GIRK2 splice variants and neuronal G protein-gated K⁺ channels: implications for channel function and behavior.

ABSTRACT: Many neurotransmitters directly inhibit neurons by activating G protein-gated inwardly rectifying K⁺ (GIRK) channels, thereby moderating the influence of excitatory input on neuronal excitability. While most neuronal GIRK channels are formed by GIRK1 and GIRK2 subunits, distinct GIRK2 isoforms generated by alternative splicing have been identified. Here, we compared the trafficking and function of two isoforms (GIRK2a and GIRK2c) expressed individually in hippocampal pyramidal neurons lacking GIRK2. GIRK2a and GIRK2c supported comparable somato-dendritic GIRK currents in Girk2 ^-/- pyramidal neurons, although GIRK2c achieved a more uniform subcellular distribution in pyramidal neurons and supported inhibitory postsynaptic currents in distal dendrites better than GIRK2a

SUBMITTER: Marron Fernandez de Velasco E 

PROVIDER: S-EPMC5431628 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature