Browsing by Subject "MATURATION"

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  • Lai, Jeffrey K. F.; Sam, I-Ching; Verlhac, Pauline; Baguet, Joel; Eskelinen, Eeva-Liisa; Faure, Mathias; Chan, Yoke Fun (2017)
    Viruses have evolved unique strategies to evade or subvert autophagy machinery. Enterovirus A71 (EV-A71) induces autophagy during infection in vitro and in vivo. In this study, we report that EV-A71 triggers autolysosome formation during infection in human rhabdomyosarcoma (RD) cells to facilitate its replication. Blocking autophagosome-lysosome fusion with chloroquine inhibited virus RNA replication, resulting in lower viral titres, viral RNA copies and viral proteins. Overexpression of the non-structural protein 2BC of EV-A71 induced autolysosome formation. Yeast 2-hybrid and co-affinity purification assays showed that 2BC physically and specifically interacted with a N-ethylmaleimide-sensitive factor attachment receptor (SNARE) protein, syntaxin-17 (STX17). Co-immunoprecipitation assay further showed that 2BC binds to SNARE proteins, STX17 and synaptosome associated protein 29 (SNAP29). Transient knockdown of STX17, SNAP29, and microtubule-associated protein 1 light chain 3B (LC3B), crucial proteins in the fusion between autophagosomes and lysosomes) as well as the lysosomal-associated membrane protein 1 (LAMP1) impaired production of infectious EV-A71 in RD cells. Collectively, these results demonstrate that the generation of autolysosomes triggered by the 2BC non-structural protein is important for EV-A71 replication, revealing a potential molecular pathway targeted by the virus to exploit autophagy. This study opens the possibility for the development of novel antivirals that specifically target 2BC to inhibit formation of autolysosomes during EV-A71 infection.
  • Colecchia, D; Stasi, M; Leonardi, M; Manganelli, F; Nolano, M; Veneziani, BM; Santoro, L; Eskelinen, Eeva-Liisa; Chiariello, M; Bucci, Cecilia (2018)
    Charcot-Marie-Tooth type 2B (CMT2B) disease is a dominant axonal peripheral neuropathy caused by 5 mutations in the RAB7A gene, a ubiquitously expressed GTPase controlling late endocytic trafficking. In neurons, RAB7A also controls neuronal-specific processes such as NTF (neurotrophin) trafficking and signaling, neurite outgrowth and neuronal migration. Given the involvement of macroautophagy/autophagy in several neurodegenerative diseases and considering that RAB7A is fundamental for autophagosome maturation, we investigated whether CMT2B-causing mutants affect the ability of this gene to regulate autophagy. In HeLa cells, we observed a reduced localization of all CMT2B-causing RAB7A mutants on autophagic compartments. Furthermore, compared to expression of RAB7AWT, expression of these mutants caused a reduced autophagic flux, similar to what happens in cells expressing the dominant negative RAB7AT22N mutant. Consistently, both basal and starvation-induced autophagy were strongly inhibited in skin fibroblasts from a CMT2B patient carrying the RAB7AV162M mutation, suggesting that alteration of the autophagic flux could be responsible for neurodegeneration.
  • Guirado, Ramon; Carceller, Hector; Castillo-Gomez, Esther; Castren, Eero; Nacher, Juan (2018)
    The quantification of the expression of different molecules is a key question in both basic and applied sciences. While protein quantification through molecular techniques leads to the loss of spatial information and resolution, immunohistochemistry is usually associated with time-consuming image analysis and human bias. In addition, the scarce automatic software analysis is often proprietary and expensive and relies on a fixed threshold binarization. Here we describe and share a set of macros ready for automated fluorescence analysis of large batches of fixed tissue samples using FIJI/ImageJ. The quantification of the molecules of interest are based on an automatic threshold analysis of immunofluorescence images to automatically identify the top brightest structures of each image. These macros measure several parameters commonly quantified in basic neuroscience research, such as neuropil density and fluorescence intensity of synaptic puncta, perisomatic innervation and col-localization of different molecules and analysis of the neurochemical phenotype of neuronal subpopulations. In addition, these same macro functions can be easily modified to improve similar analysis of fluorescent probes in human biopsies for diagnostic purposes based on the expression patterns of several molecules.
