TL;DR: It is concluded that the DNB lesion does not increase stimulus sampling globally but that it impairs performance only in those cases in which normal rats learn to ignore irrelevant stimuli.
Abstract: The role for the dorsal noradrenergic bundle (DNB) in selective attention and stimulus filtering was tested in several situations. The DNB was damaged by stereotaxically guided injections of 4 microgram of the neurotoxin 6-hydroxydopamine (6-OHDA). The latent inhibition effect was blocked by 6-OHDA-induced depletion of forebrain noradrenaline, whereas nonreversal shift performance was better in noradrenaline-depleted rats than controls. These data are interpreted to indicate that animals with DNB lesions are imparied in ignoring irrelevant stimuli. However, in situations in which control animals did not learn to ignore irrelevant stimuli, no lesion-induced difference was found. Thus, controls and animals with DNB lesions learned equally about each of two dimensions of a multiple-redundant discrimination task. This was assessed both by interpolated trials with only one dimension present and by shifts in which only one of the previous two dimensions remained relevant. It is concluded that the DNB lesion does not increase stimulus sampling globally but that it impairs performance only in those cases in which normal rats learn to ignore irrelevant stimuli.
TL;DR: Patients showed several disturbances of attentive information processing in a simple auditory discrimination task: Increased N1 to repeated stimuli suggests impaired stimulus filtering, whereas reduced P3 amplitude and latency represent the under-allocation of neural resources for infrequent, goal-relevant stimuli, and their increased speed of processing, respectively.
TL;DR: The acquisition of conditioned suppression in both lesioned groups was found to be similar to that displayed in the preexposed control group, and this pattern of results was interpreted as being attributable to a lesion-induced impairment in the ability to maintain stimulus processing, rather than a deficit in the able to filter a stimulus.
TL;DR: It is suggested that maskers can interfere with neural responses by disrupting stimulus timing information with power either within or outside the receptive fields of neurons.
Abstract: The auditory system is capable of robust recognition of sounds in the presence of competing maskers (e.g., other voices or background music). This capability arises despite the fact that masking stimuli can disrupt neural responses at the cortical level. Since the origins of such interference effects remain unknown, in this study, we work to identify and quantify neural interference effects that originate due to masking occurring within and outside receptive fields of neurons. We record from single and multi-unit auditory sites from field L, the auditory cortex homologue in zebra finches. We use a novel method called spike timing-based stimulus filtering that uses the measured response of each neuron to create an individualized stimulus set. In contrast to previous adaptive experimental approaches, which have typically focused on the average firing rate, this method uses the complete pattern of neural responses, including spike timing information, in the calculation of the receptive field. When we generate and present novel stimuli for each neuron that mask the regions within the receptive field, we find that the time-varying information in the neural responses is disrupted, degrading neural discrimination performance and decreasing spike timing reliability and sparseness. We also find that, while removing stimulus energy from frequency regions outside the receptive field does not significantly affect neural responses for many sites, adding a masker in these frequency regions can nonetheless have a significant impact on neural responses and discriminability without a significant change in the average firing rate. These findings suggest that maskers can interfere with neural responses by disrupting stimulus timing information with power either within or outside the receptive fields of neurons.
TL;DR: Data suggest that pharmacological disruption of LI may provide an animal analogue of the defective stimulus filtering thought to characterize at least some forms of schizophrenia.