Long-term influence of recurrent acute otitis media on neural involuntary attention switching in 2-year-old children

Haapala, Sini; Niemitalo-Haapola, Elina; Raappana, Antti; Kujala, Tiia; Suominen, Kalervo; Jansson-Verkasalo, Eira; Kujala, Teija

doi:10.1186/s12993-015-0086-4

Cited by 22 publications

(23 citation statements)

References 47 publications

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“…Some evidence shows that the expression of Bcl-2 was suppressed in VPA-induced ASD rats 26. BDNF plays an important role in survival and differentiation of nervous system, and BDNF is involved in the pathogenesis of a wide range of psychiatric disorders 27. The levels of BDNF and Bcl-2 were decreased in ASD patients 28,29.…”

Section: Discussionmentioning

confidence: 99%

Rapamycin modulated brain-derived neurotrophic factor and B-cell lymphoma 2 to mitigate autism spectrum disorder in rats

Zhang¹,

Li²,

Ni³

2017

NDT

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The number of children suffered from autism spectrum disorder (ASD) is increasing dramatically. However, the etiology of ASD is not well known. This study employed mammalian target of rapamycin inhibitor rapamycin to explore its effect on ASD and provided new therapeutic strategies for ASD. ASD rat model was constructed and valproic acid (VPA) was injected intraperitoneally into rats on pregnancy day 12.5. Offspring from VPA group were divided into ASD group and ASD + rapamycin (ASD + RAPA) group. Compared with normal group, the frequency and duration of social behavior and straight times of ASD group were shortened, but the grooming times were extended. Meanwhile, in ASD group, the average escape latency and the frequency of crossing plates were decreased, the apoptotic index (AI) detected by TUNEL assay was increased, and the expression of brain-derived neurotrophic factor (BDNF) and B-cell lymphoma 2 (Bcl-2) analyzed was decreased with great difference compared with normal group (P<0.01). However, rapamycin treatment in ASD rats mitigated the ASD-like social behavior, such as the frequencies of straight and grooming. Furthermore, rapamycin shortened the average escape latency, but increased the frequency of crossing plates of ASD rats. In hippocampus, rapamycin decreased the AI, but increased the levels of BDNF and Bcl-2 (P<0.01) of ASD rats. These findings revealed that rapamycin significantly mitigated the social behavior by enhancing the expression of BDNF and Bcl-2 to suppress the hippocampus apoptosis in VPA-induced ASD rats.

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Section: Discussionmentioning

confidence: 99%

Rapamycin modulated brain-derived neurotrophic factor and B-cell lymphoma 2 to mitigate autism spectrum disorder in rats

Zhang¹,

Li²,

Ni³

2017

NDT

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“…One hypothesis that explains the persistence of these behavioral deficits when occurring during childhood is that HL during a developmental critical period induces persistent changes to inhibitory synapse function that degrade central auditory processing (Sanes, 2013). Indeed, transient childhood HL is associated with altered central auditory physiology, both in the brainstem and cortex (Folsom et al, 1983;Gunnarson and Finitzo, 1991;Hall and Grose, 1993;Haapala et al, 2014Haapala et al, , 2016. Here, we ask whether developmental HL-induced auditory behavioral deficits can be rescued by maintaining or restoring normal inhibitory synaptic function.…”

Section: Introductionmentioning

confidence: 99%

Preserving Inhibition during Developmental Hearing Loss Rescues Auditory Learning and Perception

Mowery¹,

Caras²,

Hassan³

et al. 2019

J. Neurosci.

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Transient periods of childhood hearing loss can induce deficits in aural communication that persist long after auditory thresholds have returned to normal, reflecting long-lasting impairments to the auditory CNS. Here, we asked whether these behavioral deficits could be reversed by treating one of the central impairments: reduction of inhibitory strength. Male and female gerbils received bilateral earplugs to induce a mild, reversible hearing loss during the critical period of auditory cortex development. After earplug removal and the return of normal auditory thresholds, we trained and tested animals on an amplitude modulation detection task. Transient developmental hearing loss induced both learning and perceptual deficits, which were entirely corrected by treatment with a selective GABA reuptake inhibitor (SGRI). To explore the mechanistic basis for these behavioral findings, we recorded the amplitudes of GABA A and GABA B receptor-mediated IPSPs in auditory cortical and thalamic brain slices. In hearing loss-reared animals, cortical IPSP amplitudes were significantly reduced within a few days of hearing loss onset, and this reduction persisted into adulthood. SGRI treatment during the critical period prevented the hearing loss-induced reduction of IPSP amplitudes; but when administered after the critical period, it only restored GABA B receptor-mediated IPSP amplitudes. These effects were driven, in part, by the ability of SGRI to upregulate ␣1 subunitdependent GABA A responses. Similarly, SGRI prevented the hearing loss-induced reduction of GABA A and GABA B IPSPs in the ventral nucleus of the medial geniculate body. Thus, by maintaining, or subsequently rescuing, GABAergic transmission in the central auditory thalamocortical pathway, some perceptual and cognitive deficits induced by developmental hearing loss can be prevented.

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“…Do et al [4] discovered that functional coupling between striatal and cortical regions is associated with increased craving in adolescent smokers. Sutherland et al [5] observed that smoking is associated with convergent structural decreases in the left insula, right cerebellum, parahippocampus, multiple prefrontal cortex regions, and the thalamus. Mcclernon et al [6] provided evidence that abstinence-induced deficits in working memory and changes in the underlying brain function are mostly due to abstinence from nicotine rather than non-nicotine factors.…”

Section: Introductionmentioning

confidence: 99%

Regional Homogeneity Changes in Nicotine Addicts by Resting-State fMRI

Chen

2017

PLoS ONE

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ObjectiveTo reveal the brain functional changes of nicotine addicts compared with those of non-smokers and explore the objective biomarker for nicotine dependence evaluation.MethodsA total of 14 smokers and 11 non-smoking controls were recruited for this study. Resting-state functional magnetic resonance imaging and regional homogeneity (ReHo) were applied in the neural activity analysis. Two-sample t-test was performed to examine the voxel-wise difference between the smokers and the controls. Correlation analysis between the ReHo values and the Fagerstrom Test for Nicotine Dependence (FTND) scores were performed to explore the biomarkers for the clinical characteristics of smokers.ResultsThe ReHo values from the right superior frontal gyrus of the Brodmann’s area (BA) 9 to the right middle frontal gyrus and the ReHo value from the left and right precuneus (BA 23) to the left and right middle cingulum gyrus were lower in the smokers than in the non-smokers. The ReHo value in the precuneus (BA 23) was significantly and positively correlated with the FTND score of smokers.ConclusionThe ReHo values in the right superior frontal gyrus and left precuneus can be used to separate the smokers from the non-smokers. In particular, the left precuneus is a potential neuroimaging biomarker for nicotine addicts.

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Long-term influence of recurrent acute otitis media on neural involuntary attention switching in 2-year-old children

Cited by 22 publications

References 47 publications

Rapamycin modulated brain-derived neurotrophic factor and B-cell lymphoma 2 to mitigate autism spectrum disorder in rats

Rapamycin modulated brain-derived neurotrophic factor and B-cell lymphoma 2 to mitigate autism spectrum disorder in rats

Preserving Inhibition during Developmental Hearing Loss Rescues Auditory Learning and Perception

Regional Homogeneity Changes in Nicotine Addicts by Resting-State fMRI

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