Using Neural Circuit Interrogation in Rodents to Unravel Human Speech Decoding

Abstract

The neural circuits responsible for social communication are among the least understood in the brain. Human studies have made great progress in advancing our understanding of the global computations required for processing speech, and animal models offer the opportunity to discover evolutionarily conserved mechanisms for decoding these signals. In this review article, we describe some of the most well-established speech decoding computations from human studies and describe animal research designed to reveal potential circuit mechanisms underlying these processes. Human and animal brains must perform the challenging tasks of rapidly recognizing, categorizing, and assigning communicative importance to sounds in a noisy environment. The instructions to these functions are found in the precise connections neurons make with one another. Therefore, identifying circuit-motifs in the auditory cortices and linking them to communicative functions is pivotal. We review recent advances in human recordings that have revealed the most basic unit of speech decoded by neurons is a phoneme, and consider circuit-mapping studies in rodents that have shown potential connectivity schemes to achieve this. Finally, we discuss other potentially important processing features in humans like lateralization, sensitivity to fine temporal features, and hierarchical processing. The goal is for animal studies to investigate neurophysiological and anatomical pathways responsible for establishing behavioral phenotypes that are shared between humans and animals. This can be accomplished by establishing cell types, connectivity patterns, genetic pathways and critical periods that are relevant in the development and function of social communication.

Differences in temporal processing speeds between the right and left auditory cortex reflect the strength of recurrent synaptic connectivity

“…In future studies, we plan to dissect cellular and molecular mechanisms of enhanced recurrent connectivity in the right ACx. Although the results from this study were from an animal model, they support prevailing findings from the human literature, provide detailed neural mechanisms, and therefore can potentially offer insight for investigations in humans [42].…”

Auditory cortical micro-networks show differential connectivity during voice and speech processing in humans

“…A common theory postulates a sensitivity for temporal sound information in the left AC and for spectral information in the right AC 52,53 , such that the left AC might more strongly respond to speech and vocalizations, while the right AC has a higher sensitivity to frequency sweeps that might be related to prosodic elements of vocalizations [53][54][55] . While these observations point to functional asymmetry in AC, they do not help to predict asymmetries of neural network differences in AC 56,57 . A general observation in our data was a stronger integration of voice and speech processing in the left hemisphere, while these two types of processing were largely disintegrated in the right AC when looking at the connectivity patterns, suggesting therefore more separate pathways in the right hemisphere.…”

Different Heschl’s Gyrus Duplication Patterns in Deficit and Non-deficit Subtypes of Schizophrenia

“…The functional significance of this anatomical variation currently remains unclear, but may reflect inter-individual differences in the cytoarchitectonic development of the primary auditory cortex in utero ( 18 , 19 ); duplicated HG has been implicated in the development of learning disabilities ( 31 , 32 ) and the inhibition of HG activity in auditory processes ( 21 ) after birth, even in non-clinical populations. HG is a primary brain region of auditory processing, but also participates in emotional processing ( 20 ) and social communication ( 33 ). Therefore, the core clinical features of D-Sz, such as persistent blunted affect and prominent cognitive deficits, particularly in social and verbal domains ( 7 ), may be partly attributed to neurodevelopmental abnormalities associated with HG sulcus formation.…”