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Johantges, A. C.

Publications and source records attributed to Johantges, A. C..

3 recordsLinked to original sources

Dendrite-targeting inhibitory interneurons form biased circuits with deep and superficial pyramidal cells in hippocampal CA1

In CA1 hippocampus, pyramidal cells (PCs) can be classified as deep or superficial based on their radial position within the stratum pyramidale. Deep and superficial PCs form biased circuits with perisomatic-targeting PV+ basket cells, but it is unknown if such cell-type-specific circuit motifs extend to dendrite-targeting interneurons. Using male and female mice, we investigated synaptic connectivity and physiology in brain slices from four transgenic lines thought to capture distinct subsets of interneurons: SST-IRES-Cre, Nkx2.1-Cre, Chrna2-Cre, and Htr3a-GFP. First, we found that oriens-lacunosum moleculare (OLM) cells captured by the Chrna2-Cre line are a subset of Htr3a-GFP+ cells in the hippocampus. This novel finding is consistent with previous work showing Nkx2.1-Cre OLM cells are distinct from both Chrna2-Cre and Htr3a-GFP+ cells. Indeed, in paired whole-cell recordings, Nkx2.1-Cre+ interneurons in the stratum oriens, but not Chrna2-Cre+ or Htr3a-GFP+ cells, received more excitatory synaptic connections from superficial PCs relative to deep PCs. Next, we used optogenetic-assisted circuit mapping to investigate inhibition along the proximal and distal dendrites of PCs. We found that superficial PCs received stronger inhibition along their proximal dendrites than deep PCs from SST+ interneurons. Furthermore, this circuit motif was dependent on layer but not PC projection class. Finally, Chrna2-Cre OLM cells provided stronger inhibition to the distal dendrites of deep PCs relative to superficial PCs. Our data reveal that superficial and deep PCs engage in cell-type-specific circuits with dendrite-targeting interneurons. Furthermore, they support that Nkx2.1-Cre OLM cells and Chrna2-Cre/Htr3a-GFP OLM cells are distinct subtypes that form unique circuits in CA1.

neuroscience↗

Arid1b haploinsufficiency in cortical inhibitory interneurons causes cell-type-dependent changes in cellular and synaptic development

Autism spectrum disorder (ASD) presents with diverse cognitive and behavioral abnormalities beginning during early development. Although the neural circuit mechanisms remain unclear, recent work suggests pathology in cortical inhibitory interneurons (INs) plays a crucial role. However, we lack fundamental information regarding changes in the physiology of synapses to and from INs in ASD. Here, we used transgenic mice to conditionally knockout one copy of the high confidence ASD risk gene Arid1b from the progenitors of parvalbumin-expressing fast-spiking (PV-FS) INs and somatostatin-expressing non-fast-spiking (SST-NFS) INs. In brain slices, we performed paired whole-cell recordings between INs and excitatory projection neurons (PNs) to investigate changes in synaptic physiology. In neonates, we found reduced synaptic input to INs but not PNs, with a concomitant reduction in the frequency of spontaneous network events, which are driven by INs in immature circuits. In mature mice, we found a reduction in the number of PV-FS INs in cortical layers 2/3 and 5. However, changes in PV-FS IN synaptic physiology were cortical layer and PN cell-type dependent. In layer 5, synapses from PV-FS INs to subcortical-projecting PNs were weakened. In contrast, in layer 2/3, synapses to and from PV-FS INs and corticocortical-projecting PNs were strengthened, leading to enhanced feedforward inhibition of input from layer 4. Finally, we found a novel synaptic deficit among SST-NFS INs, in which excitatory synapses from layer 2/3 PNs failed to facilitate. Our data highlight that changes in unitary synaptic dynamics among INs in ASD depend on neuronal cell-type.

neuroscience↗

Satb2 regulates pyramidal cell differentiation and the development of feedforward inhibitory circuits in CA1 hippocampus

Pyramidal cells (PCs) in CA1 hippocampus can be classified by their radial position as deep or superficial and organize into subtype-specific circuits necessary for differential information processing. Specifically, superficial PCs receive fewer inhibitory synapses from parvalbumin (PV)-expressing interneurons than deep PCs, resulting in weaker feedforward inhibition of input from CA3 Schaffer collaterals. Using mice, we investigated mechanisms underlying PC differentiation and the development of this inhibitory circuit motif. We found that expression of the transcriptional regulator SATB2 is biased towards superficial PCs during early postnatal development and necessary to suppress PV+ interneuron synapse formation. In the absence of SATB2, the number of PV+ interneuron synaptic puncta surrounding superficial PCs increases during development to match deep PCs. This results in equivalent inhibitory current strength observed in paired whole-cell recordings, and equivalent feedforward inhibition of Schaffer collateral input. Thus, SATB2 is necessary for superficial PC differentiation and biased feedforward inhibition in CA1.

neuroscience↗