  • Stevenson, Nathan J.; Oberdorfer, Lisa; Tataranno, Maria-Luisa; Breakspear, Michael; Colditz, Paul B.; de Vries, Linda S.; Benders, Manon J. N. L.; Klebermass-Schrehof, Katrin; Vanhatalo, Sampsa; Roberts, James A. (2020)
    Objective A major challenge in the care of preterm infants is the early identification of compromised neurological development. While several measures are routinely used to track anatomical growth, there is a striking lack of reliable and objective tools for tracking maturation of early brain function; a cornerstone of lifelong neurological health. We present a cot-side method for measuring the functional maturity of the newborn brain based on routinely available neurological monitoring with electroencephalography (EEG). Methods We used a dataset of 177 EEG recordings from 65 preterm infants to train a multivariable prediction of functional brain age (FBA) from EEG. The FBA was validated on an independent set of 99 EEG recordings from 42 preterm infants. The difference between FBA and postmenstrual age (PMA) was evaluated as a predictor for neurodevelopmental outcome. Results The FBA correlated strongly with the PMA of an infant, with a median prediction error of less than 1 week. Moreover, individual babies follow well-defined individual trajectories. The accuracy of the FBA applied to the validation set was statistically equivalent to the training set accuracy. In a subgroup of infants with repeated EEG recordings, a persistently negative predicted age difference was associated with poor neurodevelopmental outcome. Interpretation The FBA enables the tracking of functional neurodevelopment in preterm infants. This establishes proof of principle for growth charts for brain function, a new tool to assist clinical management and identify infants who will benefit most from early intervention.
  • Sakha, Prasanna; Vesikansa, Aino; Orav, Ester; Heikkinen, Joonas; Kukko-Lukjanov, Tiina-Kaisa; Shintyapina, Alexandra; Franssila, Sami; Jokinen, Ville; Huttunen, Henri J.; Lauri, Sari E. (2016)
    Kainate type of glutamate receptors (KARs) are highly expressed during early brain development and may influence refinement of the circuitry, via modulating synaptic transmission and plasticity. KARs are also localized to axons, however, their exact roles in regulating presynaptic processes remain controversial. Here, we have used a microfluidic chamber system allowing specific manipulation of KARs in presynaptic neurons to study their functions in synaptic development and function in vitro. Silencing expression of endogenous KARs resulted in lower density of synaptophysin immunopositive puncta in microfluidically isolated axons. Various recombinant KAR subunits and pharmacological compounds were used to dissect the mechanisms behind this effect. The calcium permeable (Q) variants of the low-affinity (GluK1-3) subunits robustly increased synaptophysin puncta in axons in a manner that was dependent on receptor activity and PKA and PKC dependent signaling. Further, an associated increase in the mean active zone length was observed in electron micrographs. Selective presynaptic expression of these subunits resulted in higher success rate of evoked EPSCs consistent with higher probability of glutamate release. In contrast, the calcium-impermeable (R) variant of GluK1 or the high-affinity subunits (GluK4,5) had no effect on synaptic density or transmission efficacy. These data suggest that calcium permeable axonal KARs promote efferent connectivity by increasing the density of functional presynaptic release sites.
