GABAB receptor‐mediated inhibitory postsynaptic potentials evoked by electrical stimulation and by glutamate stimulation of interneurons in Stratum lacunosum‐moleculare in hippocampal CA1 pyramidal cells in vitro

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Abstract
Following micropressure application of glutamate (500 μM) in stratum lacunosum‐moleculare (L‐M), inhibitory postsynaptic potentials (glut‐IPSPs) were recorded in CA1 pyramidal cells. These glut‐IPSPs were blocked by tetrodotoxin (1 μM) and, thus, were probably generated by the activation of local interneurons. The effects of pharmacological antagonists on glut‐IPSPs and on electrically‐evoked early and late IPSPs were assessed in the same cells during the same application of the antagonist. Local application of the GABAB antagonist 2‐OH saclofen (1–4 mM) reduced both glut‐IPSPs and late IPSPs but not early IPSPs. In contrast, the GABAB antagonist phaclofen (20 mM) reduced late IPSPs but not early IPSPs or glut‐IPSPs. Early IPSPs were blocked by the GABAA antagonists bicuculline and picrotoxin but late IPSPs and glut‐IPSPs were not. Repetitive electrical stimulation depressed early and late IPSPs as well as glut‐IPSPs, suggesting that interneurons activated with glutamate were also stimulated electrically. Thus, interneurons in str. lacunosum‐moleculare appear to inhibit pyramidal cells via a GABAB receptor‐mediated IPSP. The discrepancy in the pharmacological profile of the GABAB glut‐IPSPs and of the GABAB late IPSPs may suggest the presence of two GABAB mechanisms in CA1 pyramidal cells.