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William A. Falls - One of the best experts on this subject based on the ideXlab platform.

  • Posttraining lesions of the Auditory thalamus, but not cortex, disrupt the inhibition of fear conditioned to an Auditory Stimulus.
    The European journal of neuroscience, 2006
    Co-Authors: Scott A. Heldt, William A. Falls
    Abstract:

    The purpose of this study was to examine the effects of lesions within the Auditory system in an effort to disrupt the processing of the noise Stimulus conditioned to inhibit fear. To accomplish this, three experiments were conducted in which rats were first given feature-negative discrimination training in which a noise was conditioned to inhibit fear to a light that signals danger. Following training, rats were given lesions of the medial geniculate body (MGB), Auditory thalamus (ADT), or Auditory cortex (CTX). Next, rats were tested for the ability to inhibit fear in the presence of the noise safety signal. The results of these experiments indicated that bilateral lesions of ADT disrupted the ability of the noise inhibitor to inhibit fear. In contrast, lesions largely restricted to the MGB or CTX did not disrupt the inhibition of fear. Along with past studies, these results suggest that an Auditory pathway(s), which includes projections from the tectum to the ADT, is used to detect the safety properties previously conditioned to an Auditory Stimulus.

  • Destruction of the Auditory thalamus disrupts the production of fear but not the inhibition of fear conditioned to an Auditory Stimulus.
    Brain research, 1998
    Co-Authors: Scott A. Heldt, William A. Falls
    Abstract:

    The Auditory thalamus is part of a neural circuit that mediates the expression of fear to Auditory stimuli. Bilateral lesions of the Auditory thalamus prevent the expression of fear to an Auditory Stimulus paired with shock. The present study assessed whether bilateral lesions of the Auditory thalamus would also disrupt the inhibition of fear to an Auditory Stimulus paired with the absence of shock. Rats were given bilateral lesions of the Auditory thalamus followed by Pavlovian conditioned inhibition training in which a light was paired with shock and a noise and light compound was presented in the absence of shock. Fear and the inhibition of fear were measured with the fear-potentiated startle effect. Lesions of the Auditory thalamus did not disrupt the ability of the noise to inhibit the expression of fear to the light. However, these lesions did disrupt the ability of the noise to produce fear-potentiated startle after it had been subsequently paired with shock. These results suggest that although the Auditory thalamus is an essential part of a neural circuit that mediates the expression of fear to Auditory stimuli, it is not an essential part of the circuit that mediates the inhibition of fear to Auditory stimuli.

  • Research report Destruction of the Auditory thalamus disrupts the production of fear but not the inhibition of fear conditioned to an Auditory Stimulus
    1998
    Co-Authors: Scott A. Heldt, William A. Falls
    Abstract:

    The Auditory thalamus is part of a neural circuit that mediates the expression of fear to Auditory stimuli. Bilateral lesions of the Auditory thalamus prevent the expression of fear to an Auditory Stimulus paired with shock. The present study assessed whether bilateral lesions of the Auditory thalamus would also disrupt the inhibition of fear to an Auditory Stimulus paired with the absence of shock. Rats were given bilateral lesions of the Auditory thalamus followed by Pavlovian conditioned inhibition training in which a light was paired with shock and a noise and light compound was presented in the absence of shock. Fear and the inhibition of fear were measured with the fear-potentiated startle effect. Lesions of the Auditory thalamus did not disrupt the ability of the noise to inhibit the expression of fear to the light. However, these lesions did disrupt the ability of the noise to produce fear-potentiated startle after it had been subsequently paired with shock. These results suggest that although the Auditory thalamus is an essential part of a neural circuit that mediates the expression of fear to Auditory stimuli, it is not an essential part of the circuit that mediates the inhibition of fear to Auditory stimuli. q 1998 Elsevier Science B.V. All rights reserved.

Scott A. Heldt - One of the best experts on this subject based on the ideXlab platform.

