TY - JOUR T1 - The Ca<sub>v</sub>3–K<sub>v</sub>4 Complex Acts as a Calcium Sensor to Maintain Inhibitory Charge Transfer during Extracellular Calcium Fluctuations JF - The Journal of Neuroscience JO - J. Neurosci. SP - 7811 LP - 7824 DO - 10.1523/JNEUROSCI.5384-12.2013 VL - 33 IS - 18 AU - Dustin Anderson AU - Jordan D. T. Engbers AU - N. Colin Heath AU - Theodore M. Bartoletti AU - W. Hamish Mehaffey AU - Gerald W. Zamponi AU - Ray W. Turner Y1 - 2013/05/01 UR - http://www.jneurosci.org/content/33/18/7811.abstract N2 - Synaptic transmission and neuronal excitability depend on the concentration of extracellular calcium ([Ca]o), yet repetitive synaptic input is known to decrease [Ca]o in numerous brain regions. In the cerebellar molecular layer, synaptic input reduces [Ca]o by up to 0.4 mm in the vicinity of stellate cell interneurons and Purkinje cell dendrites. The mechanisms used to maintain network excitability and Purkinje cell output in the face of this rapid change in calcium gradient have remained an enigma. Here we use single and dual patch recordings in an in vitro slice preparation of Sprague Dawley rats to investigate the effects of physiological decreases in [Ca]o on the excitability of cerebellar stellate cells and their inhibitory regulation of Purkinje cells. We find that a Cav3–Kv4 ion channel complex expressed in stellate cells acts as a calcium sensor that responds to a decrease in [Ca]o by dynamically adjusting stellate cell output to maintain inhibitory charge transfer to Purkinje cells. The Cav3–Kv4 complex thus enables an adaptive regulation of inhibitory input to Purkinje cells during fluctuations in [Ca]o, providing a homeostatic control mechanism to regulate Purkinje cell excitability during repetitive afferent activity. ER -