  • Syrjä, Pernilla; Anwar, Tahira; Pääkkönen, Tarja; Kyöstilä, Kaisa; Hultin Jäderlund, Karin; Cozzi, Francesca; Rohdin, Cecilia; Hahn, Kerstin; Wohlsein, Peter; Baumgärtner, Wolfgang; Henke, Diana; Oevermann, Anna; Sukura, Antti; Leeb, Tosso; Lohi, Hannes; Eskelinen, Eeva-Liisa (2017)
    A missense variant in the autophagy-related ATG4D-gene has been associated with a progressive degenerative neurological disease in Lagotto Romagnolo (LR) dogs. In addition to neural lesions, affected dogs show an extraneural histopathological phenotype characterized by severe cytoplasmic vacuolization, a finding not previously linked with disturbed autophagy in animals. Here we aimed at testing the hypothesis that autophagy is altered in the affected dogs, at reporting the histopathology of extraneural tissues and at excluding lysosomal storage diseases. Basal and starvation-induced autophagy were monitored by Western blotting and immunofluorescence of microtubule associated protein 1A/B light chain3 (LC3) in fibroblasts from 2 affected dogs. The extraneural findings of 9 euthanized LRs and skin biopsies from 4 living affected LRs were examined by light microscopy, electron microscopy, and immunohistochemistry (IHC), using antibodies against autophagosomal membranes (LC3), autophagic cargo (p62), and lysosomal membranes (LAMP2). Biochemical screening of urine and fibroblasts of 2 affected dogs was performed. Under basal conditions, the affected fibroblasts contained significantly more LC3-II and LC3-positive vesicles than did the controls. Morphologically, several cells, including serous secretory epithelium, endothelial cells, pericytes, plasma cells, and macrophages, contained cytoplasmic vacuoles with an ultrastructure resembling enlarged amphisomes, endosomes, or multivesicular bodies. IHC showed strong membranous LAMP2 positivity only in sweat glands. The results show that basal but not induced autophagy is altered in affected fibroblasts. The ultrastructure of affected cells is compatible with altered autophagic and endo-lysosomal vesicular traffic. The findings in this spontaneous disease provide insight into possible tissue-specific roles of basal autophagy.
  • Eichin, Dominik; Pessia, Alberto; Takeda, Akira; Laakkonen, Joni; Bellmann, Lydia; Kankainen, Matti; Imhof, Beat A.; Stoitzner, Patrizia; Tang, Jing; Salmi, Marko; Jalkanen, Sirpa (2021)
    CD73 is an important ectoenzyme responsible for the production of extracellular adenosine. It is involved in regulating inflammatory responses and cell migration and is overexpressed in various cancers. The functions of CD73 in blood endothelial cells are understood in detail, but its role on afferent lymphatics remains unknown. Moreover, anti‐CD73 antibodies are now used in multiple clinical cancer trials, but their effects on different endothelial cell types have not been studied. This study reveals that a previously unknown role of CD73 on afferent lymphatics is to dampen immune responses. Knocking it out or suppressing it by siRNA leads to the upregulation of inflammation‐associated genes on lymphatic endothelial cells and a more pro‐inflammatory phenotype of interacting dendritic cells in vitro and in vivo. In striking contrast, anti‐CD73 antibodies had only negligible effects on the gene expression of lymphatic‐ and blood‐endothelial cells. Our data thus reveal new functions of lymphatic CD73 and indicate a low likelihood of endothelial cell–related adverse effects by CD73 targeting therapeutic antibodies.
  • Parviainen, Tiina; Helenius, Päivi; Salmelin, Riitta (2019)
    Auditory cortex in each hemisphere shows preference to sounds from the opposite hemifield in the auditory space. Besides this contralateral dominance, the auditory cortex shows functional and structural lateralization, presumably influencing the features of subsequent auditory processing. Children have been shown to differ from adults in the hemispheric balance of activation in higher-order auditory based tasks. We studied, first, whether the contralateral dominance can be detected in 7- to 8-year-old children and, second, whether the response properties of auditory cortex in children differ between hemispheres. Magnetoencephalography (MEG) responses to simple tones revealed adult-like contralateral preference that was, however, extended in time in children. Moreover, we found stronger emphasis towards mature response properties in the right than left hemisphere, pointing to faster maturation of the right-hemisphere auditory cortex. The activation strength of the child-typical prolonged response was significantly decreased with age, within the narrow age-range of the studied child population. Our results demonstrate that although the spatial sensitivity to the opposite hemifield has emerged by 7 years of age, the population-level neurophysiological response shows salient immature features, manifested particularly in the left hemisphere. The observed functional differences between hemispheres may influence higher-level processing stages, for example, in language function.