  • Posttraining lesions of the Auditory thalamus, but not cortex, disrupt the inhibition of fear conditioned to an Auditory Stimulus.
    The European journal of neuroscience, 2006
    Co-Authors: Scott A. Heldt, William A. Falls
    Abstract:

    The purpose of this study was to examine the effects of lesions within the Auditory system in an effort to disrupt the processing of the noise Stimulus conditioned to inhibit fear. To accomplish this, three experiments were conducted in which rats were first given feature-negative discrimination training in which a noise was conditioned to inhibit fear to a light that signals danger. Following training, rats were given lesions of the medial geniculate body (MGB), Auditory thalamus (ADT), or Auditory cortex (CTX). Next, rats were tested for the ability to inhibit fear in the presence of the noise safety signal. The results of these experiments indicated that bilateral lesions of ADT disrupted the ability of the noise inhibitor to inhibit fear. In contrast, lesions largely restricted to the MGB or CTX did not disrupt the inhibition of fear. Along with past studies, these results suggest that an Auditory pathway(s), which includes projections from the tectum to the ADT, is used to detect the safety properties previously conditioned to an Auditory Stimulus.

  • Destruction of the Auditory thalamus disrupts the production of fear but not the inhibition of fear conditioned to an Auditory Stimulus.
    Brain research, 1998
    Co-Authors: Scott A. Heldt, William A. Falls
    Abstract:

    The Auditory thalamus is part of a neural circuit that mediates the expression of fear to Auditory stimuli. Bilateral lesions of the Auditory thalamus prevent the expression of fear to an Auditory Stimulus paired with shock. The present study assessed whether bilateral lesions of the Auditory thalamus would also disrupt the inhibition of fear to an Auditory Stimulus paired with the absence of shock. Rats were given bilateral lesions of the Auditory thalamus followed by Pavlovian conditioned inhibition training in which a light was paired with shock and a noise and light compound was presented in the absence of shock. Fear and the inhibition of fear were measured with the fear-potentiated startle effect. Lesions of the Auditory thalamus did not disrupt the ability of the noise to inhibit the expression of fear to the light. However, these lesions did disrupt the ability of the noise to produce fear-potentiated startle after it had been subsequently paired with shock. These results suggest that although the Auditory thalamus is an essential part of a neural circuit that mediates the expression of fear to Auditory stimuli, it is not an essential part of the circuit that mediates the inhibition of fear to Auditory stimuli.

  • Research report Destruction of the Auditory thalamus disrupts the production of fear but not the inhibition of fear conditioned to an Auditory Stimulus
    1998
    Co-Authors: Scott A. Heldt, William A. Falls
    Abstract:

    The Auditory thalamus is part of a neural circuit that mediates the expression of fear to Auditory stimuli. Bilateral lesions of the Auditory thalamus prevent the expression of fear to an Auditory Stimulus paired with shock. The present study assessed whether bilateral lesions of the Auditory thalamus would also disrupt the inhibition of fear to an Auditory Stimulus paired with the absence of shock. Rats were given bilateral lesions of the Auditory thalamus followed by Pavlovian conditioned inhibition training in which a light was paired with shock and a noise and light compound was presented in the absence of shock. Fear and the inhibition of fear were measured with the fear-potentiated startle effect. Lesions of the Auditory thalamus did not disrupt the ability of the noise to inhibit the expression of fear to the light. However, these lesions did disrupt the ability of the noise to produce fear-potentiated startle after it had been subsequently paired with shock. These results suggest that although the Auditory thalamus is an essential part of a neural circuit that mediates the expression of fear to Auditory stimuli, it is not an essential part of the circuit that mediates the inhibition of fear to Auditory stimuli. q 1998 Elsevier Science B.V. All rights reserved.

Bryan Gick - One of the best experts on this subject based on the ideXlab platform.

  • Startling speech: eliciting prepared speech using startling Auditory Stimulus.
    Frontiers in psychology, 2014
    Co-Authors: Chenhao Chiu, Bryan Gick
    Abstract:

    Speech research has recently seen a good deal of activity surrounding forward models (Tian and Poeppel, 2012; Pickering and Garrod, 2013; Scott, 2013), expanding on a long tradition of work in preprogramming of speech motor plans (e.g., Lashley, 1951; Keele, 1981; Klapp, 2003). Despite the volume of activity and interest in this area, few studies have offered insight into the detailed content of these forward plans. The content of such plans should presumably specify, at minimum, those aspects of speech that are essential in determining linguistic contrast, independent of the many aspects of a physical speech utterance that may be determined or altered through feedback mechanisms. Our previous work has attempted to uncover some of the detailed content of such forward plans using behavioral methods (Scott et al., 2013), while other studies have used neuroimaging methods (e.g., Heinks-Maldonado et al., 2006). Both approaches have given suggestive results, though not without concerns regarding interpretation (Niziolek et al., 2013). A novel experimental methodology employing startling Auditory stimuli (SAS, >120 dB) has been used to demonstrate the execution of prepared non-speech motor behaviors (e.g., head rotation and upper limb movements) with little or no interference from feedback regulation (Valls-Sole et al., 1999; Oude Nijhuis et al., 2007; Carlsen et al., 2012). Accelerated release of prepared movements (as short as 70 ms for EMG response onset) in response to SAS has been termed the StartReact effect (Valls-Sole et al., 1999, 2008). Because of their very short onset latency, SAS-induced actions may be fully executed before they are affected by sensory feedback, thus enabling study of the forward plan. It is our opinion that this experimental paradigm is ideally suited for investigating speech production and uncovering the detailed contents of forward speech plans. Early analyses hypothesized that the rapid release of SAS-induced responses is the result of triggering subcortically stored information with faster neural transmissions (Carlsen et al., 2004; see also Castellote et al., 2012; Nonnekes et al., 2014). However, recent transcranial magnetic stimulation (TMS) studies show that the StartReact effect may not be limited to subcortically stored programs, but can also be observed in cortically dependent processes (Alibiglou and MacKinnon, 2012; Stevenson et al., 2014). These studies found that, when a cortical silent period was induced by applying TMS to motor cortex, the StartReact response was delayed in startle trials. If only subcortical processes were involved, TMS should not have affected the StartReact response. The delay in the StartReact response suggests that the pathways for a StartReact response would be mediated by, rather than bypassing, cortical areas. Following these studies of finger movement, Stevenson et al. (2014) apply the startle paradigm to prepared spoken syllables, observing that voluntary lip movements were released at shorter latencies by a SAS, while the timing of kinematic displacement remained unaffected and formant profiles were performed as intended with no disruption. These results support the view that prepared syllables encode sufficient kinematic and acoustic information as part of the forward plan, and that this information may be subject to rapid release by a SAS. Extending this paradigm to pitch control in speech, Chiu and Gick (in press) show that a SAS induces an elevated pitch level in prepared syllables. Speakers show no evidence of an attempt to correct this elevated pitch to a baseline level even though Auditory and somatosensory feedback is likely available before the end of the response. These findings raise questions as to the extent to which feedback information may affect SAS-induced responses, and suggest that uncorrected contents of forward speech plans may be observable even for longer (i.e., multisyllabic) responses using SAS. The observed StartReact effect in syllable production also suggests that SAS-induced motor tasks, including upper limb, and speech movements, may involve similar neural pathways. It is noteworthy that the StartReact pathways involve similar pathways for speech production. As summarized in Carlsen et al. (2012), the StartReact response is mediated via an ascending thalamo-cortical pathway, generated by activation from reticular formation exerting on thalamus. Increased activation in thalamus provides inputs to primary motor cortex to initiate the cortically prepared movement via a descending corticospinal pathway. Similarly, speech production may also rely on thalamo-cortical circuits, and a descending corticospinal pathway. Specifically, receiving inputs from cerebellum, thalamus projects to primary motor cortex and Broca's area, and the commands are mediated via putamen and reticular formation and sent down to the phonatory motoneurones in the spine (Iwata et al., 1996; Jurgens, 2002; Guenther et al., 2006). Given that speech production involves a similar thalamo-cortical pathway to the one found in upper limb movements, upper limb movements, and speech movements may share the same StartReact pathways when elicited by a SAS. Shorter reaction times in StartReact responses are accounted for by increased neuron activation reaching faster above initiation threshold (see Carlsen et al., 2012 for details). Similar to the calculation of the required time span for voluntary limbic movements, we can also conservatively calculate the time required for a speech response. First, Schroeder and Foxe (2002) report a response latency of 10 ~ 25 ms from the onset of Auditory Stimulus to the activation in the Auditory cortex. Second, another 5 ~ 10 ms is required for the Stimulus to be conducted between the lateral lemniscus and the thalamus for auditorily-evoked responses (Stockard et al., 1977). Third, transcortical and thalamus-primary motor cortex transmissions require 2 ~ 4 ms for conduction (Guenther et al., 2006; Carlsen et al., 2012). Last, the orofacial muscle EMG response to TMS on the face area of the motor cortex has a latency of about 11 ~ 12 ms (Meyer et al., 1994) and the motor time for the muscle movement is delayed by 30 ms. Adding these values gives a minimum of 58 ~ 81 ms lag time in response to a SAS. As reported in Stevenson et al. (2014), the onset of SAS-induced responses is 75 ms, suggesting that the shared neural pathway used for limb movements and speech movements does lead to a StartReact effect for speech movement. Insofar as programming is necessary for speech production, we believe that the SAS methodology provides a new perspective that can help us to uncover the kinematic and linguistic contents of forward speech plans. Neural correlates and pathways for SAS-induced responses also support the view that SAS-induced speech responses may contain unaltered details of speech plans, allowing researchers a window into forward speech planning that bypasses afferent feedback information.

