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First published online 12 August 2008
doi: 10.1242/jcs.022368

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Homeostasis established by coordination of subcellular compartment plasticity improves spike encoding

State Key Labs for Macrobiomolecules and Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, The People's Republic of China

View larger version (64K): [in this window] [in a new window]   Fig. 1. Intracellular Ca2+ is increased by the infusion of adenophostin-A into pyramidal neurons. Adenophostin-A (AD) perfusion was carried out in a recording pipette (yellow arrow in A), which contained 100 nM AD. Ca2+ imaging was done as a control when the pipette had a cell-attached configuration on this pyramidal neuron. Suction was then added to produce whole-cell configuration. Immediately after whole-cell recording, we undertook Ca2+ imaging every 10 seconds. Superimposed image of pyramidal neurons under IR-DIC and Fluo-3-AM optics during AD perfusion (A) and in the control (B). Ca2+ transient in pyramidal neurons during AD perfusion (C) and under control (D), in which fluorescent intensities along white bars (solid line, dendrite; dotted line, soma) are measured for data presented in E,F. Ca2+ transient in the soma (E) and dendrite (F) of pyramidal neurons under AD perfusion (green line) and in the control (blue line).

View larger version (22K): [in this window] [in a new window]   Fig. 2. The elevation of intracellular Ca2+ enhances glutamatergic and GABAergic synaptic transmission. (A) Elevation of cytoplasmic [Ca2+] by infusing adenophostin-A into the neurons increases the amplitude of glutamatergic EPSCs () by 145% compared with that in the control (). Inset shows enhanced EPSC waveforms. (B) The intracellular infusions of adenophostin-A raise the amplitude of GABAergic IPSCs () by 85% compared with controls (). Inset shows IPSC waveforms. Glutamatergic EPSCs were isolated by using 10 µM bicuculline, whereas GABAergic IPSCs were isolated by adding 10 µM CNQX and 40 µM DAP-5.

View larger version (31K): [in this window] [in a new window]   Fig. 3. The elevation of intracellular Ca2+ reduces spike capacity but not precision in cortical regular-spiking neurons. Superimposed waves of spikes under control (A) and adenophostin-A (B) infusion. Vertical lines are spike-locking phases, and horizontal lines are threshold potentials (Vts). (C) The inter-spike interval (ISI) of sequential spikes under control () and adenophostin-A () infusion, in which ISI values relevant to the same number in sequential spikes are statistically different (P<0.01). (D) The standard deviation of spike timing (SDST) under control () and adenophostin-A () infusion.

View larger version (30K): [in this window] [in a new window]   Fig. 4. The elevation of intracellular Ca2+ raises the Vts and prolongs the RP of sequential spikes in regular-spiking neurons. (A) The superimposed waves of measuring absolute RP for spike 3 under control (blue traces) and adenophostin-A (red traces) infusion, where the absolute RP is defined as the duration from a complete spike to a subsequent spike evoked with 50% probability. (B) The relationship between the normalized stimuli and the absolute RP of spike 1 (S1, triangles) or spike 3 (S3, diamonds) under control (open symbols) and adenophostin-A (filled symbols) infusion, in which linear correlations are shifted upward. Values of the absolute RP-3 relevant to the similar stimulus intensity are statistically different (P<0.01). (C) The difference between Vts and Vr (Vts–Vr) for spike 1 to spike 5 under control () and adenophostin-A () infusion, where Vts values relevant to the same number in sequential spikes are statistically different (P<0.01).

