Biology subjects

Dvorakova, M.

Publications and source records attributed to Dvorakova, M..

3 recordsLinked to original sources

bioRxiv2026

Neural Speech Tracking Across the First 62 Days of Life: Effects of Language Background and Cognitive Maturation

Newborns recognise familiar language patterns experienced in utero and discriminate them from unfamiliar ones. It is as yet unclear which neural mechanisms are responsible for such early language-specific behavior. Here we focus on neural speech tracking and test whether it shows language-specific attunement in newborns and one-to-two month olds. Infants listened to infant-directed stories in their native language (Czech) and an unfamiliar language (Russian) while their EEG was recorded. First, we examined whether neural speech tracking differed between infants predominantly exposed to Czech and infants exposed primarily to other languages. Second, we assessed developmental changes by combining these data with a previously collected cohort of newborns, yielding a continuous sample spanning 1-62 days of age. Neural speech tracking was assessed in stimulus-derived delta and theta frequency bands in terms of oscillatory power and accuracy of EEG-to-speech envelope reconstruction using the backward multivariate temporal response functions. Czech-exposed infants had stronger cortical tracking of Czech speech than infants exposed to other languages. Within the Czech-exposed group, native Czech elicited stronger neural tracking than unfamiliar Russian, particularly in the delta band, indicating early language-specific tuning to the prosodic-word structure. Across the combined Czech-exposed sample, this native-language advantage gradually decreased with age, suggesting that neural speech tracking of the slow rhythms undergoes rapid reorganization during the first two months of life. These findings demonstrate that language-specific neural speech tracking is detectable from the earliest weeks of life and is jointly shaped by early, perinatal language experience as well as cognitive maturation.

neuroscience↗

bioRxiv2025

Acetaminophen inhibits diacylglycerol lipase synthesis of 2-arachidonoyl glycerol: implications for nociception

SUMMARYThough acetaminophen is a ubiquitous analgesic, its mechanism of action remains unknown. Thus, even though acetaminophen causes ∼500 deaths each year in the US it has not been possible to design safer alternatives. Because endocannabinoids may have a role in acetaminophen action, we examined interactions between the two. We now report that acetaminophen inhibits the activity of diacylglycerol lipase α (DAGLα), but not DAGLβ, decreasing production of the endocannabinoid 2-arachidonoyl glycerol. This gave rise to the counterintuitive hypothesis that decreasing endocannabinoid production by DAGLαinhibitionmay be antinociceptive in certain settings. Supporting this hypothesis, we find that DAGL inhibition by RHC80267 is antinociceptive in wildtype but not CB1 knockout mice in the hotplate test. We propose 1) that activation of DAGLα may exacerbate some forms of nociception and 2) a novel mechanism for the antinociceptive actions of acetaminophen whereby acetaminophen inhibits a DAGLα/CB1-based circuit that plays a permissive role in at least one form of nociception.

neuroscience↗

bioRxiv2021

ISL1 is an essential determinant of structural and functional tonotopic representation of sound

A cardinal feature of the auditory pathway is frequency selectivity, represented in a tonotopic map from the cochlea to the cortex. The molecular determinants of the auditory frequency map are unknown. Here, we discovered that the transcription factor ISL1 regulates the molecular and cellular features of auditory neurons, including the formation of the spiral ganglion and peripheral and central processes that shape the tonotopic representation of the auditory map. We selectively knocked out Isl1 in auditory neurons using Neurod1Cre strategies. In the absence of Isl1, spiral ganglion neurons migrate into the central cochlea and beyond, and the cochlear wiring is profoundly reduced and disrupted. The central axons of Isl1 mutants lose their topographic projections and segregation at the cochlear nucleus. Transcriptome analysis of spiral ganglion neurons shows that Isl1 regulates neurogenesis, axonogenesis, migration, neurotransmission-related machinery, and synaptic communication patterns. We show that peripheral disorganization in the cochlea affects the physiological properties of hearing in the midbrain and auditory behavior. Surprisingly, auditory processing features are preserved despite the significant hearing impairment, revealing central auditory pathway resilience and plasticity in Isl1 mutant mice. Mutant mice have a reduced acoustic startle reflex, altered prepulse inhibition, and characteristics of compensatory neural hyperactivity centrally. Our findings show that ISL1 is one of the obligatory factors required to sculpt auditory structural and functional tonotopic maps. Still, upon Isl1 deletion, the ensuing central compensatory plasticity of the auditory pathway does not suffice to overcome developmentally induced peripheral dysfunction of the cochlea.

neuroscience↗