scholarly journals Spike timing precision changes with spike rate adaptation in the owl's auditory space map

2015 ◽  
Vol 114 (4) ◽  
pp. 2204-2219 ◽  
Author(s):  
Clifford H. Keller ◽  
Terry T. Takahashi
Keyword(s):  
Carrier Frequency ◽  
Time Course ◽  
Rate Adaptation ◽  
Stimulus Level ◽  
Spike Timing ◽  
Spike Rate ◽  
Temporal Precision ◽  
Timing Precision ◽  
Spike Timing Precision

Spike rate adaptation (SRA) is a continuing change of responsiveness to ongoing stimuli, which is ubiquitous across species and levels of sensory systems. Under SRA, auditory responses to constant stimuli change over time, relaxing toward a long-term rate often over multiple timescales. With more variable stimuli, SRA causes the dependence of spike rate on sound pressure level to shift toward the mean level of recent stimulus history. A model based on subtractive adaptation (Benda J, Hennig RM. J Comput Neurosci 24: 113–136, 2008) shows that changes in spike rate and level dependence are mechanistically linked. Space-specific neurons in the barn owl's midbrain, when recorded under ketamine-diazepam anesthesia, showed these classical characteristics of SRA, while at the same time exhibiting changes in spike timing precision. Abrupt level increases of sinusoidally amplitude-modulated (SAM) noise initially led to spiking at higher rates with lower temporal precision. Spike rate and precision relaxed toward their long-term values with a time course similar to SRA, results that were also replicated by the subtractive model. Stimuli whose amplitude modulations (AMs) were not synchronous across carrier frequency evoked spikes in response to stimulus envelopes of a particular shape, characterized by the spectrotemporal receptive field (STRF). Again, abrupt stimulus level changes initially disrupted the temporal precision of spiking, which then relaxed along with SRA. We suggest that shifts in latency associated with stimulus level changes may differ between carrier frequency bands and underlie decreased spike precision. Thus SRA is manifest not simply as a change in spike rate but also as a change in the temporal precision of spiking.

scholarly journals Corticogeniculate feedback sharpens the temporal precision and spatial resolution of visual signals in the ferret

2017 ◽  
Vol 114 (30) ◽  
pp. E6222-E6230 ◽  
Author(s):  
J. Michael Hasse ◽  
Farran Briggs
Keyword(s):  
Spatial Resolution ◽  
Spike Timing ◽  
Visual Signals ◽  
Field Size ◽  
Response Latencies ◽  
Temporal Precision ◽  
V1 Neurons ◽  
Timing Precision ◽  
Spike Timing Precision

The corticogeniculate (CG) pathway connects the visual cortex with the visual thalamus (LGN) in the feedback direction and enables the cortex to directly influence its own input. Despite numerous investigations, the role of this feedback circuit in visual perception remained elusive. To probe the function of CG feedback in a causal manner, we selectively and reversibly manipulated the activity of CG neurons in anesthetized ferrets in vivo using a combined viral-infection and optogenetics approach to drive expression of channelrhodopsin2 (ChR2) in CG neurons. We observed significant increases in temporal precision and spatial resolution of LGN neuronal responses to drifting grating and white noise stimuli when CG neurons expressing ChR2 were light activated. Enhancing CG feedback reduced visually evoked response latencies, increased spike-timing precision, and reduced classical receptive field size. Increased precision among LGN neurons led to increased spike-timing precision among granular layer V1 neurons as well. Together, our findings suggest that the function of CG feedback is to control the timing and precision of thalamic responses to incoming visual signals.

scholarly journals Temperature-induced changes of spike timing precision and network synchronisation

2015 ◽  
Vol 16 (S1) ◽  
Author(s):  
Jan-Hendrik Schleimer ◽  
Janina Hesse ◽  
Susanne Schreiber
Keyword(s):  
Spike Timing ◽  
Timing Precision ◽  
Spike Timing Precision ◽  
Induced Changes

