Forschung & Innovation
Publikationen
Somatostatin sharpens the neuronal action potential by increasing K+ and decreasing Ca2+ conductances
PMU Autor*in
Therese Riedemann
Alle Autor*innen
Therese Riedemann
Fachzeitschrift
JOURNAL OF NEUROPHYSIOLOGY
Kurzfassung
Somatostatin (SST) is a neuropeptide whose biological function has initially been described in the hypothalamus. However, SST-expressing neurons are also found in the neocortex or hippocampus, and the majority of these neurons are GABAergic interneurons (INs), the so called SST-INs. Numerous studies on non-cortical cells suggest that SST acts via different K+ channels to dampen cell excitability, however questions remain as to the exact mechanisms whereby SST mediates these effects on cortical pyramidal cells (PCs). The present study analyzed the capacity of SST to inhibit action potential (AP) firing in layer II/III PCs of the anterior cingulate cortex (aCC). It is reported here that SST decreases PC excitability mainly via G protein-coupled inwardly rectifying potassium (GIRK) and Kv(7) channels. Furthermore, activation of GIRK and Kv(7) channels together with inhibition of voltage-gated Ca2+ channels (VGCCs) is responsible for SST-dependent inhibition of AP firing and increase in the afterhyperpolarization (AHP) amplitude following an AP. By analyzing single AP kinetics before and after SST exposure, this study further identifies Ca2+-activated K+ (K-Ca) channels as target molecules of SST receptor activation. In summary, the present study promotes our current understanding of the ionic mechanisms that lead to a SST-dependent loss in excitability.