GABAergic interneurons, which constitute 20% of the cortical neurons in the rodent brain, exhibit extraordinary diversity in their morphology, histochemistry, intrinsic membrane properties, and connectivity. The distinct types of interneurons play divergent roles in cortical networks.

Among them, SST⁺ interneurons differ markedly in several aspects from other subtypes interneurons and play crucial roles in early cortical circuit formation.

In a recent study published online by Cerebral Cortex, researchers at Institute of Biophysics of Chinese Academy of Sciences unveiled the critical period of the intrinsic development of somatostatin (SST) positive interneurons in the secondary motor cortex (M2) of mice, which provides a new insight into the regulation of interneuron maturation.

The functional developmental course of layer 2/3 SST⁺ interneurons of the secondary M2 in the mouse brain was traced in this study.

Researchers elucidated the intrinsic electrophysiological properties of SST⁺ interneurons during the period P1–P30 and highlighted the critical developmental period - before P15 - of SST⁺ interneuron.

By dual recording of SST⁺ interneurons and local pyramidal cells (PCs), they showed that synaptic coupling began to coordinate the integration of glutamatergic neurons and GABAergic interneurons into nascent cortical circuits at an early stage (~P5/6), with the coupling ratio and synaptic strength increasing during the first two weeks.

They then demonstrated that attenuating neuronal activity in layer 2/3 PCs at an early stage profoundly influence multiple aspects of the maturation of SST⁺ interneurons.

The observed effects of tetanus toxin (TeNT) injection and Kir2.1 overexpression support the hypothesis that early terminal activity of PCs is one of the factors influencing SST⁺ interneuron maturation before P1.

The study firstly illustrated the intrinsic electrophysiological properties of SST⁺ interneurons during the cortical development. It provided a new insight into how PC regulates the maturation of SST⁺ interneurons.

This work was supported by grants from the Chinese Ministry of Science and Technology, the Natural Science Foundation of China and the Strategic Priority Research Program of the Chinese Academy of Sciences.