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Friedrichs, D.

Publications and source records attributed to Friedrichs, D..

2 recordsLinked to original sources

Vocal Tract Disparity and Potential Implications for Speaker Recognition

Perceptual experiments show that listeners recognize female speakers with lower accuracy than male speakers. Automatic speaker recognition systems may also show performance bias against female speakers even when training data sets are gender balanced. The underlying reasons for this discrepancy are unclear. Here, we apply geometric morphometrics to quantify sex-related morphological vocal tract disparity -- the extent of shape variation -- across both resting and articulatory configurations. We find that male speakers exhibit greater disparity in both resting and articulatory configurations. This morphological idiosyncrasy may in turn generate more discriminable acoustic signatures and offer a biological explanation for higher recognition accuracies for male voices by humans and machines. Our results suggest that innate variation in vocal tract morphology may contribute to performance bias in voice technology and voice perception by human listeners.

evolutionary biology↗

Hippocampal hyperactivity in a rat model of Alzheimers disease

Neuronal network dysfunction is a hallmark of Alzheimers disease (AD). However, the underlying pathomechanisms remain unknown. We analyzed the hippocampal micronetwork in a rat model of AD at an early disease stage at the beginning of extracellular amyloid beta (A{beta}) deposition. We established two-photon Ca2+-imaging in vivo in the hippocampus of rats and found hyperactivity of CA1 neurons. Patch-clamp recordings in brain slices in vitro revealed changes in the passive properties and intrinsic excitability of CA1 pyramidal neurons. Furthermore, we observed increased neuronal input resistance and prolonged action potential width in CA1 pyramidal neurons. Surprisingly, all parameters measured to quantify synaptic inhibition and excitation onto CA1 pyramidal neurons were intact suggesting a cell immanent deficit. Our data support the view that altered intrinsic excitability of CA1 neurons may precede inhibitory dysfunction at an early stage of disease progression.

neuroscience↗