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Carolyn W. Harley - One of the best experts on this subject based on the ideXlab platform.

  • Locus Coeruleus Optogenetic Light Activation Induces Long-Term Potentiation of Perforant Path Population Spike Amplitude in Rat Dentate Gyrus.
    Frontiers in systems neuroscience, 2019
    Co-Authors: Meghan A. L. Quinlan, Carolyn W. Harley, Vanessa M. Strong, Darlene M. Skinner, Gerard M. Martin, Susan G. Walling
    Abstract:

    Norepinephrine (NE) in dentate gyrus (DG) produces NE-dependent long-term potentiation (NE-LTP) of the perforant path-evoked potential Population Spike both in vitro and in vivo. Chemical activators infused near locus coeruleus (LC), the source of DG NE, produce a NE-LTP that is associative, i.e., requires concurrent pairing with perforant path (PP) input. Here, we ask if LC optogenetic stimulation that allows us to activate only LC neurons can induce NE-LTP in DG. We use an adeno-associated viral vector containing a depolarizing channel (AAV8-Ef1a-DIO-eChR2(h134r)-EYFP-WPRE) infused stereotaxically into the LC of TH:Cre rats to produce light-sensitive LC neurons. A co-localization of ~62% in LC neurons was observed for these channels. Under urethane anesthesia, we demonstrated that 5-10 s 10 Hz trains of 30 ms light pulses in LC reliably activated neurons near an LC optoprobe. Ten minutes of the same train paired with 0.1 Hz PP electrical stimulation produced a delayed NE-LTP of Population Spike amplitude, but not EPSP slope. A leftward shift in the Population Spike input/output curve at the end of the experiment was also consistent with long-term Population Spike potentiation. LC neuron activity during the 10 min light train was unexpectedly transient. Increased LC neuronal firing was seen only for the first 2 min of the light train. NE-LTP was more delayed and less robust than reported with LC chemo-activation. Previous estimates of LC axonal conduction times suggest acute release of NE occurs 40-70 ms after an LC neuron action potential. We used single LC light pulses to examine acute effects of NE release and found potentiated Population Spike amplitude when a light pulse in LC occurred 40-50 ms, but not 20-30 ms, prior to a PP pulse, consistent with conduction estimates. These effects of LC optogenetic activation reinforce evidence for a continuum of NE potentiation effects in DG. The single pulse effects mirror an earlier report using LC electrical stimulation. These acute effects support an attentional role of LC activation. The LTP of PP responses induced by optogenetic LC activation is consistent with the role of LC in long-term learning and memory.

  • idazoxan increases perforant path evoked epsp slope paired pulse inhibition and reduces perforant path evoked Population Spike paired pulse facilitation in rat dentate gyrus
    Brain Research, 2006
    Co-Authors: John Knight, Carolyn W. Harley
    Abstract:

    Abstract Norepinephrine, acting via β-adrenoceptors, enhances the perforant path-evoked potential in dentate gyrus. Using systemic idazoxan to increase norepinephrine, and paired perforant path pulses to probe early inhibition, previous investigators reported that idazoxan increased initial Spike amplitude and increased somatic feedback inhibition. Here, feedback inhibition was re-examined in idazoxan-treated (5 mg/kg) rats under urethane anesthesia. To control for initial increased Spike amplitude after idazoxan, evoked potentials were matched, pre- and post-idazoxan, on initial Population Spike. Input–output current profiles were also compared pre- and post-idazoxan. Saline- and timolol-filled micropipettes permitted evaluation of a contribution of local β-adrenoceptors. As previously observed, initial Spike amplitude was potentiated by idazoxan. Comparable Spike potentiation was not seen on the timolol micropipette. Paired pulse inhibition of Spike amplitude apparently increased, but input–output curve comparisons revealed a loss of feedback facilitation rather than an increase in feedback inhibition. Initial EPSP slopes were depressed after idazoxan in input–output curve data. EPSP slope feedback ratios were significantly reduced following idazoxan.These data suggest idazoxan has multiple effects on perforant path input to the dentate gyrus. Spike potentiation following idazoxan has previously been shown to depend on intact norepinephrine input. Here, the reduction in Spike potentiation on the timolol pipette is consistent with other evidence that norepinephrine-mediated potentiation of the perforant path-evoked potential is dependent on local β-adrenoceptor activation. The input–output data suggest a decrease in feedback facilitation after idazoxan is likely to account for the apparent increase in feedback inhibition previously reported. Decreased EPSP slope ratios with similar paired pulse intervals have been reported in novel environments. Since exposure to novel environments activates locus coeruleus neurons, norepinephrine may mediate the change in EPSP slope inhibition reported in awake rats.In summary, these results are consistent with the hypothesis that idazoxan potentiates granule cell responses to perforant path input in the dentate gyrus via increases in norepinephrine that lead to β-adrenoceptor activation, and, further, that idazoxan reduces paired pulse feedback Spike facilitation and enhances EPSP slope, but not Spike, feedback inhibition.

