168 research outputs found

    Regulation of auditory plasticity during critical periods and following hearing loss

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    Sensory input has profound effects on neuronal organization and sensory maps in the brain. The mechanisms regulating plasticity of the auditory pathway have been revealed by examining the consequences of altered auditory input during both developmental critical periods—when plasticity facilitates the optimization of neural circuits in concert with the external environment—and in adulthood—when hearing loss is linked to the generation of tinnitus. In this review, we summarize research identifying the molecular, cellular, and circuit-level mechanisms regulating neuronal organization and tonotopic map plasticity during developmental critical periods and in adulthood. These mechanisms are shared in both the juvenile and adult brain and along the length of the auditory pathway and serve to regulate disinhibitory networks, synaptic structure and function, as well as structural barriers to plasticity. Regulation of plasticity also involves both neuromodulatory circuits, which link plasticity with learning and attention, as well as ascending and descending auditory circuits, which link the auditory cortex and lower structures. Further work identifying the interplay of molecular and cellular mechanisms associating hearing loss induced plasticity with brain changes observed as part of tinnitus should advance strategies to treat tinnitus by molecularly modulating plasticity

    Lesões do cabo longo do bíceps: tenotomia versus tenodese

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    ResumoAs lesões da cabeça longa do tendão bicipital (CLB) são comuns na prática clínica e podem ter causas degenerativas, inflamatórias, instabilidades (subluxação ou luxação) ou traumáticas. Geralmente, elas estão associadas a outras doenças do ombro, principalmente a lesões do manguito rotador. Atualmente, existem controvérsias quanto às indicações dos tratamentos cirúrgicos e à escolha da melhor técnica para cada caso, devido à possibilidade de deformidade estética, perda da força muscular e dor residual.O objetivo deste estudo foi identificar as indicações do tratamento cirúrgico, a melhor técnica cirúrgica e as vantagens e desvantagens de cada técnica descritas na literatura médica ortopédica no tratamento das lesões da CLB.Foi realizada revisão da literatura médica ortopédica disponível na base de dados da Biblioteca Regional de Medicina (BIREME), Medline, PubMed, Cochrane Library e Google Scholar, incluindo artigos publicados no período de 1991 a 2015.AbstractDisorders of the long head of biceps tendon are common in clinical practice. Their causes could be degenerative, inflammatory, instability (subluxation or luxation) or traumatic. They are generally associated to other diseases of the shoulder, mainly rotator cuff injuries. Currently, there is controversy in the literature regarding the indications for surgical treatment and the choice of the best technique for each case, due to the possibility of esthetic deformity, loss of muscle strength, and residual pain.The objective of this study was to identify the indications for surgical treatment, the best surgical technique, and the advantages and disadvantages of each technique described in the orthopedic literature for the treatment of long head of biceps tendon injuries.A revision of the orthopedic medical literature on the following databases: Biblioteca Regional de Medicina (BIREME), Medline, PubMed, Cochrane Library and Google Scholar, comprising articles published in the period from 1991 to 2015

    Recovery time between weigh-in and first match in State level judo competitions

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    Rapid weight loss is highly prevalent among combat sport athletes. After the weigh-in, there is a period in which athletes can refeed and rehydrate before the combats. The length of this recovery period is determinant for performance in the subsequent combats. No study, however, has determined the time patterns of such period. The purpose of this study was to determine the patterns of recovery time between the weigh-in and the first combats during judo competitions. One hundred and seventeen juvenile, junior and senior male athletes were analyzed during two São Paulo state competitions. The time at which each athlete has finished the weight-in and the time at which they have started the first combat were recorded and then the recovery period between weigh-in and combats was calculated. Average recovery time was approximately four hours. Most athletes had a 2.5 to 5-hour recovery time between the weigh-in and the first combat. Senior athletes had a significant longer recovery time compared to junior and juvenile (p < 0.001). Junior athletes also had a significant longer recovery time in comparison to juvenile athletes (p < 0.001). In conclusion, the patterns for recovery time presented in this study are likely to be a standard if competitions of similar size and organization are considered. Recovery period for the majority of athletes is enough to allow them to refeed and rehydrate, so the impact of weight loss on performance would be minimal. This can stimulate athletes to engage in potentially harmful rapid weight loss procedures.A perda rápida de peso é altamente prevalente entre atletas de luta. No judô, há um período entre a pesagem e o início da competição no qual atletas podem se recuperar da perda de peso. Apesar desse tempo ser determinante para o desempenho, nenhum estudo avaliou seu padrão de duração. Este estudo objetivou determinar o padrão de duração do tempo entre a pesagem e o início das lutas em competições oficiais de judô. Foram analisados 117 atletas do sexo masculino (classes juvenil, júnior e sênior) durante duas competições oficiais. Registraram-se o horário de término da pesagem e do início da primeira luta de cada atleta. O tempo médio de recuperação foi de aproximadamente quatro horas. A maior parte dos atletas teve aproximadamente 2,5 - 5 horas entre a pesagem e o início das lutas. O período para a classe sênior foi significantemente maior do que o das classes júnior e juvenil (p < 0,01) e o da classe júnior foi significantemente maior do que o da classe juvenil (p < 0,01). Conclui-se que os tempos de recuperação aqui registrados são provavelmente padrões para competições de mesmo porte e esquema organizacional, embora os tempos específicos para as classes etárias possam se modificar. O período que a maioria dos atletas teve para recuperar-se é suficiente para adequada ingestão de alimentos e líquidos, o que minimiza o impacto da perda de peso sobre o desempenho e estimula a pratica de métodos agressivos de perda rápida de peso

