TY - JOUR T1 - GABAergic Synaptic Transmission Triggers Action Potentials in Thalamic Reticular Nucleus Neurons JF - The Journal of Neuroscience JO - J. Neurosci. SP - 7782 LP - 7790 DO - 10.1523/JNEUROSCI.0839-12.2012 VL - 32 IS - 23 AU - Yan-Gang Sun AU - Chia-Shan Wu AU - John J. Renger AU - Victor N. Uebele AU - Hui-Chen Lu AU - Michael Beierlein Y1 - 2012/06/06 UR - http://www.jneurosci.org/content/32/23/7782.abstract N2 - GABAergic neurons in the thalamic reticular nucleus (TRN) form powerful inhibitory connections with several dorsal thalamic nuclei, thereby controlling attention, sensory processing, and synchronous oscillations in the thalamocortical system. TRN neurons are interconnected by a network of GABAergic synapses, but their properties and their role in shaping TRN neuronal activity are not well understood. Using recording techniques aimed to minimize changes in the intracellular milieu, we show that synaptic GABAA receptor activation triggers postsynaptic depolarizations in mouse TRN neurons. Immunohistochemical data indicate that TRN neurons express very low levels of the Cl− transporter KCC2. In agreement, perforated-patch recordings show that intracellular Cl− levels are high in TRN neurons, resulting in a Cl− reversal potential (ECl) significantly depolarized from rest. Additionally, we find that GABAA receptor-evoked depolarizations are amplified by the activation of postsynaptic T-type Ca2+ channels, leading to dendritic Ca2+ increases and the generation of burst firing in TRN neurons. In turn, GABA-evoked burst firing results in delayed and long-lasting feedforward inhibition in thalamic relay cells. Our results show that GABA-evoked depolarizations can interact with T-type Ca2+ channels to powerfully control spike generation in TRN neurons. ER -