Emery N. Brown - One of the best experts on this subject based on the ideXlab platform.

  • The effect of different spectro-temporal representations of an input Auditory Stimulus on the fitting of a point process model of Auditory neurons
    2012 11th International Conference on Information Science Signal Processing and their Applications (ISSPA), 2012
    Co-Authors: Eric Plourde, Emery N. Brown
    Abstract:

    We compare the effect of the use of three different spectro-temporal representations of an input Auditory Stimulus on the fitting of a point process model of Auditory neuron firing. The three spectro-temporal representations considered are the spectrogram, a gammatone filterbank and the Hilbert spectrum. We firstly investigate how the model fits the recorded neuronal data when using either one of the three representations and secondly how well do the estimated parameters of the model correspond to their experimentally measured counterparts. It is observed that all three representations yield a model that fits well the recorded data. However, the characteristic frequencies obtained with the spectro-temporal parameters of the model using the gammatone filterbank corresponds better to the experimentally measured characteristic frequency than the characteristic frequency obtained with the models using the other two spectro-temporal representations. Therefore, it is concluded that the quality of the fitted parameters can be affected by the choice of the spectro-temporal representation and that, as could have been expected, the gammatone filterbank seems to more accurately extract the relevant spectro-temporal characteristics of the input Auditory Stimulus.

  • ISSPA - The effect of different spectro-temporal representations of an input Auditory Stimulus on the fitting of a point process model of Auditory neurons
    2012 11th International Conference on Information Science Signal Processing and their Applications (ISSPA), 2012
    Co-Authors: Eric Plourde, Emery N. Brown
    Abstract:

    We compare the effect of the use of three different spectro-temporal representations of an input Auditory Stimulus on the fitting of a point process model of Auditory neuron firing. The three spectro-temporal representations considered are the spectrogram, a gammatone filterbank and the Hilbert spectrum. We firstly investigate how the model fits the recorded neuronal data when using either one of the three representations and secondly how well do the estimated parameters of the model correspond to their experimentally measured counterparts. It is observed that all three representations yield a model that fits well the recorded data. However, the characteristic frequencies obtained with the spectro-temporal parameters of the model using the gammatone filterbank corresponds better to the experimentally measured characteristic frequency than the characteristic frequency obtained with the models using the other two spectro-temporal representations. Therefore, it is concluded that the quality of the fitted parameters can be affected by the choice of the spectro-temporal representation and that, as could have been expected, the gammatone filterbank seems to more accurately extract the relevant spectro-temporal characteristics of the input Auditory Stimulus.

Jinglong Wu - One of the best experts on this subject based on the ideXlab platform.

  • Modulation of Auditory Stimulus processing by visual spatial or temporal cue: an event-related potentials study
    Neuroscience Letters, 2013
    Co-Authors: Xiaoyu Tang, Chunlin Li, Weiping Yang, Soushirou Ishikawa, Jingjing Yang, Jinglong Wu
    Abstract:

    Abstract Utilizing the high temporal resolution of event-related potentials (ERPs), we examined how visual spatial or temporal cues modulated the Auditory Stimulus processing. The visual spatial cue (VSC) induces orienting of attention to spatial locations; the visual temporal cue (VTC) induces orienting of attention to temporal intervals. Participants were instructed to respond to Auditory targets. Behavioral responses to Auditory stimuli following VSC were faster and more accurate than those following VTC. VSC and VTC had the same effect on the Auditory N1 (150–170 ms after Stimulus onset). The mean amplitude of the Auditory P1 (90–110 ms) in VSC condition was larger than that in VTC condition, and the mean amplitude of late positivity (300–420 ms) in VTC condition was larger than that in VSC condition. These findings suggest that modulation of Auditory Stimulus processing by visually induced spatial or temporal orienting of attention were different, but partially overlapping.