scholarly journals Gap detection in modulated noise: Across-frequency facilitation and interference

2008 ◽  
Vol 123 (2) ◽  
pp. 998-1007 ◽  
Author(s):  
John H. Grose ◽  
Emily Buss ◽  
Joseph W. Hall
Keyword(s):  
Gap Detection ◽  
Frequency Facilitation

scholarly journals Gap detection in modulated noise: Across‐frequency facilitation and interference

2007 ◽  
Vol 121 (5) ◽  
pp. 3198-3198
Author(s):  
John H. Grose ◽  
Joseph W. Hall ◽  
Emily Buss
Keyword(s):  
Gap Detection ◽  
Frequency Facilitation

Temporal-Gap Detection by Cochlear Prosthesis Users

1989 ◽  
Vol 32 (4) ◽  
pp. 849-856 ◽  
Author(s):  
John P. Preece ◽  
Richard S. Tyler
Keyword(s):  
Magnitude Estimation ◽  
Stimulus Level ◽  
Electrode Placement ◽  
Frequency Effect ◽  
Gap Detection ◽  
Cochlear Prosthesis ◽  
Sensation Level

Minimum-detectable gaps for sinusoidal stimuli were measured for three users of a multi electrode cochlear prosthesis as functions of stimulus level, frequency, and electrode place within the cochlea. Stimulus level was scaled by sensation level and by growth-of-loudness functions generated for each condition by direct magnitude estimation. Minimum-detectable gaps decreased with increase in either sensation level or loudness, up to a plateau. When compared at equal sensation levels, the minimum-detectable gaps decreased with frequency increases. The frequency effect on minimum-detectable gaps is reduced if the data are considered at equal loudness. Comparison across place of stimulation within the cochlea showed minimum-detectable gaps to be shorter for more basal electrode placement at low stimulus levels. No differences in minimum-detectable gap as a function of place were found at higher stimulus levels.

scholarly journals Audiograms, gap detection thresholds, and frequency difference limens in cannabinoid receptor 1 knockout mice

2016 ◽  
Vol 332 ◽  
pp. 217-222 ◽  
Author(s):  
Katrina L. Toal ◽  
Kelly E. Radziwon ◽  
David P. Holfoth ◽  
Matthew A. Xu-Friedman ◽  
Micheal L. Dent
Keyword(s):  
Knockout Mice ◽  
Cannabinoid Receptor ◽  
Frequency Difference ◽  
Gap Detection ◽  
Cannabinoid Receptor 1 ◽  
Detection Thresholds

Correlations among within-Channel and between-Channel Auditory Gap-Detection Thresholds in Normal Listeners

Perception ◽  
10.1068/p5116 ◽  
2004 ◽  
Vol 33 (3) ◽  
pp. 371-378 ◽  
Author(s):  
Dennis P Phillips ◽  
Jennifer C Smith
Keyword(s):  
Gap Detection ◽  
Detection Thresholds

Facilitation at the Lobster Neuromuscular Junction: A Stimulus-Dependent Mobilization Model

1997 ◽  
Vol 78 (1) ◽  
pp. 417-428 ◽  
Author(s):  
Mary Kate Worden ◽  
Maria Bykhovskaia ◽  
John T. Hackett
Keyword(s):  
Neuromuscular Junction ◽  
Kinetic Equations ◽  
Nerve Impulse ◽  
Stimulation Frequency ◽  
Synaptic Activity ◽  
Quantal Content ◽  
Physiological Basis ◽  
Low Frequencies ◽  
Average Probability ◽  
Frequency Facilitation

