The effects of 2-APB on the time–frequency distributions of γ oscillations in rat hippocampal slices

We investigated the influence of 2-APB (2-aminoethoxy-diphenylborate) acute exposure on hippocampal oscillations using time-frequency analysis methods including continuous wavelet transform and short-time Fourier transform. We hypothesized that acute exposure to 2-APB drastically reduced the hippocampal gamma oscillations. We estimated the hippocampal oscillations' time-frequency representations from 24 hippocampal slices in five rats. Our results indicated that it took at least 100 ms to see any hippocampal activities in response to the 100 Hz stimulus. The hippocampal oscillations' spectral energies dominated in the 31-60 Hz and 61-90 Hz frequency bands in the early time (100-200 ms) segment post-stimulus and in the 31-60 Hz and 61-90 Hz frequency bands after 200 ms until 400 ms post-stimulus. They were noticeably reduced in the late time segment (above 400 ms). The hippocampal oscillations' spectral energies in the 31-60 and 61-90 Hz frequency bands still dominated the early time segment after the acute 2-APB exposure. The 2-APB exposure never changed the energy content in all three frequency bands in the early time segment (p > 0.01). The exposure significantly reduced the energy content in both the mid-time segment and in the 31-60 Hz frequency band (p < 0.001) and in both the second time segment and in the 61-90 Hz frequency band (p < 0.01). Additionally, in the late time segment, the energy content in all three frequency bands was notably reduced post-drug exposure (p < 0.001).

[1]  O. Mignen,et al.  ARC channels: a novel pathway for receptor-activated calcium entry. , 2004, Physiology.

[2]  W. Regehr,et al.  Short-term synaptic plasticity. , 2002, Annual review of physiology.

[3]  Dennis Gabor,et al.  Theory of communication , 1946 .

[4]  O. Mignen,et al.  Reciprocal Regulation of Capacitative and Arachidonate-regulated Noncapacitative Ca2+ Entry Pathways* , 2001, The Journal of Biological Chemistry.

[5]  T. Murray,et al.  Role of α7-nicotinic acetylcholine receptors in tetanic stimulation-induced γ oscillations in rat hippocampal slices , 2005, Neuropharmacology.

[6]  Richard S Lewis,et al.  Potentiation and inhibition of Ca2+ release‐activated Ca2+ channels by 2‐aminoethyldiphenyl borate (2‐APB) occurs independently of IP3 receptors , 2001, The Journal of physiology.

[7]  K. Mikoshiba,et al.  2APB, 2-aminoethoxydiphenyl borate, a membrane-penetrable modulator of Ins(1,4,5)P3-induced Ca2+ release. , 1997, Journal of biochemistry.

[8]  R. Fisher,et al.  Gamma oscillation underlies hyperthermia-induced epileptiform-like spikes in immature rat hippocampal slices , 2001, BMC Neuroscience.

[9]  Sandip Patel,et al.  NAADP Mobilizes Ca2+ from Reserve Granules, Lysosome-Related Organelles, in Sea Urchin Eggs , 2002, Cell.

[10]  J. Voipio,et al.  Long-Lasting GABA-Mediated Depolarization Evoked by High-Frequency Stimulation in Pyramidal Neurons of Rat Hippocampal Slice Is Attributable to a Network-Driven, Bicarbonate-Dependent K+ Transient , 1997, The Journal of Neuroscience.

[11]  A. Galione,et al.  Nicotinic acid adenine dinucleotide phosphate triggers Ca2+ release from brain microsomes , 1999, Current Biology.

[12]  G. Buzsáki,et al.  Gamma (40-100 Hz) oscillation in the hippocampus of the behaving rat , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[13]  Metin Akay,et al.  Time frequency and wavelets in biomedical signal processing , 1998 .

[14]  H. Meves.  Modulation of ion channels by arachidonic acid , 1994, Progress in Neurobiology.

[15]  K. Mikoshiba,et al.  ATTENUATION OF INTRACELLULAR CA2+ AND SECRETORY RESPONSES BY INS(1,4,5)P3-INDUCED CA2+ RELEASE MODULATOR, 2APB, IN RAT PANCREATIC ACINAR CELLS , 1997 .