  • β-Adrenergic blockade in the dentate gyrus in vivo prevents high frequency-induced long-term potentiation of EPSP slope, but not long-term potentiation of Population Spike amplitude
    Hippocampus, 2001
    Co-Authors: Catherine A.m. Munro, Susan G. Walling, John H. Evans, Carolyn W. Harley
    Abstract:

    High frequency (HF)-induced and norepinephrine (NE)-induced long-term potentiation have been hypothesized to utilize common mechanisms of induction and expression in the dentate gyrus. In vitro data tend to support this hypothesis, but few studies have been done in vivo. The present study records perforant path-evoked potentials simultaneously on two micropipettes, one filled with saline and the other with the beta-antagonist, timolol. Stimulation of the paragigantocellularis nucleus (PGi) was used as a method of producing NE release in the dentate gyrus, and thus, to assess the efficacy of beta-receptor blockade on the timolol pipette. Beta-blockade by timolol attenuated PGi-induced Spike potentiation. HF-induced potentiation of the excitatory post-synaptic potential (EPSP) slope was also blocked by timolol, but HF-induced Spike amplitude potentiation was unaffected. These results are consistent with an earlier report examining HF-long-term potentiation (LTP) following 6-OHDA-induced NE depletion, which showed that the EPSP slope LTP depended, for its full expression, on NE, but potentiation of the Population Spike amplitude component of HF-induced LTP did not. In the present study, PGi-induced potentiation of Spike amplitude on the saline pipette was normal after HF-induced saturation of Spike amplitude potentiation, suggesting that the mechanisms for expression of Spike potentiation, as well as induction of Spike potentiation, are separate for HF and NE stimulation.

  • Glutamatergic activation of the medial septum complex: an enhancement of the dentate gyrus Population Spike and accompanying EEG and unit changes.
    Brain research, 2000
    Co-Authors: G P Carre, Carolyn W. Harley
    Abstract:

    Abstract A large number of cells from the medial septum complex (MSC) innervate the dentate gyrus of the hippocampus. Electrical prestimulation of the MSC enhances perforant path-dentate gyrus evoked field potentials. Considering the large number of fibres that pass through this region, the effects glutamatergic stimulation of the MSC had on dentate gyrus field potentials, and accompanying changes in units, and EEG, was investigated in urethane-anaesthetized rats. The perforant path was stimulated at a rate of 0.1 Hz, evoking an EPSP and a Population Spike recorded in the dentate gyrus granule cell layer. l -glutamate was delivered by pressure ejection. Glutamate ejection to the MSC produced a significant enhancement of the Population Spike. The duration of enhancement ranged from 1 to 49 min (~=10.5 min). A consistent, but relatively short increase in the EPSP slope was also demonstrated. MSC activation induced a theta rhythm in 7 of 10 animals (duration=20–112 s). Theta rhythm induction preceded Spike enhancement and occurred for a shorter duration than the enhancement. The effects on spontaneous unit activity were mixed. However, all changes in firing rate preceded Spike enhancement, and their duration rarely coincided with the duration of the Spike enhancement. The Population Spike enhancement usually occurred without evidence of a change in paired-pulse inhibition.

