GABA<sub>B</sub>‐ and GABA<sub>A</sub>‐receptor‐mediated regulation of Up and Down states across development

Kaplanian, Ani; Vinos, Michael; Skaliora, Irini

doi:10.1113/jp282736

Cited by 3 publications

(4 citation statements)

References 134 publications

(147 reference statements)

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“…Thus, GABAbRs control SST-IN activity indirectly via the regulation of glutamatergic synaptic drive. This might be due to regulation of presynaptic release at Pyr-SST synapses, or by more complex circuit level effects 21 , 22 .…”

Section: Resultsmentioning

confidence: 99%

Somatostatin-expressing interneurons modulate neocortical network through GABAb receptors in a synapse-specific manner

Kanigowski

Bogaj

Barth

et al. 2023

Sci Rep

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The firing activity of somatostatin-expressing inhibitory neurons (SST-INs) can suppress network activity via both GABAa and GABAb receptors (Rs). Although SST-INs do not receive GABAaR input from other SST-INs, it is possible that SST-IN-released GABA could suppress the activity of SST-INs themselves via GABAbRs, providing a negative feedback loop. Here we characterized the influence of GABAbR modulation on SST-IN activity in layer 2/3 of the somatosensory cortex in mice. We compared this to the effects of GABAbR activation on parvalbumin-expressing interneurons (PV-INs). Using in vitro whole-cell patch clamp recordings, pharmacological and optogenetic manipulations, we found that the firing activity of SST-INs suppresses excitatory drive to themselves via presynaptic GABAbRs. Postsynaptic GABAbRs did not influence SST-IN spontaneous activity or intrinsic excitability. Although GABAbRs at pre- and postsynaptic inputs to PV-INs are modestly activated during cortical network activity in vitro, the spontaneous firing of SST-INs was not the source of GABA driving this GABAbR activation. Thus, SST-IN firing regulates excitatory synaptic strength through presynaptic GABAbRs at connections between pyramidal neurons (Pyr-Pyr) and synapses between pyramidal neurons and SST-INs (Pyr-SST), but not Pyr-PV and PV-Pyr synapses. Our study indicates that two main types of neocortical inhibitory interneurons are differentially modulated by SST-IN-mediated GABA release.

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Section: Resultsmentioning

confidence: 99%

Somatostatin-expressing interneurons modulate neocortical network through GABAb receptors in a synapse-specific manner

Kanigowski

Bogaj

Barth

et al. 2023

Sci Rep

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“…Given that synchronous inhibitory activity to the distal apical dendrites from low threshold spiking SST‐positive interneurons entails the oscillatory frequency of the network in the beta band (Li et al, 2013), the decrease in the beta oscillation power is quite conceivable after selective Satb1 knockout. Finally, we should consider that the Up‐Down state activity (UDS) is a developmentally regulated network phenomenon, as we have previously shown (Kaplanian et al, 2022; Rigas et al, 2015), and future studies should examine whether the alterations we report during this developmental period persist into adulthood.…”

Section: Discussionmentioning

confidence: 64%

“…LFP traces were exported to MATLAB format and analyzed with the use of LFPAnalyzer, an in‐house‐developed software (Kaplanian et al, 2022; Tsakanikas et al, 2017). Briefly, for the automatic detection of LFP bursts: (i) input signals were pre‐processed by DC offset subtraction and low‐pass filtering at 200 Hz; (ii) two feature sequences were extracted for each segment, based on two complementary mathematical transformations (Hilbert and Short energy); (iii) a dynamic, data‐driven threshold‐based on Gaussian mixture models was estimated for each feature sequence and used to create a mask; and (iv) the two masks were combined using a logical OR operator and used for the detection of the onset and offset of the LFP events.…”

Section: Methodsmentioning

confidence: 99%

The role of selective SATB1 deletion in somatostatin expressing interneurons on endogenous network activity and the transition to epilepsy

