Familial hemiplegic migraine type 1 (FHM1) is a subtype of migraine with aura caused by mutations in CaV 2.1 (P/Q-type) Ca2+ channels. We previously reported gain of function of excitatory neurotransmission at pyramidal cell (Pyr) synapses but unaltered inhibitory neurotransmission at fast-spiking interneuron synapses suggesting that the balance between excitation (E) and inhibition (I) could be altered in FHM1 (Tottene et al.,2009). Another polysynaptic inhibitory subcircuit important for dynamic regulation of the cortical E-I balance involves somatostatin (SOM+) interneurons. By performing in vitro dual patch-clamp recordings in somatosensory cortex of GIN (GFP-expressing Inhibitory Neurons) mice, we characterized synaptic transmission and short term plasticity at the excitatory and reciprocal inhibitory synapses between layer 2/3 Pyrs and specific SOM+ interneurons. Pharmacological investigation of the types of Ca2+ channels controlling neurotransmitter release at these synapses revealed a predominant role of P/Q-type Ca2+ channels. Therefore, we are now investigating the effect of FHM1 mutation on Pyr-SOM+ interneurons synapses. To accomplish this task we created a new transgenic mouse line by crossbreeding FHM1 R192Q KI mice with GIN mice