  • Locus coeruleus activation induces perforant path-evoked Population Spike potentiation in the dentate gyrus of awake rat.
    Experimental brain research, 1994
    Co-Authors: George Klukowski, Carolyn W. Harley
    Abstract:

    In vitro norepinephrine (NE) induces both short and long-term β-receptor-mediated potentiation of the perforant path-evoked Population Spike in the dentate gyrus. NE or locus coeruleus (LC) activation in vivo also produces a β-receptor dependent potentiation of Population Spike amplitude in anesthetized rat. Studies of behavioral state modulation of Population Spike amplitude in awake rats, and in rats depleted of NE, however, have led to the hypothesis that LC-NE activation should act to suppress or reduce Population Spike amplitude in the dentate gyrus of unanesthetized rat. Using glutamate activation of LC in awake unrestrained rats (n=12), the present study provides evidence that LC activation in the awake rat does not reduce, but potentiates, Population Spike amplitude. The potentiation effect was long-lasting (>25min) in 50% of the experiments. In addition glutamate ejections in the third lobe of cerebellar rostral vermis produced potentiation of Population Spike amplitude (n=3) and Population excitatory postsynaptic potential slope. Ejections at sites outside the LC and rostral vermis were ineffective (n=5). Behavioral effects of glutamate ejection did not predict the occurrence of potentiation. These data support the hypothesis that phasic activation of LC cells is likely to induce short-term, and possibly long-term, potentiation of dentate gyrus throughput in alert animals.

Hiroshi Kato - One of the best experts on this subject based on the ideXlab platform.

  • Temperature Dependence of Synaptic Responses in Guinea Pig Hippocampal CA1 Neurons in Vitro
    Cellular and Molecular Neurobiology, 2002
    Co-Authors: Satoshi Fujii, Ken-ichi Ito, Hiroshi Sasaki, Kenya Kaneko, Hiroshi Kato
    Abstract:

    1. Temperature-dependent properties of synaptic transmission were studied by recording orthodromic responses of the Population Spike and excitatory postsynaptic potential in CA1 pyramidal neurons of guinea pig hippocampal slices. 2. Increasing the temperature of the perfusing medium from 30 to 43°C resulted in a decrease in the amplitude of the Population Spike (A-PS) and a reduced slope of the excitatory postsynaptic potential (S-EPSP). Bath application of the γ-aminobutyric acid receptor antagonist, picrotoxin, or a change in the calcium concentration of the perfusate did not affect the A-PS during heating. 3. Increasing the strength of the synaptic input to that eliciting a PS with an amplitude 50, 75, or 100% of maximal at 30°C resulted in a significant increase in the A-PS during the middle phase of hyperthermia (35–39°C). 4. The long-term potentiation (LTP) induced at either 30 or 37°C showed the same percentage increase in both the amplitude of the Population Spike and the S-EPSP after delivery of a tetanus (100 Hz, 100 pulses) to CA1 synapses. 5. The results of the present study, therefore, indicate that the decrease in CA1 field potential was linearly related to the temperature of the slice preparation, while LTP was induced in these responses during heating from 30 to 37°C.

  • Adenosine (A2) antagonist inhibits induction of long-term potentiation of evoked synaptic potentials but not of the Population Spike in hippocampal CA1 neurons.
    Biochemical and biophysical research communications, 1991
    Co-Authors: Yuko Sekino, Ken-ichi Ito, Hiroyoshi Miyakawa, Hiroshi Kato, Yoichiro Kuroda
    Abstract:

    Abstract The effects of adenosine A2 receptor antagonist (CP-66713) on long-term potentiation were studied using guinea pig hippocampal slices in a perfusion system. Tetanic stimulation of Schaffer collateral input which was applied during perfusion of CP-66713 (10 μM), did not induce long-term potentiation but rather long-term depression of evoked synaptic potentials (field EPSP), but induced long-term potentiation of the Population Spike in CA1 neurons. Thus, adenosine derivatives which accumulate in the synaptic cleft during the tetanic stimulation may be involved in induction of the long-term potentiation via A2 receptors at the synapse. The clear discrimination between long-term depression of the field EPSP and long-term potentiation of the Population Spike suggests EPSP-Spike potentiation at the postsynaptic sites.

