title: The ionic mechanism of membrane potential oscillations and membrane resonance in striatal LTS interneurons.
abstract: Striatal low-threshold spiking (LTS) interneurons spontaneously transition to a depolarized, oscillating state similar to that seen after sodium channels are blocked. In the depolarized state, whether spontaneous or induced by sodium channel blockade, the neurons express a 3- to 7-Hz oscillation and membrane impedance resonance in the same frequency range. The membrane potential oscillation and membrane resonance are expressed in the same voltage range (greater than -40 mV). We identified and recorded from LTS interneurons in striatal slices from a mouse that expressed green fluorescent protein under the control of the neuropeptide Y promoter. The membrane potential oscillation depended on voltage-gated calcium channels. Antagonism of L-type calcium currents (CaV1) reduced the amplitude of the oscillation, whereas blockade of N-type calcium currents (CaV2.2) reduced the frequency. Both calcium sources activate a calcium-activated chloride current (CaCC), the blockade of which abolished the oscillation. The blocking of any of these three channels abolished the membrane resonance. Immunohistochemical staining indicated anoctamin 2 (ANO2), and not ANO1, as the CaCC source. Biophysical modeling showed that CaV1, CaV2.2, and ANO2 are sufficient to generate a membrane potential oscillation and membrane resonance, similar to that in LTS interneurons. LTS interneurons exhibit a membrane potential oscillation and membrane resonance that are both generated by CaV1 and CaV2.2 activating ANO2. They can spontaneously enter a state in which the membrane potential oscillation dominates the physiological properties of the neuron.
authors.affiliation: Department of Biology, The University of Texas at San Antonio, San Antonio, Texas; and.
authors.forename: S C
authors.initials: SC
authors.lastname: Song
authors.affiliation: Department of Biology, The University of Texas at San Antonio, San Antonio, Texas; and Department of Physiology, Michigan State University, East Lansing, Michigan.
authors.forename: J A
authors.initials: JA
authors.lastname: Beatty
authors.affiliation: Department of Biology, The University of Texas at San Antonio, San Antonio, Texas; and charles.wilson@utsa.edu.
authors.forename: C J
authors.initials: CJ
authors.lastname: Wilson
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers; D003342:Corpus Striatum / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D049452:Green Fluorescent Proteins / Q000235:genetics / Q000378:metabolism; D007150:Immunohistochemistry; D007395:Interneurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D007473:Ion Channels / Q000037:antagonists & inhibitors / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology*; D008822:Mice, Transgenic; D008958:Models, Molecular; D008959:Models, Neurological; D009478:Neuropeptide Y / Q000235:genetics / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D010507:Periodicity; D011401:Promoter Regions, Genetic; D046509:Tissue Culture Techniques
chemical_list: D002121:Calcium Channel Blockers; D007473:Ion Channels; D009478:Neuropeptide Y; D018377:Neurotransmitter Agents; D049452:Green Fluorescent Proteins
keywords: LTS interneuron; calcium-activated chloride current; oscillation; resonance; striatum