non-N-methyl-D-aspartate and N-methyl-D-aspartate-mediated excitation of inhibitory interneurons. Under physiological conditions slow inhibition may act as an important synaptic filtering mechanism, but when N-methyl-D-aspartate-mediated excitation increases, slow inhibition is further recruited, providing an important means to offset excessive excitation.
    [Abstract] [Full Text] [Related] [New Search]