Gabriel Curio - One of the best experts on this subject based on the ideXlab platform.

  • EPV 14. Non-invasive single-trial detection of human Population Spike responses in somatosensory evoked potentials in a realistic clinical setting
    Clinical Neurophysiology, 2016
    Co-Authors: G. Waterstraat, Gabriel Curio
    Abstract:

    Introduction High-frequency EEG oscillations ( ≈ 600 Hz; HFO) evoked by median nerve stimulation and recorded above the human somatosensory cortex are non-invasive correlates of cortical Population Spikes. Recently, it was shown that spatiotemporal filtering and multivariate classification enables single-trial HFO detection using 29-channel low-impedance ( Ω ) low-noise EEG in an electromagnetically shielded recording chamber. It is an open question, whether this can be achieved in a realistic clinical setting. Methods With a custom-built CE-certified low-noise EEG amplifier, median nerve SEPs were recorded in 10 healthy subjects using 8 electrodes (impedances ≈ 1 k Ω ) in a standard unshielded hospital environment. After band-pass filtering (500–900 Hz), a subset of the trials (N = 2000) was used to train the two-step single-trial HFO detector, which is composed of spatiotemporal filter optimization and nonlinear classification. The performance of the algorithm was assessed using an independent set of additional trials (N = 5200). Results In the present group of 10 subjects, on average the algorithm detected evoked HFOs in 64.9% of the single trials in the correct latency window (around ≈ 20 ms) with a positive predictive value (PPV) of 61.9%. Notably, in several subjects with a higher signal-plus-noise-to-noise ratio (SNNR), detection rate (DR) and PPV were above 80% (peak values: SNNR = 2.0, DR = 95.2%, PPV = 98.5%). Conclusions A non-invasive single-trial detection of human Population Spike responses in somatosensory evoked potentials can be achieved also in a realistic unshielded clinical setting. The increase in sensitivity brought about by combined hardware and algorithmic improvements enables the analysis of single-trial variability and might be extended also to pathological components, such as the non-invasive detection of epileptic neocortical high-frequency oscillations.

  • Non-invasive single-trial detection of variable Population Spike responses in human somatosensory evoked potentials.
    Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology, 2015
    Co-Authors: G. Waterstraat, Manuel Scheuermann, Gabriel Curio
    Abstract:

    Abstract Objective Somatosensory evoked potentials (SEPs) around 600 Hz (‘σ-bursts’) are correlates of cortical Population Spikes. Recently, single-trial σ-bursts were detected in human scalp EEG using 29-channel low-noise recordings in an electromagnetically shielded room. To achieve clinical applicability, this study aimed to establish a protocol using only 8 EEG channels in an unshielded environment and to quantify the variability of σ-bursts. Methods Median nerve SEPs were recorded in 10 healthy subjects using a custom-built low-noise EEG amplifier. A detection algorithm for single-trial σ-bursts was trained as combination of spatio-temporal filters and a non-linear classifier. The single-trial responses were probed for the presence of significant increases of amplitude and variability. Results Single-trial σ-burst detection succeeded with Detection Rates and Positive Predictive Values above 80% in subjects with high SNR. A significant inter-trial variability in the amplitudes of early low-frequency SEPs and σ-bursts could be demonstrated. Conclusions Single-trial σ-bursts can be detected on scalp-EEG using only 8 EEG channels in an electromagnetically disturbed environment. The combination of dedicated hardware and detection algorithms allows quantifying and describing their variability. Significance The variability of Population Spikes in the human somatosensory cortex can be traced non-invasively in a clinical setting.

Toshio Ishikawa - One of the best experts on this subject based on the ideXlab platform.