  • Popova, Dina; Castren, Eero; Taira, Tomi (2017)
    Recent studies demonstrate that chronic administration of the widely used antidepressant fluoxetine (FLX) promotes neurogenesis, synaptogenesis and synaptic plasticity in the adult hippocampus, cortex and amygdala. However, the mechanisms underlying these effects and how are they related to the clinical antidepressant efficacy are still poorly understood. We show here that chronic FLX administration decreases hippocampus-associated neophobia in naive mice. In parallel, electrophysiological recordings in hippocampal CA3-CA1 circuitry revealed that the FLX treatment resulted in increased short and long-term plasticity likely attributed to changes in presynaptic function. These changes were accompanied by enhancement in the expression of proteins related to vesicular trafficking and release, namely synaptophysin, synaptotagmin 1, MUNC 18 and syntaxin 1. Thus, chronic FLX administration is associated with enhanced synaptic dynamics atypical of mature CA1 synapses, elevated hippocampal plasticity, improved hippocampus-dependent behavior as well as altered expression of synaptic proteins regulating neurotransmitter trafficking and release. The results support the idea that antidepressants can promote neuronal plasticity and show that they can increase the functional dynamic range and information processing in synaptic circuitries. (C) 2017 Elsevier Ltd. All rights reserved.
  • Gonzalez, Marta Lopez; Oosterhoff, Dinja; Lindenberg, Jelle J.; Milenova, Ioanna; Lougheed, Sinead M.; Martianez, Tania; Dekker, Henk; Quixabeira, Dafne Carolina Alves; Hangalapura, Basav; Joore, Jos; Piersma, Sander R.; Cervera-Carrascon, Victor; Santos, Joao Manuel; Scheper, Rik J.; Verheul, Henk M. W.; Jimenez, Connie R.; Van De Ven, Rieneke; Hemminki, Akseli; Van Beusechem, Victor W.; De Gruijl, Tanja D. (2019)
    In patients with cancer, the functionality of Dendritic Cells (DC) is hampered by high levels of tumor-derived suppressive cytokines, which interfere with DC development and maturation. Poor DC development can limit the efficacy of immune checkpoint blockade and in vivo vaccination approaches. Interference in intracellular signaling cascades downstream from the receptors of major tumor-associated suppressive cytokines like IL-10 and IL-6, might improve DC development and activation, and thus enhance immunotherapy efficacy. We performed exploratory functional screens on arrays consisting of >1000 human kinase peptide substrates to identify pathways involved in DC development and its inhibition by IL-10 or IL-6. The resulting alterations in phosphorylation of the kinome substrate profile pointed to glycogen-synthase kinase-3 beta (GSK3 beta) as a pivotal kinase in both DC development and suppression. GSK3 beta inhibition blocked human DC differentiation in vitro, which was accompanied by decreased levels of IL-12p70 secretion, and a reduced capacity for T cell priming. More importantly, adenoviral transduction of monocytes with a constitutively active form of GSK3 beta induced resistance to the suppressive effects of IL-10 and melanoma-derived supernatants alike, resulting in improved DC development, accompanied by up-regulation of co-stimulatory markers, an increase in CD83 expression levels in mature DC, and diminished release of IL-10. Moreover, adenovirus-mediated intratumoral manipulation of this pathway in an in vivo melanoma model resulted in DC activation and recruitment, and in improved immune surveillance and tumor control. We propose the induction of constitutive GSK3 beta activity as a novel therapeutic means to bolster DC functionality in the tumor microenvironment.