View larger version (39K): [in this window] [in a new window]   Fig. 5. Ca2+-induced potentiation of excitatory and inhibitory synaptic transmission improves spike capacity and timing precision. Effect of intracellular Ca2+-induced synaptic potentiation on spike encoding and neuronal intrinsic properties. The potentiation of excitatory and inhibitory synaptic inputs was mimicked by strong depolarization and hyperpolarization pulses. Data were obtained under control conditions (), adenophostin-A infusion alone (gray triangles) or adenophostin-A together with strong depolarization (new threshold stimuli, Tsti') and AHP (). (A) Strong depolarization pulses reduce adenophostin-A-induced prolongation of the absolute RP. There is no statistical difference between adenophostin-A-treated () and control () RPs in spike 1; however, a difference was observed with spike 3 for adenophostin-A infusion alone versus control ( versus , respectively). (B) The mixture of strong depolarization/AHP pulses lowers adenophostin-raised Vts–Vr () compared with that recorded with adenophostin-A alone (gray triangles, P<0.05). (C) Spike waveforms superimposed from 20 traces with adenophostin-A treatment alone. (D) Waveforms from 20 traces under adenophostin-A infusion with strong depolarization and AHP. (E) ISI values for corresponding spikes 2-4 between the three conditions are statistically different (P<0.01). (F) SDST values for spikes 2-5 under strong depolarization and AHP are significantly different (P<0.01) to those in adenophostin-A-treated and control.

View larger version (15K): [in this window] [in a new window]   Fig. 6. The current pulses integrated from Ca2+-induced potentiation at glutamatergic and GABAergic synapses improve spike encoding. (A) Superimposed waveforms of spikes evoked by currents integrated from GABAergic and glutamatergic synaptic transmission in the control (left panel) and with adenophostin-A-induced synaptic potentiation (right). The integrative effect of adenophostin-A on neuronal encoding is an increase in the number of sequential spikes. (B) SDST values of sequential spikes under control and adenophostin-A infusion, in which SDST is significantly different for spike 3 (P<0.01).

View larger version (41K): [in this window] [in a new window]   Fig. 7. The excitability of cell body and axon measured at cortical pyramidal neurons. (A) Tungsten electrodes at an axon output electrical pulses (0.1 mseconds) to evoke axonal excitation. A whole-cell pipette at the soma injects depolarization pulses (100 mseconds) to excite the neuron, and records electrical signal from soma and axon. (B) Threshold stimulation to the cell body or the axon (TSCB or TSAx, respectively) evoke single spikes at soma (left) and axon (antidromic, right) with 50% probability, which measure subcellular excitability. (C) TSAx and TSCB do not change over 35 minutes of recording (n=14).

View larger version (26K): [in this window] [in a new window]   Fig. 8. Intensive activity at axons induces inverse changes in axonal and somatic excitability. (A) Axonal HFA lowers threshold stimuli at axons (TSAx, ) and raises threshold stimuli at cell bodies (TSCB, ; n=10). (B) Axonal HFA increases TSAx (filled symbols) and decreases TSCB (open symbols; n=9). (C) Single spikes elicited by threshold stimuli (50% probability of spike firing) at axons (right) and soma (left) before (blue traces) and after HFA (red traces). TSCB rises and TSAx is reduced after axonal HFA.

View larger version (31K): [in this window] [in a new window]   Fig. 9. Intracellular Ca2+ signaling pathways are essential to the inverse plasticity of axonal and somatic excitability induced by axonal HFA. BAPTA, CaMK(284-302) and CaN autoinhibitory peptide (CaN-AIP) were infused into the neurons via the recording pipette. (A) BAPTA prevents axonal HFA-induced plasticity of excitability dissociated at axons () and soma (, n=8). (B) CaMK(284-302) blocks the inverse plasticity of axonal () and somatic excitability (, n=11). (C) CaN-AIP lowers threshold stimuli at the axon (TSAx, ) and raises threshold stimuli at cell body (TSCB, ; n=7). (D) CaN-AIP increases TSAx () and decreases TSCB (; n=8). All results are means ± s.e.m.

View larger version (50K): [in this window] [in a new window]   Fig. 10. Intracellular Ca2+-signaling pathways induce plastic changes at subcellular compartments. The potentiation at the glutamatergic synapse enhances neuronal activity (red); the potentiation at the GABA synapse inhibits neuronal activity (blue); and the weakness in the soma (blue) is inversely associated with axonal potentiation (red), or vice versa. The integrated effects on neuronal programming are homeostatic in nature. ARP, absolute refractory period; CaM, calmodulin; CaN, calcineurin; GABA-R, GABA receptor; Glu-R, glutamine receptor; IP3R, inositol (1,4,5)-trisphosphate receptor; Pks, protein kinases; VGSC, Voltage-gated sodium channel; Vts, threshold potential.

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