  • Studies on long-term potentiation of the Population Spike component of hippocampal field potential by the tetanic stimulation of the perforant path in rats: effects of a dopamine agonist, SKF-38393
    Brain research, 1992
    Co-Authors: Ryuya Yanagihashi, Toshio Ishikawa
    Abstract:

    Abstract Long-term potentiation of the field potentials recorded in the dentate gyrus of the hippocampus was observed in freely-moving rats by delivering a brief tetanic stimulation to the perforant path, and the effects of the D 1 agonist, SKF-38393, on it was investigated. The field potential was divided into two components; excitatory postsynaptic potential (EPSP) and Population Spike. In Expt. I, synaptic stimulus-response (S-R) relationship, Spike S-R relationship, and EPSP-Spike (E-S) relationship were plotted. The estimated slope of the regression line in the Spike S-R relationship was enhanced after delivery of the tetanic stimulation (10 pulse at 400 Hz), where that in synaptic S-R relationship was not enhanced. The estimated slope of the regression line in the E-S relationship was also enhanced by the tetanic stimulation. In Expt. II, time-dependent change of the field potential after tetanic stimulation was investigated. The Population Spike was enhanced significantly for about 2 h following tetanic stimulation, while p EPSP did not change sigficantly. The changes following tetanic stimulation in Expt. I and II were significantly inhibited by previous administration of SKF-38393 (10 mg/kg, i.p.), and the effect of this drug was dose-dependently antagonized by the D 1 antagonist, SCH-23390 (0.1, 0.2 and 0.5 mg/kg, i.p.). These results suggest that a brief tetanic stimulation of the perforant path induces long-term potentiation of the Population Spike without potentiating the synaptic input in the perforant path-dentate synapses, and that potentiation of the Population Spike is inhibited by the dopaminergic D 1 mechanism.

Nicholas A. Lesica - One of the best experts on this subject based on the ideXlab platform.

  • Analysis and modelling of variability and covariability of Population Spike trains across multiple time scales.
    Network (Bristol England), 2012
    Co-Authors: Dmitry R. Lyamzin, Jose A. Garcia-lazaro, Nicholas A. Lesica
    Abstract:

    As multi-electrode and imaging technology begin to provide us with simultaneous recordings of large neuronal Populations, new methods for modelling such data must also be developed. We present a model of responses to repeated trials of a sensory stimulus based on thresholded Gaussian processes that allows for analysis and modelling of variability and covariability of Population Spike trains across multiple time scales. The model framework can be used to specify the values of many different variability measures including Spike timing precision across trials, coefficient of variation of the interSpike interval distribution, and Fano factor of Spike counts for individual neurons, as well as signal and noise correlations and correlations of Spike counts across multiple neurons. Using both simulated data and data from different stages of the mammalian auditory pathway, we demonstrate the range of possible independent manipulations of different variability measures, and explore how this range depends on the sensory stimulus. The model provides a powerful framework for the study of experimental and surrogate data and for analyzing dependencies between different statistical properties of neuronal Populations.

  • Modeling Population Spike trains with specified time-varying Spike rates, trial-to-trial variability, and pairwise signal and noise correlations
    Frontiers in computational neuroscience, 2010
    Co-Authors: Dmitry R. Lyamzin, Jakob H. Macke, Nicholas A. Lesica
    Abstract:

    As multi-electrode and imaging technology begin to provide us with simultaneous recordings of large neuronal Populations, new methods for modeling such data must also be developed. Here, we present a model for the type of data commonly recorded in early sensory pathways: responses to repeated trials of a sensory stimulus in which each neuron has it own time-varying Spike rate (as described by its PSTH) and the dependencies between cells are characterized by both signal and noise correlations. This model is an extension of previous attempts to model Population Spike trains designed to control only the total correlation between cells. In our model, the response of each cell is represented as a binary vector given by the dichotomized sum of a deterministic "signal" that is repeated on each trial and a Gaussian random "noise" that is different on each trial. This model allows the simulation of Population Spike trains with PSTHs, trial-to-trial variability, and pairwise correlations that match those measured experimentally. Furthermore, the model also allows the noise correlations in the Spike trains to be manipulated independently of the signal correlations and single-cell properties. To demonstrate the utility of the model, we use it to simulate and manipulate experimental responses from the mammalian auditory and visual systems. We also present a general form of the model in which both the signal and noise are Gaussian random processes, allowing the mean Spike rate, trial-to-trial variability, and pairwise signal and noise correlations to be specified independently. Together, these methods for modeling Spike trains comprise a potentially powerful set of tools for both theorists and experimentalists studying Population responses in sensory systems.