Vasilopoulos

Kaplanian

Vinos

et al. 2022

J of Neuroscience Research

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Somatostatin (SST) expressing interneurons are the second most abundant group of inhibitory neurons in the neocortex. They mainly target the apical dendrites of excitatory pyramidal cells and are implicated in feedforward and feedback inhibition. In the present study, we employ a conditional knockout mouse, in which the transcription factor Satb1 is selectively deleted in SST‐expressing interneurons resulting to the reduction of their number across the somatosensory barrel field. Our goal was to investigate the effect of the reduced number of Satb1 mutant SST‐interneurons on (i) the endogenous cortical network activity (spontaneously recurring Up/Down states), and (ii) the transition to epileptiform activity. By conducting LFP recordings in acute brain slices from young male and female mice, we demonstrate that mutant animals exhibit significant changes in network excitability, reflected in increased Up state occurrence, decreased Up state duration and higher levels of extracellular spiking activity. Epileptiform activity was induced through two distinct and widely used in vitro protocols: the low magnesium and the 4‐Aminopyridine (4‐AP) model. In the former, slices from mutant animals manifested shorter latency for the expression of stable seizure‐like events. In contrast, when epilepsy was induced by 4‐AP, no significant differences were reported. We conclude that normal SST‐interneuron function has a significant role both in the regulation of the endogenous network activity, and in the transition to seizure‐like discharges in a context‐dependent manner.

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Section: Resultsmentioning

confidence: 99%

SST interneurons modulate neocortical network through GABAb receptors in a synapse- specific manner

Kanigowski

Bogaj

Barth

et al. 2023

Preprint

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The firing activity of somatostatin-expressing inhibitory neurons (SST-INs) can suppress network activity via both GABAa and GABAb receptors (Rs). Although SST-INs do not receive GABAaR input from other SST-INs, it is possible that SST-IN-released GABA could suppress the activity of SST-INs themselves via GABAbRs, providing a negative feedback loop. Here we characterized the influence of GABAbR modulation on SST-IN activity in layer 2/3 of the somatosensory cortex in mice. We compared this to the effects of GABAbR activation on parvalbumin-expressing interneurons (PV-INs). Using in vitrowhole-cell patch clamp recordings, pharmacological and optogenetic manipulations, we found that the firing activity of SST-INs suppresses excitatory drive to themselves via presynaptic GABAbRs. Postsynaptic GABAbRs did not influence SST-IN spontaneous activity or intrinsic excitability. Although GABAbRs at pre- and postsynaptic inputs to PV-INs are modestly activated during cortical network activity in vitro, the spontaneous firing of SST-INs was not the source of GABA driving this GABAbR activation. Thus, SST-IN firing regulates excitatory synaptic strength through presynaptic GABAbRs at connections between pyramidal neurons (Pyr-Pyr) and synapses between pyramidal neurons and SST-INs (Pyr-SST), but not Pyr-PV and PV-Pyr synapses. Our study indicates that two main types of neocortical inhibitory interneurons are differentially modulated by SST-IN-mediated GABA release.

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GABA_B‐ and GABA_A‐receptor‐mediated regulation of Up and Down states across development

Abstract: support-information-section).

Cited by 3 publications

References 134 publications

Somatostatin-expressing interneurons modulate neocortical network through GABAb receptors in a synapse-specific manner

Somatostatin-expressing interneurons modulate neocortical network through GABAb receptors in a synapse-specific manner

The role of selective SATB1 deletion in somatostatin expressing interneurons on endogenous network activity and the transition to epilepsy

SST interneurons modulate neocortical network through GABAb receptors in a synapse- specific manner

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GABAB‐ and GABAA‐receptor‐mediated regulation of Up and Down states across development

Abstract: support-information-section).

Cited by 3 publications

References 134 publications

Somatostatin-expressing interneurons modulate neocortical network through GABAb receptors in a synapse-specific manner

Somatostatin-expressing interneurons modulate neocortical network through GABAb receptors in a synapse-specific manner

The role of selective SATB1 deletion in somatostatin expressing interneurons on endogenous network activity and the transition to epilepsy

SST interneurons modulate neocortical network through GABAb receptors in a synapse- specific manner

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GABA_B‐ and GABA_A‐receptor‐mediated regulation of Up and Down states across development