Forward masking of auditory nerve fiber responses

1979 ◽  
Vol 42 (4) ◽  
pp. 1083-1107 ◽  
Author(s):  
D. M. Harris ◽  
P. Dallos

1. Responses of single fibers were obtained from the auditory nerve of chinchillas. Tone-burst stimuli consisted of a masking stimulus followed by a probe stimulus. Forward masking of a fiber's response is defined as a reduction in the magnitude of the probe-evoked response caused by the addition of the masking stimulus. 2. The recovery of probe response magnitude as a function of the time interval between masker offset and probe onset (delta T) follows an exponential time course. A relationship between the time course or magnitude of poststimulus recovery and the characteristic frequency (CF) of a fiber was not detected. 3. The iso-forward masking contour near the threshold of the masking effect across masker frequencies approximates a fiber's frequency threshold curve (FTC). In other words, forward masking tuning curves are essentially the same as frequency threshold curves. 4. The frequency dependence of forward masking is compared to that of two-tone suppression. Tonal stimuli outside the boundaries of a fiber's FTC that produce two-tone suppression are ineffective forward maskers. Certain frequency/intensity combinations within the FTC may produce both suppression and forward masking and tones within the remaining area of the FTC produce no suppression but are effective forward maskers. 5. Both the time course and the magnitude of the forward masking effect are dependent on the discharge rate evoked by the masker regardless of the masker's absolute level or spectral content. An increase in masker-evoked excitation causes an increase in time constant and a greater reduction in probe response magnitude, rd. The function relating rd to masker level parallels the firing rate/masker level function up to 40 dB above response threshold. 6. A decrease in masker duration from 100 ms leads to a decrease in both rd and the time constant of recovery. There is no significant difference between the 100 and 200 ms duration conditions. 7. Forward masking in single fibers is related to the period of poststimulus recovery of spontaneous activity, a component of a fiber's response pattern to the masker, and this component is tentatively identified as a period of recovery from short-term adaptation.

2007 ◽  
Vol 24 (2) ◽  
pp. 177-181 ◽  
Author(s):  
BERNT C. SKOTTUN ◽  
JOHN R. SKOYLES

In metacontrast a masking stimulus reduces the visibility of an adjacent target stimulus. This effect has been interpreted in terms of magno-/parvocellular interactions. It has also been found that a second masking stimulus, which precedes the primary mask by about 90 ms reduces the masking effect. This reduction, which is termed “target recovery,” has been hypothesized to reflect parvocellular inhibition of the magnocellular system. However, this is problematic because the time course of this effect is much larger than would be expected from magno-/parvocellular interactions. For this and other reasons, it is difficult to understand metacontrast in terms of magno- and parvocellular mechanisms.


1994 ◽  
Vol 72 (1) ◽  
pp. 326-336 ◽  
Author(s):  
M. Andreasen ◽  
J. J. Hablitz

1. Whole-cell patch-clamp recordings were used to study paired-pulse facilitation (PPF) of the lateral perforant path input to the dentate gyrus in thin hippocampal slices. 2. Orthodromic stimulation of the lateral perforant pathway evoked a excitatory postsynaptic current (EPSC) with a latency of 3.3 +/- 0.1 ms (mean +/- SE) that fluctuated in amplitude. The EPSC had a rise time (10-90%) of 2.79 +/- 0.06 ms (n = 35) and decayed with a single exponential time course with a time-constant of 9.14 +/- 0.24 ms (n = 35). No correlation was found between the amplitude of the EPSC and the rise time or decay time-constant. The non-N-methyl-D-aspartate (NMDA) antagonist 6-cyano-7-nitroquinoxaline-2,3-dione completely blocked the EPSC whereas the NMDA antagonist D-aminophosphonovaleric acid (APV) had modest effects. 3. When a test (T-)EPSC was preceded at an interval of 100 ms by a conditioning (C-)EPSC, a significant increase in the amplitude of the T-EPSC was seen in 38 out of 44 trials analyzed from a total of 27 granule cells. The average amount of PPF was 35.7 +/- 2.1%. There was no apparent correlation between the amount of PPF and the stimulation intensity or mean amplitude of the C-EPSC. The time course of the facilitated T-EPSC was not significantly different from that of the C-EPSC. 4. No correlation was found between the amplitude of the C-EPSC and that of the T-EPSC. Estimates of quantal content (mcv) were determined by calculating the ratio of the squared averaged EPSC amplitude (from 48 responses) to the variance of these responses (M2/sigma 2) whereas quantal amplitudes (qcv) were estimated by calculating the ratio of the response variance to average EPSC amplitude (sigma 2/M). PPF was found to be associated with an average increase in mcv of 64.8 +/- 7.2% (n = 38) whereas qcv was decreased by 12.1 +/- 3.8%. 5. The time course of PPF was studied by varying the interval between the C- and T-pulse from 10 to 400 ms while keeping the stimulation intensity constant. Maximal facilitation of the T-EPSC was obtained with interpulse intervals < or = 25 ms where the average facilitation amounted to approximately 70% (n = 6). The decline of facilitation was nearly exponential and was no longer evident with intervals > 350 ms.(ABSTRACT TRUNCATED AT 400 WORDS