  • Torvik, Fartein Ask; Flato, Martin; McAdams, Tom A.; Colman, Ian; Silventoinen, Karri; Stoltenberg, Camilla (2021)
    Purpose: On average, boys have lower academic achievement than girls. We investigated whether the timing of puberty is associated with academic achievement, and whether later puberty among boys contributes to the sex difference in academic achievement. Method: Examination scores at age 16 were studied among 13,477 British twins participating in the population-based Twins Early Development Study. A pubertal development scale, a height based proxy of growth spurt, and age at menarche were used as indicators of puberty. Associations between puberty, sex, and academic achievement were estimated in phenotypic mediation models and biometric twin models. Results: Earlier puberty was associated with higher academic achievement both in boys and girls. The exception was early age at menarche in girls, which associated with lower academic achievement. More than half of the sex differences in academic achievement could be linked to sex differences in pubertal development, but part of this association appeared to be rooted in prepubertal differences. The biometric twin modelling indicated that the association between puberty and academic achievement was due to shared genetic risk factors. Genetic influences on pubertal development accounted for 7%-8% of the phenotypic variation in academic achievement. Conclusions: Pubertal maturation relates to the examination scores of boys and of girls. This can give genes related to pubertal maturation an influence on outcomes in education and beyond. Sex differences in pubertal maturation can explain parts of the sex difference in academic achievement. Grading students when they are immature may not accurately measure their academic potential. (c) 2021 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
  • Vesikansa, Aino; Sakha, Prasanna; Kuja-Panula, Juha; Molchanova, Svetlana; Rivera Baeza, Claudio; Huttunen, Henri J.; Rauvala, Heikki; Taira, Tomi; Lauri, Sari E. (2012)
  • Steinzeig, Anna; Cannarozzo, Cecilia; Castren, Eero (2019)
    Heightened neuronal plasticity expressed during early postnatal life has been thought to permanently decline once critical periods have ended. For example, monocular deprivation is able to shift ocular dominance in the mouse visual cortex during the first months of life, but this effect is lost later in life. However, various treatments, such as the antidepressant fluoxetine, can reactivate a critical period-like plasticity in the adult brain. When monocular deprivation is supplemented with chronic fluoxetine administration, a major shift in ocular dominance is produced after the critical period has ended. In the current study, we characterized the temporal patterns of fluoxetine-induced plasticity in the adult mouse visual cortex, using in vivo optical imaging. We found that artificially induced plasticity in ocular dominance extended beyond the duration of the naturally occurring critical period and continued as long as fluoxetine was administered. However, this fluoxetine-induced plasticity period ended as soon as the drug was not given. These features of antidepressant-induced plasticity may be useful when designing treatment strategies involving long-term antidepressant treatment in humans.
  • Hagihara, Hideo; Fujita, Masayo; Umemori, Juzoh; Hashimoto, Makoto; Miyakawa, Tsuyoshi (2018)
    AIM: Maturation abnormalities of the brain cells have been suggested in several neuropsychiatric disorders, including schizophrenia, bipolar disorder, autism spectrum disorders, and epilepsy. In this study, we examined the expression patterns of neuronal maturation markers in the brain of a mouse model of dementia with Lewy body-linked mutant β-synuclein (βS), especially in the hippocampus, to explore whether such brain abnormalities occur in neurodegenerative disorders as well. METHODS: Quantitative PCR (qPCR) and immunohistochemical analyses were performed using the hippocampus of 14-month-old P123H βS transgenic (Tg) mice to evaluate the expression of molecular markers for maturation of dentate granule cells. RESULTS: Based on qPCR results, expression of Tdo2 and Dsp (markers of mature granule cells) was decreased and that of Drd1a (a marker of immature granule cells) was increased in the hippocampus of P123H βS Tg mice compared to that in wild-type controls. Immunohistochemical analysis revealed decreased expression of mature granule cell markers Calb1 and Gria1, along with increased expression of the microglial marker Iba1, in the hippocampal dentate gyrus region of P123H βS Tg mice. P123H βS Tg mice exhibited immature-like neuronal molecular expression patterns and microgliosis in the hippocampus. Pseudo-immaturity of dentate granule cells, associated with neuroinflammation, may be a shared endophenotype in the brains of at least a subgroup of patients with neuropsychiatric disorders and neurodegenerative diseases.
