title: Voltage-independent sodium channels emerge for an expression of activity-induced spontaneous spikes in GABAergic neurons.
abstract: BACKGROUND
  Cerebral overexcitation needs inhibitory neurons be functionally upregulated to rebalance excitation vs. inhibition. For example, the intensive activities of GABAergic neurons induce spontaneous spikes, i.e., activity-induced spontaneous spikes (AISS). The mechanisms underlying AISS onset remain unclear. We investigated the roles of sodium channels in AISS induction and expression at hippocampal GABAergic neurons by electrophysiological approach.
  
  
  RESULTS
  AISS expression includes additional spike capability above evoked spikes, and the full spikes in AISS comprise early phase (spikelets) and late phase, implying the emergence of new spikelet component. Compared with the late phase, the early phase is characterized as voltage-independent onset, less voltage-dependent upstroke and sensitivity to TTX. AISS expression and induction are independent of membrane potential changes. Therefore, AISS's spikelets express based on voltage-independent sodium channels. In terms of AISS induction, the facilitation of voltage-gated sodium channel (VGSC) activation accelerates AISS onset, or vice versa.
  
  
  CONCLUSIONS
  AISS expression in GABAergic neurons is triggered by the spikelets based on the functional emergence of voltage-independent sodium channels, which is driven by intensive VGSCs' activities.
authors.forename: Wei
authors.initials: W
authors.lastname: Lu
authors.forename: Bo
authors.initials: B
authors.lastname: Wen
authors.forename: Fengyu
authors.initials: F
authors.lastname: Zhang
authors.affiliation: State Key lab for Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, 15 Datun Road, Beijing 100101, China. jhw@sun5.ibp.ac.cn.
authors.forename: Jin-Hui
authors.initials: JH
authors.lastname: Wang
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology; D001369:Axons / Q000187:drug effects / Q000502:physiology; D015220:Calcium Channels / Q000378:metabolism; D003064:Cnidarian Venoms / Q000633:toxicity; D063388:Endocannabinoids / Q000494:pharmacology; D059330:GABAergic Neurons / Q000187:drug effects / Q000502:physiology*; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology; D015640:Ion Channel Gating / Q000187:drug effects / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D053284:Polyunsaturated Alkamides / Q000494:pharmacology; D015222:Sodium Channels / Q000378:metabolism*; D013779:Tetrodotoxin / Q000633:toxicity
chemical_list: D001095:Arachidonic Acids; D015220:Calcium Channels; D003064:Cnidarian Venoms; D063388:Endocannabinoids; D053284:Polyunsaturated Alkamides; D015222:Sodium Channels; D013779:Tetrodotoxin; C028800:toxin II (Anemonia sulcata); C078814:anandamide