1991 ◽  
Vol 97 (2) ◽  
pp. 303-320 ◽  
Author(s):  
A Castellano ◽  
J López-Barneo

Voltage-gated Na+ and Ca2+ conductances of freshly dissociated septal neurons were studied in the whole-cell configuration of the patch-clamp technique. All cells exhibited a large Na+ current with characteristic fast activation and inactivation time courses. Half-time to peak current at -20 mV was 0.44 +/- 0.18 ms and maximal activation of Na+ conductance occurred at 0 mV or more positive membrane potentials. The average value was 91 +/- 32 nS (approximately 11 mS cm-2). At all membrane voltages inactivation was well fitted by a single exponential that had a time constant of 0.44 +/- 0.09 ms at 0 mV. Recovery from inactivation was complete in approximately 900 ms at -80 mV but in only 50 ms at -120 mV. The decay of Na+ tail currents had a single time constant that at -80 mV was faster than 100 microseconds. Depolarization of septal neurons also elicited a Ca2+ current that peaked in approximately 6-8 ms. Maximal peak Ca2+ current was obtained at 20 mV, and with 10 mM external Ca2+ the amplitude was 0.35 +/- 0.22 nA. During a maintained depolarization this current partially inactivated in the course of 200-300 ms. The Ca2+ current was due to the activity of two types of conductances with different deactivation kinetics. At -80 mV the closing time constants of slow (SD) and fast (FD) deactivating channels were, respectively, 1.99 +/- 0.2 and 0.11 +/- 0.03 ms (25 degrees C). The two kinds of channels also differed in their activation voltage, inactivation time course, slope of the conductance-voltage curve, and resistance to intracellular dialysis. The proportion of SD and FD channels varied from cell to cell, which may explain the differential electrophysiological responses of intracellularly recorded septal neurons.


1992 ◽  
Vol 67 (6) ◽  
pp. 1698-1701 ◽  
Author(s):  
S. M. Thompson ◽  
B. H. Gahwiler

1. The effects of the gamma-aminobutyric acid (GABA) uptake blocker tiagabine on inhibitory synaptic potentials (IPSPs) were examined with microelectrode and whole-cell recording from CA3 pyramidal cells in rat hippocampal slice cultures. 2. Tiagabine (10-25 microM) greatly prolonged the duration of monosynaptic IPSPs elicited in the presence of excitatory amino acid antagonists but had no effect on their amplitude. Part of the prolonged time course resulted from a GABAB receptor-mediated component that was not detectable under control conditions. 3. The mean decay time constant of the underlying GABAA receptor-mediated synaptic current was increased from 16 to 250 ms. Spontaneous miniature IPSPs recorded with whole-cell clamp were unaffected by tiagabine. Pentobarbital sodium, in contrast, increased the decay time constant of both evoked and spontaneous GABAA-mediated currents. 4. Tiagabine (25 microM) inhibited spontaneous and evoked epileptiform bursting induced by increasing the extracellular potassium concentration to 8 mM. 5. We conclude that GABA uptake plays a significant role in determining the time course of evoked IPSPs and also limits the likelihood that GABAB receptors are activated.


1999 ◽  
Vol 82 (5) ◽  
pp. 2120-2129 ◽  
Author(s):  
Pascal Legendre

Electrophysiological recordings of outside-out patches to fast-flow applications of glycine were made on patches derived from the Mauthner cells of the 50-h-old zebrafish larva. As for glycinergic miniature inhibitory postsynaptic currents (mIPSCs), depolarizing the patch produced a broadening of the transient outside-out current evoked by short applications (1 ms) of a saturating concentration of glycine (3 mM). When the outside-out patch was depolarized from −50 to +20 mV, the peak current varied linearly with voltage. A 1-ms application of 3 mM glycine evoked currents that activated rapidly and deactivated biexponentially with time constants of ≈5 and ≈30 ms (holding potential of −50 mV). These two decay time constants were increased by depolarization. The fast deactivation time constant increased e-fold per 95 mV. The relative amplitude of the two decay components did not significantly vary with voltage. The fast component represented 64.2 ± 2.8% of the total current at −50 mV and 54.1 ± 10% at +20 mV. The 20–80% rise time of these responses did not show any voltage dependence, suggesting that the opening rate constant is insensitive to voltage. The 20–80% rise time was 0.2 ms at −70 mV and 0.22 ms at +20 mV. Responses evoked by 100–200 ms application of a low concentration of glycine (0.1 mM) had a biphasic rising phase reflecting the complex gating behavior of the glycine receptor. The time constant of these two components and their relative amplitude did not change with voltage, suggesting that modal shifts in the glycine-activated channel gating mode are not sensitive to the membrane potential. Using a Markov model to simulate glycine receptor gating behavior, we were able to mimic the voltage-dependent change in the deactivation time course of the responses evoked by 1-ms application of 3 mM glycine. This kinetics model incorporates voltage-dependent closing rate constants. It provides a good description of the time course of the onset of responses evoked by the application of a low concentration of glycine at all membrane potentials tested.