Worden, Mary Kate, Maria Bykhovskaia, and John T. Hackett. Facilitation at the lobster neuromuscular junction: a stimulus-dependent mobilization model. J. Neurophysiol. 78: 417–428, 1997. Frequency facilitation is a process whereby neurosecretion increases as a function of stimulation frequency during repetitive synaptic activity. To examine the physiological basis underlying facilitation, we have estimated the frequency dependence of the synaptic parameters n (number of units capable of responding to a nerve impulse) and P (average probability of responding) at the lobster neuromuscular junction. Both n and P increase as a function of frequency, suggesting that the efficiency of quantal docking and quantal fusion is regulated by repetitive synaptic activity. In experiments in which facilitation is strong and quantal content does not saturate over the frequency range tested, the value of P saturates at low frequencies of stimulation, and increases in quantal content at higher frequencies of stimulation are due to an increase in n. Therefore the value of P does not limit facilitation. We propose that transmitter release is limited by the rates of quantal mobilization and demobilization, and that each excitatory stimulus causes additional mobilization of quanta to dock at the presynaptic release sites. In such a model the binomial parameter n will correspond to the number of quanta docked at the release sites and available for release. We have developed and solved kinetic equations that describe how the number of docked quanta changes as a function of time and of stimulation frequency. The stimulus-dependent mobilization model of facilitation predicts that the reciprocal value of the quantal content depends linearly on the reciprocal product of the stimulation frequency and the probability of release. Fits of the experimental data confirm the accuracy of this prediction, showing that the model proposed here quantitatively describes frequency facilitation. The model predicts that high rates of quantal demobilization will produce strong frequency facilitation.

Neural Responses in Primary Auditory Cortex Mimic Psychophysical, Across-Frequency-Channel, Gap-Detection Thresholds

2000 ◽  
Vol 84 (3) ◽  
pp. 1453-1463 ◽  
Author(s):  
Jos J. Eggermont
Keyword(s):  
Auditory Cortex ◽  
Cortical Neurons ◽  
Primary Auditory Cortex ◽  
Noise Burst ◽  
Gap Detection ◽  
Frequency Content ◽  
Neural Responses ◽  
Frequency Channel ◽  
Interval Representations ◽  
Onset Response

Responses of single- and multi-units in primary auditory cortex were recorded for gap-in-noise stimuli for different durations of the leading noise burst. Both firing rate and inter-spike interval representations were evaluated. The minimum detectable gap decreased in exponential fashion with the duration of the leading burst to reach an asymptote for durations of 100 ms. Despite the fact that leading and trailing noise bursts had the same frequency content, the dependence on leading burst duration was correlated with psychophysical estimates of across frequency channel (different frequency content of leading and trailing burst) gap thresholds in humans. The duration of the leading burst plus that of the gap was represented in the all-order inter-spike interval histograms for cortical neurons. The recovery functions for cortical neurons could be modeled on basis of fast synaptic depression and after-hyperpolarization produced by the onset response to the leading noise burst. This suggests that the minimum gap representation in the firing pattern of neurons in primary auditory cortex, and minimum gap detection in behavioral tasks is largely determined by properties intrinsic to those, or potentially subcortical, cells.

scholarly journals Altered Short-Term Synaptic Plasticity in Mice Lacking the Metabotropic Glutamate Receptor mGlu7

2002 ◽  
Vol 2 ◽  
pp. 730-737 ◽  
Author(s):  
Trevor J. Bushell ◽  
Gilles Sansig ◽  
Valerie J. Collett ◽  
Herman van der Putten ◽  
Graham L. Collingridge
Keyword(s):  
Synaptic Plasticity ◽  
Molecular Mechanisms ◽  
Pyramidal Neurons ◽  
Metabotropic Glutamate Receptor ◽  
Long Term Potentiation ◽  
Short Term ◽  
Metabotropic Glutamate ◽  
Term Potentiation ◽  
Commissural Pathway ◽  
Frequency Facilitation

Eight subtypes of metabotropic glutamate (mGlu) receptors have been identified of which two, mGlu5 and mGlu7, are highly expressed at synapses made between CA3 and CA1 pyramidal neurons in the hippocampus. This input, the Schaffer collateral-commissural pathway, displays robust long-term potentiation (LTP), a process believed to utilise molecular mechanisms that are key processes involved in the synaptic basis of learning and memory. To investigate the possible function in LTP of mGlu7 receptors, a subtype for which no specific antagonists exist, we generated a mouse lacking this receptor, by homologous recombination. We found that LTP could be induced in mGlu7-/- mice and that once the potentiation had reached a stable level there was no difference in the magnitude of LTP between mGlu7-/- mice and their littermate controls. However, the initial decremental phase of LTP, known as short-term potentiation (STP), was greatly attenuated in the mGlu7-/- mouse. In addition, there was less frequency facilitation during, and less post-tetanic potentiation following, a high frequency train in the mGlu7-/- mouse. These results show that the absence of mGlu7 receptors results in alterations in short-term synaptic plasticity in the hippocampus.

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