GABA-B RECEPTOR-MEDIATED INHIBITORY POSTSYNAPTIC POTENTIALS-EVOKED BY ELECTRICAL-STIMULATION AND BY GLUTAMATE STIMULATION OF INTERNEURONS IN STRATUM-LACUNOSUM-MOLECULARE IN HIPPOCAMPAL CA1 PYRAMIDAL CELLS-INVITRO

Following micropressure application of glutamate (500-mu-M) 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-mu-M) 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 GABA(B) antagonist 2-OH saclofen (1-4 mM) reduced both glut-IPSPs and late IPSPs but not early IPSPs. In contrast, the GABA(B) antagonist phaclofen (20 mM) reduced late IPSPs but not early IPSPs or glut-IPSPs. Barium (1 mM), a blocker of some K+ channels, diminished late IPSPs but not early IPSPs or glut-IPSPs. Early IPSPs were blocked by the GABA(A) 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 GABA(B) receptor-mediated IPSP. The discrepancy in the pharmacological profile of the GABA(B) glut-IPSPs and of the GABA(B) late IPSPs may suggest the presence of two GABA(B) mechanisms in CA1 pyramidal cells.