Neural responses to sensory novelty with and without conscious access.

Detection of novel stimuli that violate statistical regularities in the sensory scene is of paramount importance for the survival of biological organisms. Event-related potentials, phasic increases in pupil size, and evoked changes in oscillatory power have been proposed as markers of sensory novelty detection. However, how conscious access to novelty modulates these different brain responses is not well understood. Here, we studied the neural responses to sensory novelty in the auditory modality with and without conscious access. We identified individual thresholds for conscious auditory discrimination and presented to our participants sequences of tones, where the last stimulus could be another standard, a subthreshold target or a suprathreshold target. Participants were instructed to report whether the last tone of each sequence was the same or different from those preceding it. Results indicate that attentional orientation to behaviorally relevant stimuli and overt decision-making mechanisms, indexed by the P3 event-related response and reaction times, best predict whether a novel stimulus will be consciously accessed. Theta power and pupil size do not predict conscious access to novelty, but instead reflect information maintenance and unexpected sensory uncertainty. These results highlight the interplay between bottom-up and top-down mechanisms and how the brain weights neural responses to novelty and uncertainty during perception and goal-directed behavior.

Chronic stress induces dendritic atrophy in the rat medial geniculate nucleus: effects on auditory conditioning.

Chronic stress induces dendritic atrophy in the inferior colliculus (IC, auditory mesencephalon) and impairs auditory avoidance conditioning. The aim of this study was to determine in Golgi preparations and in cued fear conditioning whether stress affects other auditory components, like the thalamic medial geniculate nucleus (MG) or the posterior thalamic nucleus (PO), in Sprague-Dawley rats. Chronic restraint stress produced a significant dendritic atrophy in the MG (stress: 407+/-55 microm; control: 808+/-120 microm; p<0.01) but did not affect auditory fear conditioning. The last result was in apparent contrast with the fact that stress impairs both the acquisition of auditory avoidance conditioned responses and the dendritic structure in two major nuclei of the auditory system. In order to analyze this disagreement, we investigated whether the stress-related freezing to tone occurring in the fear conditioning protocol corresponded to a conditioned or an unconditioned fear response, using changes in tone instead of light throughout conditioning trials. Chronic stress significantly enhanced visual fear conditioning in stressed animals compared to controls (stress: 58.9+/-8.42%, control: 23.31+/-8.01%; p<0.05), but this fear enhancement was related to unconditioned fear. Conversely, chronic stress did not affect the morphology of the PO (subserving both auditory and somatosensory information) or the corresponding auditory and somatosensory unconditioned responses (acoustic startle response and escape behavior). Our results suggest that the auditory conditioned stimulus can be processed in part independently of the IC and MG in the stressed animals, and sent to the amygdala via the PO inducing unconditioned fear. Comparable alterations could be produced in major depression.

AChE-rich magnopyramidal neurons have a left-right size asymmetry in Broca's area.

Acetylcholinesterase-rich neurons (AChERN) are a particular group of pyramidal neurons, displaying a specific laminar and ontogenetic pattern in the cerebral cortex of human and nonhuman primates. Using histochemistry and morphometrical methods, we have found a layer 3 magnopyramidal AChERN left-right size asymmetry restricted to Brodmann's area 45, a component of Broca's language area. This structural feature could be related to functional lateralization associated to syntactic processing and phonological working memory, and is consistent with a non-cholinergic role of AChE possibly linked to neuroplastic processes in the human neocortex.