[16]  W Singer,et al.  Visual feature integration and the temporal correlation hypothesis. , 1995, Annual review of neuroscience.

[17]  J. Paton,et al.  Mechanism of nitric oxide action on inhibitory GABAergic signaling within the nucleus tractus solitarii , 2006, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[18]  G. Buzsáki,et al.  Hippocampal network patterns of activity in the mouse , 2003, Neuroscience.

[19]  D. Paterson,et al.  Nitric oxide and autonomic control of heart rate: a question of specificity , 2002, Trends in Neurosciences.

[20]  Metin Akay,et al.  Hypoxia silences the neural activities in the early phase of the phrenic neurogram of eupnea in the piglet , 2005, Journal of NeuroEngineering and Rehabilitation.

[21]  Vitaly Filippov,et al.  Nitric Oxide Signals Parallel Fiber Activity to Bergmann Glial Cells in the Mouse Cerebellar Slice , 2001, Molecular and Cellular Neuroscience.

[22]  P. Somogyi,et al.  Brain-state- and cell-type-specific firing of hippocampal interneurons in vivo , 2003, Nature.

[23]  M Knaflitz,et al.  Time-frequency methods applied to muscle fatigue assessment during dynamic contractions. , 1999, Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology.

[24]  Jing Shi,et al.  Sustained depolarization-induced propagation of [Ca2+]i oscillations in cultured DRG neurons: The involvement of extracellular ATP and P2Y receptor activation , 2008, Brain Research.

[25]  T. Sharp,et al.  Widespread Distribution of Binding Sites for the Novel Ca2+-mobilizing Messenger, Nicotinic Acid Adenine Dinucleotide Phosphate, in the Brain* , 2000, The Journal of Biological Chemistry.

[26]  Jun Yu,et al.  Time-frequency analysis of myoelectric signals during dynamic contractions: a comparative study , 2000, IEEE Transactions on Biomedical Engineering.

[27]  F. Moccia,et al.  NAADP activates a Ca2+ current that is dependent on F‐actin cytoskeleton , 2003, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[28]  S. Goldman,et al.  Astrocyte-mediated potentiation of inhibitory synaptic transmission , 1998, Nature Neuroscience.

[29]  F. Michelangeli,et al.  Inhibition of the type 1 inositol 1,4,5-trisphosphate receptor by 2-aminoethoxydiphenylborate. , 2002, Cellular signalling.

[30]  Diptiman D. Bose,et al.  Activation of ryanodine receptors induces calcium influx in a neuroblastoma cell line lacking calcium influx factor activity. , 2005, The Biochemical journal.

[31]  K. Mikoshiba,et al.  2-Aminoethoxydiphenyl borate inhibits agonist-induced Ca2+ signals by blocking inositol trisphosphate formation in acutely dissociated mouse pancreatic acinar cells , 2004, Pflügers Archiv.

[32]  Hon Cheung Lee,et al.  A Derivative of NADP Mobilizes Calcium Stores Insensitive to Inositol Trisphosphate and Cyclic ADP-ribose (*) , 1995, The Journal of Biological Chemistry.

[33]  J. Deuchars,et al.  Nitroxergic Modulation in the NTS: Implications for Cardiovascular Function , 2005 .

[34]  H. Seller,et al.  Effects of nitric oxide on sympathetic baroreflex transmission in the nucleus tractus solitarii and caudal ventrolateral medulla in cats , 1995, Neuroscience Letters.

[35]  P. Somogyi,et al.  Spike timing of dendrite-targeting bistratified cells during hippocampal network oscillations in vivo , 2004, Nature Neuroscience.

[36]  R. Traub,et al.  Synchronized oscillations in interneuron networks driven by metabotropic glutamate receptor activation , 1995, Nature.

[37]  J. Rosado,et al.  The inositol trisphosphate receptor antagonist 2-aminoethoxydiphenylborate (2-APB) blocks Ca2+ entry channels in human platelets: cautions for its use in studying Ca2+ influx. , 2001, Cell calcium.

[38]  Alan Fine,et al.  Calcium Stores in Hippocampal Synaptic Boutons Mediate Short-Term Plasticity, Store-Operated Ca2+ Entry, and Spontaneous Transmitter Release , 2001, Neuron.