Isoproterenol facilitates GABAergic autapses in fast-spiking cells of rat insular cortex.

In the cerebral cortex, fast-spiking (FS) cells are the principal GABAergic interneurons and potently suppress neural activity in targeting neurons. Some FS neurons make synaptic contacts with themselves. Such synapses are called autapses and contribute to self-inhibition of FS neural activity. β-Adrenoceptors have a crucial role in regulating GABAergic synaptic inputs from FS cells to pyramidal (Pyr) cells; however, the β-adrenergic functions on FS autapses are unknown. To determine how the β-adrenoceptor agonist isoproterenol modulates inhibitory synaptic transmission in the autapses of FS cells, paired whole-cell patch-clamp recordings were obtained from FS and Pyr cells in layer V of rat insular cortex. Previous studies found that isoproterenol (100 μM) had pleiotropic effects on unitary inhibitory postsynaptic currents (uIPSCs) in FS→Pyr connections, whereas autapses in FS cells were always facilitated by isoproterenol. Facilitation of autapses by isoproterenol was accompanied by decreases in the paired-pulse ratio of second to first uIPSC amplitudes and the coefficient of variation of the uIPSC amplitude, which suggests that β-adrenergic facilitation is likely mediated by presynaptic mechanisms. The discrepancy between isoproterenol-induced modulation of uIPSCs in FS autapses and in FS→Pyr connections may reflect the presence of different presynaptic mechanisms of GABA release in each synapse.