1996 ◽  
Vol 76 (1) ◽  
pp. 17-29 ◽  
Author(s):  
K. Parham ◽  
H. B. Zhao ◽  
D. O. Kim

1. To elucidate the peripheral contribution to "echo" processing in the auditory system, we examined the characteristics of auditory nerve responses to click-pair stimuli in unanesthetized, decerebrate cats. We used equilevel click pairs at peak levels of 45, 65, and 85 dB SPL re 20 microPa. The interclick intervals ranged from 1 to 32 ms. This study reports results from 78 auditory nerve fibers in 7 cats. The fibers were divided into 2 groups: 33 low- and 45 high-spontaneous rate (SR), with SRs less than and > or = 20 spikes/s, respectively. A method was introduced to quantify the second-click response, and its recovery was examined as a function of the interclick interval. 2. In general, auditory nerve fibers showed a gradual recovery of the second-click response as interclick interval was increased. Noticeable differences in the second-click response recovery functions emerged among fiber populations that were related to the SR. Low-SR fibers showed little change in the recovery functions of the second-click response as the click level was increased from 45 to 85 dB SPL. In contrast, high-SR fibers showed slower recoveries with increasing click level from 45 to 85 dB SPL. At 45 and 65 dB SPL, the recovery functions of the two SR groups were similar. At 85 dB SPL, high-SR fibers exhibited slower recovery than low-SR fibers, regardless of fiber characteristic frequency. The interclick intervals at 50% second-click response ranged from 1 to 6 ms (mean, 1.4 ms) among low-SR fibers. The interclick intervals at 50% second-click response for high-SR fibers, whereas similar to those for the low-SR fibers at 45 and 65 dB SPL, ranged from 2 to 16 ms (mean, 3 ms) for high-SR fibers, at 85 dB SPL. 3. We also examined auditory nerve compound action potentials (CAPs) evoked by click-pair stimuli for various interclick intervals and click levels. With increasing interclick interval, the amplitude of the second-click CAP increased, and with increasing level, the second-click CAP showed slower recovery. At 45 dB SPL, the recovery functions of the second-click CAP were similar to those of the high- and low-SR fibers. At higher levels, the CAP exhibited lower second-click response values than both high- and low-SR fiber populations for interclick intervals < 4-8 ms. At 85 dB SPL, as interclick interval increased, between 8 and 16 ms, the CAP second-click response converged with that of the high-SR fibers, and by 32 ms, the second-click response values were similar for the CAP, high- and low-SR fibers. 4. The present results are consistent with those of forward masking studies at the level of the auditory nerve in that both demonstrate a short-term reduction of the neural responses. However, the two results differ in that we observed that high-SR fibers exhibited slower recovery than low-SR fibers in response to click-pair stimuli, opposite of the trend observed in the forward masking studies of responses to pure-tone bursts. 5. The present results on auditory nerve fiber responses to click-pair stimuli provide a reference for comparison with responses of central auditory neurons to similar stimuli. This information should serve to elucidate the peripheral contribution to the processing of echoes in the auditory system.


1963 ◽  
Vol 204 (1) ◽  
pp. 31-34 ◽  
Author(s):  
Paul C. Johnson ◽  
Kenneth M. Hanson

The pressure volume characteristics of the intestinal venous vasculature were studied in vivo by a weight technique. The pressure-volume relationship was linear over the range 0–20 mm Hg. In a few experiments the volume increment appeared to be reduced at venous pressures above 30 mm Hg. The average compliance of the intestinal veins was 0.34 ml/mm Hg 100 g tissue. The time course of the blood volume change was also examined. Rapid elevation of venous pressure to a higher level caused blood volume to increase at an exponentially declining rate. Therefore, the phenomenon of creep in the intestinal veins appears to be a simple exponential process. The half time of the increase in venous volume averaged 7.5 sec while the time constant was 10.9 sec. The magnitude of the time constant suggests the presence of elements of rather high viscosity in the venous wall.


Like the axolemma of the giant nerve fibre of the squid, the nodal membrane of frog myelinated nerve fibres after blocking transmembrane ionic currents exhibits asymmetrical displacement currents during and after hyperpolarizing and depolarizing voltage clamp pulses of equal size. The steady-state distribution of charges as a function of membrane potential is consistent with Boltzmann’s law (midpoint potential —33.7 mV; saturation value 17200 charges/(μm 2 ). The time course of the asymmetry current and the voltage dependence of its time constant are consistent with the notion that due to a sudden change in membrane potential the charges undergo a first order transition between two configurations. Size and voltage dependence of the time constant are similar to those of the activation of the sodium conductance assuming m 2 h kinetics, The results suggest the presence of ten times more sodium channels (5000/μm2) in the node of Ranvier than in the squid giant axon with similar sodium conductance per channel (2-3 pS),


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