The Development of Phasic and Tonic Inhibition in the Rat Visual Cortex

Jang, Hyun Jong; Cho, Kwang Hyun; Park, Sung Won; Kim, Myung Joon; Yoon, Shin Hee; Rhie, Duck-Joo

doi:10.4196/kjpp.2010.14.6.399

Cited by 15 publications

(14 citation statements)

References 49 publications

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“…In accordance with the previous result, in the present study an increase of ∼20% in GABA A R‐mediated currents by diazepam was enough to suppress the induction of LTP at 5 weeks. We have also demonstrated that GABAergic inhibition continued to increase until 8 weeks of age (Jang et al, ) when plasticity was lower than at 5 weeks. Thus, an increase in the amplitude and the decay time constant of GABA A R‐mediated currents might be responsible for the developmental decrease in synaptic plasticity in the visual cortex.…”

Section: Discussionsupporting

confidence: 54%

“…The changes in the subunit ratio shorten NMDAR currents (Carmignoto and Vicini, 1992) because NMDARs containing GluN2A subunits exhibit fast opening and closing kinetics (Paoletti, 2011). The subunit composition of GABA A Rs also appears to change during the critical period because the kinetics of GABA A R-mediated currents change at this period (Jang et al, 2010). It has been suggested that the changes in NMDAR and GABA A R interact to regulate synaptic plasticity (He et al, 2006;Philpot et al, 2007).…”

mentioning

confidence: 99%

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GluN2B‐containing N‐methyl‐D‐aspartate receptors compensate for the inhibitory control of synaptic plasticity during the early critical period in the rat visual cortex

Lee

Joo

Kim

et al. 2015

J of Neuroscience Research

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In the visual cortex, synaptic plasticity is very high during the early developmental stage known as the critical period and declines with development after the critical period. Changes in the properties of N-methyl-D-aspartate receptor (NMDAR) and γ-aminobutyric acid type A receptor (GABAA R) have been suggested to underlie the changes in the characteristics of plasticity. However, it is largely unknown how the changes in the two receptors interact to regulate synaptic plasticity. The present study investigates the changes in the properties of NMDAR and GABAA R from 3 to 5 weeks of age in layer 2/3 pyramidal neurons of the rat visual cortex. The impact of these changes on the characteristics of long-term potentiation (LTP) is also investigated. The amplitude and decay time constant of GABAA R-mediated currents increased during this period. However, the decay time constant of NMDAR-mediated currents decreased as a result of the decrease in the proportion of the GluN2B subunit-mediated component. Induction of NMDAR-dependent LTP at 3 weeks depended on the GluN2B subunit, but LTP at 5 weeks did not. Enhancement of GABAA R-mediated inhibition suppressed the induction of LTP only at 5 weeks. However, partial inhibition of the GluN2B subunit with a low concentration of ifenprodil allowed the GABAA R-mediated suppression of LTP at 3 weeks. These results suggest that changes in the properties of NMDAR- and GABAA R-mediated synaptic transmission interact to determine the characteristics of synaptic plasticity during the critical period in the visual cortex.

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Section: Discussionsupporting

confidence: 54%

mentioning

confidence: 99%

GluN2B‐containing N‐methyl‐D‐aspartate receptors compensate for the inhibitory control of synaptic plasticity during the early critical period in the rat visual cortex

Lee

Joo

Kim

et al. 2015

J of Neuroscience Research

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“…In a previous study investigating the E-I ratio [ 15 ], we noticed that IPSPs increased with time when measured at 0 mV of membrane potential. In this study, we investigated the underlying mechanism for the increase in IPSP and elucidated the signaling pathways involved in the maintenance and regulation of phasic and tonic GABA A R-mediated inhibition.…”

Section: Resultsmentioning

confidence: 92%

Phasic and Tonic Inhibition are Maintained Respectively by CaMKII and PKA in the Rat Visual Cortex

Joo

Yoon

Rhie

et al. 2014

Korean J Physiol Pharmacol

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Phasic and tonic γ-aminobutyric acidA (GABAA) 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 GABAA receptor blocker bicuculline. Basal tone of phasic inhibition was maintained by intracellular Ca2+ and Ca2+/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 Ca2+ 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.

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“…Unlike the somatosensory cortex, in the visual cortex tonic GABA A -mediated currents increase with age (Jang et al, 2010). This may be related to the role of GABA in shaping neuronal circuits during a well-defined period of early postnatal development called critical period (Sale et al, 2010).…”

Section: Early In Postnatal Development Tonic Gabaergic Currents Difmentioning

confidence: 99%

Functional role of ambient GABA in refining neuronal circuits early in postnatal development

Cellot¹,

Cherubini²

2013

Front. Neural Circuits

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Early in development, γ-aminobutyric acid (GABA), the primary inhibitory neurotransmitter in the mature brain, depolarizes and excites targeted neurons by an outwardly directed flux of chloride, resulting from the peculiar balance between the cation-chloride importer NKCC1 and the extruder KCC2. The low expression of KCC2 at birth leads to accumulation of chloride inside the cell and to the equilibrium potential for chloride positive respect to the resting membrane potential. GABA exerts its action via synaptic and extrasynaptic GABAA receptors mediating phasic and tonic inhibition, respectively. Here, recent data on the contribution of “ambient” GABA to the refinement of neuronal circuits in the immature brain have been reviewed. In particular, we focus on the hippocampus, where, prior to the formation of conventional synapses, GABA released from growth cones and astrocytes in a calcium- and SNARE (soluble N-ethylmaleimide-sensitive-factor attachment protein receptor)-independent way, diffuses away to activate in a paracrine fashion extrasynaptic receptors localized on distal neurons. The transient increase in intracellular calcium following the depolarizing action of GABA leads to inhibition of DNA synthesis and cell proliferation. Tonic GABA exerts also a chemotropic action on cell migration. Later on, when synapses are formed, GABA spilled out from neighboring synapses, acting mainly on extrasynaptic α5, β2, β3, and γ containing GABAA receptor subunits, provides the membrane depolarization necessary for principal cells to reach the window where intrinsic bursts are generated. These are instrumental in triggering calcium transients associated with network-driven giant depolarizing potentials which act as coincident detector signals to enhance synaptic efficacy at emerging GABAergic and glutamatergic synapses.

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The Development of Phasic and Tonic Inhibition in the Rat Visual Cortex

Cited by 15 publications

References 49 publications

GluN2B‐containing N‐methyl‐D‐aspartate receptors compensate for the inhibitory control of synaptic plasticity during the early critical period in the rat visual cortex

GluN2B‐containing N‐methyl‐D‐aspartate receptors compensate for the inhibitory control of synaptic plasticity during the early critical period in the rat visual cortex

Phasic and Tonic Inhibition are Maintained Respectively by CaMKII and PKA in the Rat Visual Cortex

Functional role of ambient GABA in refining neuronal circuits early in postnatal development

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