  • Pryazhnikov, Evgeny; Mugantseva, Ekaterina; Casarotto, Plinio; Kolikova, Julia; Fred, Senem Merve; Toptunov, Dmytro; Afzalov, Ramil; Hotulainen, Pirta; Voikar, Vootele; Terry-Lorenzo, Ryan; Engel, Sharon; Kirov, Sergei; Castren, Eero; Khiroug, Leonard (2018)
    Ketamine, a well-known anesthetic, has recently attracted renewed attention as a fast-acting antidepressant. A single dose of ketamine induces rapid synaptogenesis, which may underlie its antidepressant effect. To test whether repeated exposure to ketamine triggers sustained synaptogenesis, we administered a sub-anesthetic dose of ketamine (10 mg/kg i.p.) once-daily for 5 days, and repeatedly imaged dendritic spines of the YFP-expressing pyramidal neurons in somatosensory cortex of awake female mice using in vivo two-photon microscopy. We found that the spine formation rate became significantly higher at 72-132 h after the first ketamine injection (but not at 6-24 h), while the rate of elimination of pre-existing spines remained unchanged. In contrast to the net gain of spines observed in ketamine-treated mice, the vehicle-injected control mice exhibited a net loss typical for young-adult animals undergoing synapse pruning. Ketamine-induced spinogenesis was correlated with increased PSD-95 and phosphorylated actin, consistent with formation of new synapses. Moreover, structural synaptic plasticity caused by ketamine was paralleled by a significant improvement in the nest building behavioral assay. Taken together, our data show that subchronic low-dose ketamine induces a sustained shift towards spine formation.
  • Mavrovic, Martina; Uvarov, Pavel; Delpire, Eric; Vutskits, Laszlo; Kaila, Kai; Puskarjov, Martin (2020)
    KCC2, encoded in humans by the SLC12A5 gene, is a multifunctional neuron-specific protein initially identified as the chloride (Cl-) extruder critical for hyperpolarizing GABA(A) receptor currents. Independently of its canonical function as a K-Cl cotransporter, KCC2 regulates the actin cytoskeleton via molecular interactions mediated through its large intracellular C-terminal domain (CTD). Contrary to the common assumption that embryonic neocortical projection neurons express KCC2 at non-significant levels, here we show that loss of KCC2 enhances apoptosis of late-born upper-layer cortical projection neurons in the embryonic brain. In utero electroporation of plasmids encoding truncated, transport-dead KCC2 constructs retaining the CTD was as efficient as of that encoding full-length KCC2 in preventing elimination of migrating projection neurons upon conditional deletion of KCC2. This was in contrast to the effect of a full-length KCC2 construct bearing a CTD missense mutation (KCC2(R952H)), which disrupts cytoskeletal interactions and has been found in patients with neurological and psychiatric disorders, notably seizures and epilepsy. Together, our findings indicate ion transport-independent, CTD-mediated regulation of developmental apoptosis by KCC2 in migrating cortical projection neurons.
  • Putkinen, Vesa; Tervaniemi, Mari; Huotilainen, Minna (2019)
    The influence of musical experience on brain development has been mostly studied in school-aged children with formal musical training while little is known about the possible effects of less formal musical activities typical for preschool-aged children (e.g., before the age of seven). In the current study, we investigated whether the amount of musical group activities is reflected in the maturation of neural sound discrimination from toddler to preschool-age. Specifically, we recorded event-related potentials longitudinally (84 recordings from 33 children) in a mismatch negativity (MMN) paradigm to different musically relevant sound changes at ages 2-3, 4-5 and 6-7 years from children who attended a musical playschool throughout the follow-up period and children with shorter attendance to the same playschool. In the first group, we found a gradual positive to negative shift in the polarities of the mismatch responses while the latter group showed little evidence of age-related changes in neural sound discrimination. The current study indicates that the maturation of sound encoding indexed by the MMN may be more protracted than once thought and provides first longitudinal evidence that even quite informal musical group activities facilitate the development of neural sound discrimination during early childhood.