Band-Pass Response Properties of Rat SI Neurons

2003 ◽  
Vol 90 (3) ◽  
pp. 1379-1391 ◽  
Author(s):  
Catherine E. Garabedian ◽  
Stephanie R. Jones ◽  
Michael M. Merzenich ◽  
Anders Dale ◽  
Christopher I. Moore
Keyword(s):  
Inhibitory Neuron ◽  
Stimulus Onset ◽  
Spike Timing ◽  
Spike Rate ◽  
Frequency Range ◽  
Response Properties ◽  
Temporal Precision ◽  
Band Pass ◽  
Temporal Measures ◽  
Vector Strength

Rats typically employ 4- to 12-Hz “whisking” movements of their vibrissae during tactile exploration. The intentional sampling of signals in this frequency range suggests that neural processing of tactile information may be differentially engaged in this bandwidth. We examined action potential responses in rat primary somatosensory cortex (SI) to a range of frequencies of vibrissa motion. Single vibrissae were mechanically deflected with 5-s pulse trains at rates ≤40 Hz. As previously reported, vibrissa deflection evoked robust neural responses that consistently adapted to stimulus rates ≥3 Hz. In contrast with this low-pass feature of the response, several other characteristics of the response revealed bandpass response properties. While average evoked response amplitudes measured 0–35 ms after stimulus onset typically decreased with increasing frequency, the later components of the response (>15 ms post stimulus) were augmented at frequencies between 3 and 10 Hz. Further, during the steady state, both rate and temporal measures of neural activity, measured as total spike rate or vector strength (a measure of temporal fidelity of spike timing across cycles), showed peak signal values at 5–10 Hz. A minimal biophysical network model of SI layer IV, consisting of an excitatory and inhibitory neuron and thalamocortical input, captured the spike rate and vector strength band-pass characteristics. Further analyses in which specific elements were selectively removed from the model suggest that slow inhibitory influences give rise to the band-pass peak in temporal precision, while thalamocortical adaptation can account for the band-pass peak in spike rate. The presence of these band-pass characteristics may be a general property of thalamocortical circuits that lead rodents to target this frequency range with their whisking behavior.

scholarly journals Spike Timing Precision and Neural Error Correction: Local Behavior

2005 ◽  
Vol 17 (7) ◽  
pp. 1577-1601 ◽  
Author(s):  
Michael Stiber
Keyword(s):  
Error Correction ◽  
Dynamical Behavior ◽  
Error Recovery ◽  
Spike Timing ◽  
Local Behavior ◽  
Postsynaptic Spike ◽  
Timing Precision ◽  
Presynaptic Spike ◽  
Spike Timing Precision ◽  
High Degree

The effects of spike timing precision and dynamical behavior on error correction in spiking neurons were investigated. Stationary discharges—phase locked, quasiperiodic, or chaotic—were induced in a simulated neuron by presenting pacemaker presynaptic spike trains across a model of a prototypical inhibitory synapse. Reduced timing precision was modeled by jittering presynaptic spike times. Aftereffects of errors—in this communication, missed presynaptic spikes—were determined by comparing postsynaptic spike times between simulations identical except for the presence or absence of errors. Results show that the effects of an error vary greatly depending on the ongoing dynamical behavior. In the case of phase lockings, a high degree of presynaptic spike timing precision can provide significantly faster error recovery. For nonlocked behaviors, isolated missed spikes can have little or no discernible aftereffects (or even serve to paradoxically reduce uncertainty in postsynaptic spike timing), regardless of presynaptic imprecision. This suggests two possible categories of error correction: high-precision locking with rapid recovery and low-precision nonlocked with error immunity.

scholarly journals Temporal coding of taste in the parabrachial nucleus of the pons of the rat

2011 ◽  
Vol 105 (4) ◽  
pp. 1889-1896 ◽  
Author(s):  
Andrew M. Rosen ◽  
Jonathan D. Victor ◽  
Patricia M. Di Lorenzo
Keyword(s):  
Time Course ◽  
Temporal Dynamics ◽  
Spike Timing ◽  
Temporal Coding ◽  
Taste Quality ◽  
Spike Count ◽  
Parabrachial Nucleus ◽  
Similar Proportion ◽  
Temporal Characteristics ◽  
Temporal Precision

