title: GABA(B)  receptor-mediated presynaptic inhibition reverses inter-columnar covariability of synaptic actions by intracortical axons in the rat barrel cortex.
abstract: Intracortical axons originating from pyramidal cells in layer 3 of the rat somatosensory cortex are shared between adjacent columns, and receive the presynaptic inhibition that is mediated by the GABA(B)  receptor. Synaptic actions by intracortical axons of single layer 3 pyramidal cells covary between the two adjacent columns in response to stimulation of layer 3 of either column. We examined whether GABA(B)  receptor-mediated presynaptic inhibition affects the covariability of synaptic actions by intracortical axons between adjacent columns in slice preparations of the rat barrel cortex. Paired stimulations of superficial layer 3 evoked first and second excitatory postsynaptic currents (EPSCs) of varying amplitudes, yielding varying paired-pulse depression of EPSCs in layer 3 pyramidal cells that were located in the stimulated column, but not in its adjacent column. The amplitude of the second EPSC was inversely proportional to that of the first EPSC in layer 3 pyramidal cells in the stimulated column, yielding a negative correlation coefficient between the first and second EPSCs. Baclofen and CGP55845 attenuated paired-pulse depression and abolished the inverse relationship. Simultaneous recordings from two layer 3 pyramidal cells in the stimulated and adjacent columns revealed a positive correlation between the paired first EPSC amplitudes and a negative correlation between the paired second EPSC amplitudes, which, respectively, indicate the positive and negative covariability of synaptic actions by intracortical axons between the two adjacent columns. These results suggest that GABA(B)  receptor-mediated presynaptic inhibition can reverse the positive covariability of inter-columnar synaptic actions, which may serve as a basis for inter-columnar desynchronisation.
authors.affiliation: Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, Suita, Osaka, Japan.
authors.forename: Hajime
authors.initials: H
authors.lastname: Sato
authors.forename: Hiroki
authors.initials: H
authors.lastname: Toyoda
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Saito
authors.forename: Masayuki
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Daniel
authors.initials: D
authors.lastname: Althof
authors.forename: Ákos
authors.initials: Á
authors.lastname: Kulik
authors.forename: Youngnam
authors.initials: Y
authors.lastname: Kang
mesh_terms: D000818:Animals; D001369:Axons / Q000378:metabolism / Q000502:physiology; D001418:Baclofen / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials; D058786:GABA-B Receptor Agonists / Q000494:pharmacology; D058788:GABA-B Receptor Antagonists / Q000494:pharmacology; D009433:Neural Inhibition; D017966:Pyramidal Cells / Q000378:metabolism* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D018080:Receptors, GABA-B / Q000378:metabolism*; D013003:Somatosensory Cortex / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D013569:Synapses / Q000378:metabolism* / Q000502:physiology
chemical_list: D058786:GABA-B Receptor Agonists; D058788:GABA-B Receptor Antagonists; D018080:Receptors, GABA-B; D001418:Baclofen