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Duck-Joo Rhie,Ho Young Kang,Gyeong Ryul Ryu,Myung-Jun Kim,Shin Hee Yoon,Sang June Hahn,Do Sik Min,Yang-Hyeok Jo,Myung-Suk Kim 대한생리학회-대한약리학회 2003 The Korean Journal of Physiology & Pharmacology Vol.13 No.4
Interneuron diversity is one of the key factors to hinder understanding the mechanism of cortical neural network functions even with their important roles. We characterized inhibitory interneurons in layer II/III of the rat primary visual cortex, using patch-clamp recording and confocal reconstruction, and classified inhibitory interneurons into fast spiking (FS), late spiking (LS), burst spiking (BS), and regular spiking non-pyramidal (RSNP) neurons according to their electrophysiological characteristics. Global parameters to identify inhibitory interneurons were resting membrane potential (<FONT FACE= 바탕 >>70 mV) and action potential (AP) width (<FONT FACE= 바탕 ><0.9 msec at half amplitude). FS could be differentiated from LS, based on smaller amplitude of the AP (<FONT FACE= 바탕 ><∼50 mV) and shorter peak-to-trough time (P-T time) of the afterhyperpolarization (<FONT FACE= 바탕 ><4 msec). In addition to the shorter AP width, RSNP had the higher input resistance (<FONT FACE= 바탕 >>200 M<FONT FACE= 바탕 >Ω) and the shorter P-T time (<FONT FACE= 바탕 ><20 msec) than those of regular spiking pyramidal neurons. Confocal reconstruction of recorded cells revealed characteristic morphology of each subtype of inhibitory interneurons. Thus, our results provide at least four subtypes of inhibitory interneurons in layer II/III of the rat primary visual cortex and a classification scheme of inhibitory interneurons.
Rhie, Duck-Joo,Kang, Ho-Young,Ryu, Gyeong-Ryul,Kim, Myung-Jun,Yoon, Shin-Hee,Hahn, Sang-June,Min, Do-Sik,Jo, Yang-Hyeok,Kim, Myung-Suk The Korean Society of Pharmacology 2003 The Korean Journal of Physiology & Pharmacology Vol.7 No.6
Interneuron diversity is one of the key factors to hinder understanding the mechanism of cortical neural network functions even with their important roles. We characterized inhibitory interneurons in layer II/III of the rat primary visual cortex, using patch-clamp recording and confocal reconstruction, and classified inhibitory interneurons into fast spiking (FS), late spiking (LS), burst spiking (BS), and regular spiking non-pyramidal (RSNP) neurons according to their electrophysiological characteristics. Global parameters to identify inhibitory interneurons were resting membrane potential (>-70 mV) and action potential (AP) width (<0.9 msec at half amplitude). FS could be differentiated from LS, based on smaller amplitude of the AP (<∼50 mV) and shorter peak-to-trough time (P-T time) of the afterhyperpolarization (<4 msec). In addition to the shorter AP width, RSNP had the higher input resistance (>200 $M{Omega}$) and the shorter P-T time (<20 msec) than those of regular spiking pyramidal neurons. Confocal reconstruction of recorded cells revealed characteristic morphology of each subtype of inhibitory interneurons. Thus, our results provide at least four subtypes of inhibitory interneurons in layer II/III of the rat primary visual cortex and a classification scheme of inhibitory interneurons.
Phasic and Tonic Inhibition are Maintained Respectively by CaMKII and PKA in the Rat Visual Cortex
Joo, Kayoung,Yoon, Shin Hee,Rhie, Duck-Joo,Jang, Hyun-Jong The Korean Society of Pharmacology 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.6
Phasic and tonic ${\gamma}$-aminobutyric acidA ($GABA_A$) receptor-mediated inhibition critically regulate neuronal information processing. As these two inhibitory modalities have distinctive features in their receptor composition, subcellular localization of receptors, and the timing of receptor activation, it has been thought that they might exert distinct roles, if not completely separable, in the regulation of neuronal function. Inhibition should be maintained and regulated depending on changes in network activity, since maintenance of excitation-inhibition balance is essential for proper functioning of the nervous system. In the present study, we investigated how phasic and tonic inhibition are maintained and regulated by different signaling cascades. Inhibitory postsynaptic currents were measured as either electrically evoked events or spontaneous events to investigate regulation of phasic inhibition in layer 2/3 pyramidal neurons of the rat visual cortex. Tonic inhibition was assessed as changes in holding currents by the application of the $GABA_A$ receptor blocker bicuculline. Basal tone of phasic inhibition was maintained by intracellular $Ca^{2+}$ and $Ca^{2+}$/calmodulin-dependent protein kinase II (CaMKII). However, maintenance of tonic inhibition relied on protein kinase A activity. Depolarization of membrane potential (5 min of 0 mV holding) potentiated phasic inhibition via $Ca^{2+}$ and CaMKII but tonic inhibition was not affected. Thus, phasic and tonic inhibition seem to be independently maintained and regulated by different signaling cascades in the same cell. These results suggest that neuromodulatory signals might differentially regulate phasic and tonic inhibition in response to changes in brain states.
Joo, Kayoung,Cho, Kwang-Hyun,Youn, Sung-Hee,Jang, Hyun-Jong,Rhie, Duck-Joo Elsevier 2019 Brain Research Vol.1712 No.-
<P><B>Abstract</B></P> <P>Neuromodulatory facilitation of long-term synaptic plasticity is important in learning, memory, and experience-dependent cortical plasticity. Although muscarinic-induced long-term depression (mLTD) in the visual cortex is well known, its cellular mechanisms are not fully understood yet. Since endocannabinoid signaling mediates presynaptic expression of LTD in various brain areas including the primary visual cortex of rats, we investigated the involvement of endocannabinoids in the induction of mLTD in different dendritic compartments of layer 2/3 pyramidal neurons. With an unloading experiment of FM1-43 as an indicator of synaptic vesicle recycling, we confirmed that layer 1 and layer 4 stimulations mainly activated distal apical (in layer 1) and perisomatic (in layer 2/3) dendritic compartments, respectively. Bath application of muscarine (10 min) induced LTD in synaptic inputs activated by stimulation of layers 1 (L1-mLTD) and 4 (L2/3-mLTD). Both mLTDs were blocked by intracellular Ca<SUP>2+</SUP> chelator BAPTA and bath application of NMDA receptor antagonist <SMALL>D</SMALL>-AP5. However, only L2/3-mLTD exhibited an increase in paired-pulse ratio. In addition, only L2/3-mLTD was blocked by treatment with CB<SUB>1</SUB> receptor antagonist AM251. Both mLTDs were blocked by intracellular NMDA receptor antagonist MK801, but not by glia-specific metabolic inhibitor fluoroacetate, implying that neither presynaptic NMDA receptors nor astrocytes are involved in mLTD. These results suggest that L2/3-mLTD is expressed presynaptically via retrograde endocannabinoid signaling while L1-mLTD is endocannabinoid independent in layer 2/3 pyramidal neurons of the visual cortex. Therefore, layer-specific involvement of endocannabinoids in the induction of mLTD might play an important role in cortical development and information processing in the neocortex.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Endocannabinoids are involved in muscarinic-induced LTD. </LI> <LI> Endocannabinoid signaling is dendritic-compartment specific in layer 2/3 neurons. </LI> <LI> Muscarine induces endocannabinoid-dependent LTD in a layer-specific manner. </LI> <LI> Neither presynaptic NMDA receptors nor astrocytes are involved in LTD. </LI> </UL> </P>