Prepulse inhibition (PPI) of startle is the suppression of the startle reflex when a weaker sensory stimulus (the prepulse) shortly precedes the startling stimulus. PPI can be attentionally enhanced in both humans and laboratory animals. This study investigated whether the following three forebrain structures, which are critical for initial cortical processing of auditory signals, auditory fear conditioning/memories, and spatial attention, respectively, play a role in the top-down modulation of PPI in rats: the primary auditory cortex (A1), lateral nucleus of the amygdala (LA), and posterior parietal cortex (PPC). The results show that, under the noise-masking condition, PPI was enhanced by fear conditioning of the prepulse in a prepulse-specific manner, and the conditioning-induced PPI enhancement was further increased by perceptual separation between the conditioned prepulse and the noise masker. Reversibly blocking glutamate receptors in the A1 with 2 mmkynurenic acid eliminated both the conditioning-induced and perceptual separation-induced PPI enhancements. Blocking the LA eliminated the conditioning-induced but not the perceptual separation-induced PPI enhancement, and blocking the PPC specifically eliminated the perceptual separation-induced PPI enhancement. The two types of PPI enhancements were also eliminated by the extinction manipulation. Thus, the top-down modulation of PPI is differentially organized and depends on operations of various forebrain structures. Due to the fine-tuned modulation by higher-order cognitive processes, functions of PPI can be more flexible to complex environments. The top-down enhancements of PPI in rats are also useful for modeling some mental disorders, such as schizophrenia, attention deficit/hyperactivity disorder, and posttraumatic stress disorder.

Human listeners are able to selectively attend to target speech in a noisy environment with multiple-people talking. Using recordings of scalp electroencephalogram (EEG), this study investigated how selective attention facilitates the cortical representation of target speech under a simulated “cocktail-party” listening condition with speech-on-speech masking. The result shows that the cortical representation of target-speech signals under the multiple-people talking condition was specifically improved by selective attention relative to the non-selective-attention listening condition, and the beta-band activity was most strongly modulated by selective attention. Moreover, measured with the Granger causality (GC) value, selective attention to the single target speech in the mixed-speech complex enhanced the following 4 causal connectivities for the beta-band oscillation: the ones (1) from site FT7 to the right motor area, (2) from the left frontal area to the right motor area, (3) from the central frontal area to the right motor area, and (4) from the central frontal area to the right frontal area. However, the selective-attention-induced change in beta-band causal connectivity from the central frontal area to the right motor area, but not other beta-band causal connectivities, was significantly correlated with the selective-attention-induced change in the cortical beta-band representation of target speech. These findings suggest that under the “cocktail-party” listening condition, the beta band oscillation in EEGs to target speech is specifically facilitated by selective attention to the target speech that is embedded in the mixed-speech complex. The selective attention-induced unmasking of target speech may be associated with the improved beta-band functional connectivity from the central frontal area to the right motor area, suggesting a top-down attentional modulation of the speech-motor process.