    Early Seizures Prematurely Unsilence Auditory Synapses to Disrupt Thalamocortical Critical Period Plasticity

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    Heightened neural excitability in infancy and childhood results in increased susceptibility to seizures. Such early-life seizures are associated with language deficits and autism that can result from aberrant development of the auditory cortex. Here, we show that early-life seizures disrupt a critical period (CP) for tonotopic map plasticity in primary auditory cortex (A1). We show that this CP is characterized by a prevalence of “silent,” NMDA-receptor (NMDAR)-only, glutamate receptor synapses in auditory cortex that become “unsilenced” due to activity-dependent AMPA receptor (AMPAR) insertion. Induction of seizures prior to this CP occludes tonotopic map plasticity by prematurely unsilencing NMDAR-only synapses. Further, brief treatment with the AMPAR antagonist NBQX following seizures, prior to the CP, pre

    Hearing Loss Prevents the Maturation of GABAergic Transmission in the Auditory Cortex

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    Inhibitory neurotransmission is a critical determinant of neuronal network gain and dynamic range, suggesting that network properties are shaped by activity during development. A previous study demonstrated that sensorineural hearing loss (SNHL) in gerbils leads to smaller inhibitory potentials in L2/3 pyramidal neurons in the thalamorecipient auditory cortex, ACx. Here, we explored the mechanisms that account for proper maturation of γ-amino butyric acid (GABA)ergic transmission. SNHL was induced at postnatal day (P) 10, and whole-cell voltage-clamp recordings were obtained from layer 2/3 pyramidal neurons in thalamocortical slices at P16–19. SNHL led to an increase in the frequency of GABAzine-sensitive (antagonist) spontaneous (s) and miniature (m) inhibitory postsynaptic currents (IPSCs), accompanied by diminished amplitudes and longer durations. Consistent with this, the amplitudes of minimum-evoked IPSCs were also reduced while their durations were longer. The α1- and β2/3 subunit–specific agonists zolpidem and loreclezole increased control but not SNHL sIPSC durations. To test whether SNHL affected the maturation of GABAergic transmission, sIPSCs were recorded at P10. These sIPSCs resembled the long SNHL sIPSCs. Furthermore, zolpidem and loreclezole were ineffective in increasing their durations. Together, these data strongly suggest that the presynaptic release properties and expression of key postsynaptic GABAA receptor subunits are coregulated by hearing

    Emergence of self-organized amoeboid movement in a multi-agent approximation of Physarum polycephalum

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    The giant single-celled slime mould Physarum polycephalum exhibits complex morphological adaptation and amoeboid movement as it forages for food and may be seen as a minimal example of complex robotic behaviour. Swarm computation has previously been used to explore how spatio-temporal complexity can emerge from, and be distributed within, simple component parts and their interactions. Using a particle-based swarm approach we explore the question of how to generate collective amoeboid movement from simple non-oscillatory component parts in a model of P. polycephalum. The model collective behaves as a cohesive and deformable virtual material, approximating the local coupling within the plasmodium matrix. The collective generates de-novo and complex oscillatory patterns from simple local interactions. The origin of this motor behaviour distributed within the collective rendering is morphologically adaptive, amenable to external influence and robust to simulated environmental insult. We show how to gain external influence over the collective movement by simulated chemo-attraction (pulling towards nutrient stimuli) and simulated light irradiation hazards (pushing from stimuli). The amorphous and distributed properties of the collective are demonstrated by cleaving it into two independent entities and fusing two separate entities to form a single device, thus enabling it to traverse narrow, separate or tortuous paths. We conclude by summarizing the contribution of the model to swarm-based robotics and soft-bodied modular robotics and discuss the future potential of such material approaches to the field. © 2012 IOP Publishing Ltd

    Developmental disruption of perineuronal nets in the medial prefrontal cortex after maternal immune activation

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    © The Author(s) 2016. Maternal infection during pregnancy increases the risk of offspring developing schizophrenia later in life. Similarly, animal models of maternal immune activation (MIA) induce behavioural and anatomical disturbances consistent with a schizophrenia-like phenotype in offspring. Notably, cognitive impairments in tasks dependent on the prefrontal cortex (PFC) are observed in humans with schizophrenia and in offspring after MIA during pregnancy. Recent studies of post-mortem tissue from individuals with schizophrenia revealed deficits in extracellular matrix structures called perineuronal nets (PNNs), particularly in PFC. Given these findings, we examined PNNs over the course of development in a well-characterized rat model of MIA using polyinosinic-polycytidylic acid (polyI:C). We found selective reductions of PNNs in the PFC of polyI:C offspring which did not manifest until early adulthood. These deficits were not associated with changes in parvalbumin cell density, but a decrease in the percentage of parvalbumin cells surrounded by a PNN. Developmental expression of PNNs was also significantly altered in the amygdala of polyI:C offspring. Our results indicate MIA causes region specific developmental abnormalities in PNNs in the PFC of offspring. These findings confirm the polyI:C model replicates neuropathological alterations associated with schizophrenia and may identify novel mechanisms for cognitive and emotional dysfunction in the disorder
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