  • Antinmaa, Jaana; Lapinleimu, Helena; Salonen, Jaakko; Stolt, Suvi; Kaljonen, Anne; Jääskeläinen, Satu (2020)
    Aim: To study whether auditory function measured with brainstem auditory evoked potential and brainstem audiometry recordings in the neonatal period associates with language development 1 year later in preterm infants.Methods: This retrospective study included 155 preterm infants (birthweight ≤1500 g and/or birth ≤32 gestational weeks) born between 2007 and 2012 at the Turku University Hospital. Auditory function was recorded in neonatal period. Information of language development was gathered at the mean corrected age of 1 year by using the Finnish version of the MacArthur Communicative Development Inventory.Results: Slower auditory processing (longer interpeak interval, IPI I-V) in the right ear in the neonatal brainstem auditory evoked potential recording associated with smaller receptive lexicon size at 1 year (P = .043). Infants with longer IPI I-V were more likely to have a deviant (≤17 words) receptive lexicon size (P = .033). The ab-sence of a contralateral response with right ear stimulation increased the risk for deviant lexicon size (P = .049).Conclusion: The results suggest that impaired auditory function in the neonatal pe-riod in preterm infants may lead to a poorer receptive language outcome 1 year later. Auditory pathway function assessment provides information for the identification of preterm children at risk for weak language development.
  • Kostilainen, Kaisamari; Partanen, Eino; Mikkola, Kaija; Wikström, Valtteri; Pakarinen, Satu; Fellman, Vineta; Huotilainen, Minna (2020)
    Objective: Auditory change-detection responses provide information on sound discrimination and memory skills in infants. We examined both the automatic change-detection process and the processing of emotional information content in speech in preterm infants in comparison to full-term infants at term age. Methods: Preterm (n = 21) and full-term infants' (n = 20) event-related potentials (ERP) were recorded at term age. A challenging multi-feature mismatch negativity (MMN) paradigm with phonetic deviants and rare emotional speech sounds (happy, sad, angry), and a simple one-deviant oddball paradigm with pure tones were used. Results: Positive mismatch responses (MMR) were found to the emotional sounds and some of the phonetic deviants in preterm and full-term infants in the multi-feature MMN paradigm. Additionally, late positive MMRs to the phonetic deviants were elicited in the preterm group. However, no group differences to speech-sound changes were discovered. In the oddball paradigm, preterm infants had positive MMRs to the deviant change in all latency windows. Responses to non-speech sounds were larger in preterm infants in the second latency window, as well as in the first latency window at the left hemisphere electrodes (F3, C3). Conclusions: No significant group-level differences were discovered in the neural processing of speech sounds between preterm and full-term infants at term age. Change-detection of non-speech sounds, however, may be enhanced in preterm infants at term age. Significance: Auditory processing of speech sounds in healthy preterm infants showed similarities to full-term infants at term age. Large individual variations within the groups may reflect some underlying differences that call for further studies.
  • Heikkila, Jenni; Tiippana, Kaisa; Loberg, Otto; Leppänen, Paavo H. T. (2018)
    Seeing articulatory gestures enhances speech perception. Perception of auditory speech can even be changed by incongruent visual gestures, which is known as the McGurk effect (e.g., dubbing a voice saying /mi/ onto a face articulating /ni/, observers often hear /ni/). In children, the McGurk effect is weaker than in adults, but no previous knowledge exists about the neural-level correlates of the McGurk effect in school-age children. Using brain event-related potentials, we investigated change detection responses to congruent and incongruent audiovisual speech in school-age children and adults. We used an oddball paradigm with a congruent audiovisual /mi/ as the standard stimulus and a congruent audiovisual /ni/ or McGurk A/mi/V/ni/ as the deviant stimulus. In adults, a similar change detection response was elicited by both deviant stimuli. In children, change detection responses differed between the congruent and the McGurk stimulus. This reflects a maturational difference in the influence of visual stimuli on auditory processing.