Recent studies have provided evidence that temporal coding contributes significantly to encoding taste stimuli at the first central relay for taste, the nucleus of the solitary tract (NTS). However, it is not known whether this coding mechanism is also used at the next synapse in the central taste pathway, the parabrachial nucleus of the pons (PbN). In the present study, electrophysiological responses to taste stimuli (sucrose, NaCl, HCl, and quinine) were recorded from 44 cells in the PbN of anesthetized rats. In 29 cells, the contribution of the temporal characteristics of the response to the discrimination of various taste qualities was assessed. A family of metrics that quantifies the similarity of two spike trains in terms of spike count and spike timing was used. Results showed that spike timing in 14 PbN cells (48%) conveyed a significant amount of information about taste quality, beyond what could be conveyed by spike count alone. In another 14 cells (48%), the rate envelope (time course) of the response contributed significantly more information than spike count alone. Across cells there was a significant correlation ( r = 0.51; P < 0.01) between breadth of tuning and the proportion of information conveyed by temporal dynamics. Comparison with previous data from the NTS (Di Lorenzo PM and Victor JD. J Neurophysiol 90: 1418–31, 2003 and J Neurophysiol 97: 1857–1861, 2007) showed that temporal coding in the NTS occurred in a similar proportion of cells and contributed a similar fraction of the total information at the same average level of temporal precision, even though trial-to-trial variability was higher in the PbN than in the NTS. These data suggest that information about taste quality conveyed by the temporal characteristics of evoked responses is transmitted with high fidelity from the NTS to the PbN.

scholarly journals Spike-Timing Precision and Neuronal Synchrony Are Enhanced by an Interaction between Synaptic Inhibition and Membrane Oscillations in the Amygdala

PLoS ONE ◽  
2012 ◽  
Vol 7 (4) ◽  
pp. e35320 ◽  
Author(s):  
Steven J. Ryan ◽  
David E. Ehrlich ◽  
Aaron M. Jasnow ◽  
Shabrine Daftary ◽  
Teresa E. Madsen ◽  
...  
Keyword(s):  
Spike Timing ◽  
Synaptic Inhibition ◽  
Neuronal Synchrony ◽  
Timing Precision ◽  
Spike Timing Precision ◽  
Membrane Oscillations

scholarly journals Circuit mechanisms revealed by spike-timing correlations in macaque area MT

2013 ◽  
Vol 109 (3) ◽  
pp. 851-866 ◽  
Author(s):  
Xin Huang ◽  
Stephen G. Lisberger
Keyword(s):  
Time Course ◽  
Neural Circuit ◽  
Temporal Cortex ◽  
Intracortical Inhibition ◽  
Central Peak ◽  
Spike Timing ◽  
Temporal Precision ◽  
Outward Currents ◽  
Cross Correlations ◽  
The Individual

We recorded simultaneously from pairs of motion-sensitive neurons in the middle temporal cortex (MT) of macaque monkeys and used cross-correlations in the timing of spikes between neurons to gain insights into cortical circuitry. We characterized the time course and stimulus dependency of the cross-correlogram (CCG) for each pair of neurons and of the auto-correlogram (ACG) of the individual neurons. For some neuron pairs, the CCG showed negative flanks that emerged next to the central peak during stimulus-driven responses. Similar negative flanks appeared in the ACG of many neurons. Negative flanks were most prevalent and deepest when the neurons were driven to high rates by visual stimuli that moved in the neurons' preferred directions. The temporal development of the negative flanks in the CCG coincided with a parallel, modest reduction of the noise correlation between the spike counts of the neurons. Computational analysis of a model cortical circuit suggested that negative flanks in the CCG arise from the excitation-triggered mutual cross-inhibition between pairs of excitatory neurons. Intracortical recurrent inhibition and afterhyperpolarization caused by intrinsic outward currents, such as the calcium-activated potassium current of small conductance, can both contribute to the negative flanks in the ACG. In the model circuit, stronger intracortical inhibition helped to maintain the temporal precision between the spike trains of pairs of neurons and led to weaker noise correlations. Our results suggest a neural circuit architecture that can leverage activity-dependent intracortical inhibition to adaptively modulate both the synchrony of spike timing and the correlations in response variability.

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