Synaptic plasticity has been extensively studied in principal neurons of the neocortex, but less work has been done on GABAergic interneurons. Interneurons consist of multiple subtypes and their synaptic properties vary between subtypes. In the present study, we have examined long-term potentiation (LTP) of excitatory synapses on somatostatin (SS)-expressing interneurons in neocortex using transgenic mice that express enhanced green fluorescent protein in these interneurons. We found that a strong theta burst stimulation was required to induce LTP in SS interneurons. LTP was associated with a reduction in paired-pulse facilitation and was not blocked by an N-methyl-D-aspartate receptor (NMDAR) antagonist. LTP was not affected by chelating postsynaptic Ca2+ with BAPTA, a fast Ca2+ chelator, and blocking L-type voltage-dependent Ca2+ channels with nimodipine. Application of forskolin, an activator of adenylate cyclase that increases cyclic adenosine monophosphate (cAMP) concentration, enhanced synaptic transmission and occluded subsequent induction of LTP. Finally, we found that LTP was blocked by protein kinase A (PKA) inhibitors. Our results suggest that excitatory synapses on SS interneurons express a presynaptic form of LTP that is not dependent on NMDARs or postsynaptic Ca2+ rise but is dependent on the cAMP-PKA signaling pathway.
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