Summary
Inhibitory modulation of glutamatergic information processing is a prerequisite for proper network function. Among the many groups of interneurons, somatostatin-expressing interneurons (SOM-INs) seem to play an important role in the maintenance of physiological brain activity. We have previously shown that bath application of somatostatin (SOM) causes a reduction in pyramidal cell (PC) excitability. However, the mechanisms of action of the peptide on cortical synaptic circuits are still unclear. To gain further insight into the function of SOM-INs, we analyzed the effect of SOM on synaptic transmission in PCs, in SOM-INs and in layer 1 interneurons (L1-INs) of the anterior cingulate cortex. We found that SOM produced pronounced postsynaptic effects in PCs while having little or no postsynaptic effects on either IN type. Accordingly, it is proposed here, that SOM - by acting differentially on SOM-INs and L1-INs - increases spontaneous GABAergic transmission, while at the same time, decreasing spontaneous glutamatergic transmission. In addition, we show that SOM specifically modulates GABAB receptor (GABABR)-mediated synaptic transmission but has little effect on GABAA receptor-mediated (GABAAR) transmission.
Competing Interest Statement
The authors have declared no competing interest.
