title: Enhanced lateral inhibition in the barrel cortex by deletion of phospholipase C-related catalytically inactive protein-1/2 in mice.
abstract: We previously demonstrated that the deletion of phospholipase C-related catalytically inactive protein-1/2 (PRIP-1/2) enhances the desensitization of GABAA receptors (GABAARs), while it facilitates their resensitization at the offset of GABA puff, causing a hump-like tail current (tail-I) in layer 3 (L3) pyramidal cells (PCs) of the barrel cortex. In the present study, we investigated whether inhibitory synaptic transmission in L3 PCs in the barrel cortex is altered in the PRIP-1/2 double-knockout (PRIP-DKO) mice, and if so, how the interaction between excitation and inhibition is subsequently modified. PRIP-1/2 deletion resulted in the prolongation of the decay phase of inhibitory postsynaptic currents/potentials (IPSCs/IPSPs) in L3 PCs evoked by stimulation of L3, leaving the overall features of miniature IPSCs unchanged. An optical imaging revealed that the spatiotemporal profile of a horizontal excitation spread across columns in L2/3 caused by L4 stimulation in the barrel cortex was more restricted in PRIP-DKO mice compared to the wild type, while those obtained in the presence of bicuculline were almost identical between the two genotypes. These findings suggest that PRIP-1/2 deletion enhances the lateral inhibition by prolonging inhibitory synaptic actions to limit the intercolumnar integration in the barrel cortex. Considering the present findings together with our previous study including a mathematical simulation, the prolongation of inhibitory synaptic actions is likely to result from an enhancement of desensitization followed by an enhanced resensitization in GABAARs.
authors.affiliation: Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, 1-8, Yamadaoka, Suita, Osaka, 565-0871, Japan.
authors.forename: Hiroki
authors.initials: H
authors.lastname: Toyoda
authors.affiliation: Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, 1-8, Yamadaoka, Suita, Osaka, 565-0871, Japan.
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Saito
authors.affiliation: Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, 1-8, Yamadaoka, Suita, Osaka, 565-0871, Japan.
authors.forename: Hajime
authors.initials: H
authors.lastname: Sato
authors.affiliation: Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, 1-8, Yamadaoka, Suita, Osaka, 565-0871, Japan.
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Kawano
authors.affiliation: Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, 1-8, Yamadaoka, Suita, Osaka, 565-0871, Japan.|Nourishment Function Laboratory, Health Care Division, Morinaga & Co., Ltd., Yokohama, Kanagawa, 230-8504, Japan.
authors.forename: Shinpei
authors.initials: S
authors.lastname: Kawakami
authors.affiliation: Department of Fixed Prosthodontics, Osaka University Graduate School of Dentistry, Suita, Osaka, 565-0871, Japan.
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Yatani
authors.affiliation: Department of Dental Pharmacology, Division of Integrated Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, 734-8553, Japan.
authors.forename: Takashi
authors.initials: T
authors.lastname: Kanematsu
authors.affiliation: Laboratory of Molecular and Cellular Biochemistry, Faculty of Dental Science, Kyushu University, Fukuoka, 812-8582, Japan.
authors.forename: Masato
authors.initials: M
authors.lastname: Hirata
authors.affiliation: Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, 1-8, Yamadaoka, Suita, Osaka, 565-0871, Japan. kang@dent.osaka-u.ac.jp.
authors.forename: Youngnam
authors.initials: Y
authors.lastname: Kang
mesh_terms: D048868:Adaptor Proteins, Signal Transducing / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D005260:Female; D017353:Gene Deletion; D053444:Inhibitory Postsynaptic Potentials; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D017966:Pyramidal Cells / Q000378:metabolism* / Q000502:physiology; D013003:Somatosensory Cortex / Q000166:cytology / Q000378:metabolism* / Q000502:physiology
chemical_list: D048868:Adaptor Proteins, Signal Transducing; D047908:Intracellular Signaling Peptides and Proteins; C496391:Plcl1 protein, mouse; C530633:Plcl2 protein, mouse