Perinatal Asphyxia Affects Rat Auditory Processing: Implications for Auditory Perceptual Impairments in Neurodevelopmental Disorders

Perinatal asphyxia, a naturally and commonly occurring risk factor in birthing, represents one of the major causes of neonatal encephalopathy with long term consequences for infants. Here, degraded spectral and temporal responses to sounds were recorded from neurons in the primary auditory cortex (A1) of adult rats exposed to asphyxia at birth. Response onset latencies and durations were increased. Response amplitudes were reduced. Tuning curves were broader. Degraded successive-stimulus masking inhibitory mechanisms were associated with a reduced capability of neurons to follow higher-rate repetitive stimuli. The architecture of peripheral inner ear sensory epithelium was preserved, suggesting that recorded abnormalities can be of central origin. Some implications of these findings for the genesis of language perception deficits or for impaired language expression recorded in developmental disorders, such as autism spectrum disorders, contributed to by perinatal asphyxia, are discussed

What we learn and when we learn it: sensitive periods in development

The impact of training or experience is not the same at all points in development. Children who receive music lessons, or learn a second language before age 7-8 are more proficient as adults. Early exposure to drugs or trauma makes people more likely to become addicted or depressed later life. Rat pups exposed to specific frequencies from 9-13 days post-partum show expanded cortical representations of these frequencies. Young birds must hear and copy their native song within 1-2 months of birth or they may never learn it at all. These are examples of sensitive periods: developmental windows where maturation and specific experience interact to produce differential long-term effects on the brain and behavior. While still controversial, evidence for the existence of sensitive periods has grown, as has our understanding of the underlying mechanisms of brain plasticity. Behavioral evidence from studies of language, psychopathology or vision in humans has been complemented by evidence elucidating molecular, gene and hormonal mechanisms in animals. It has been proposed that sensitive periods can be both opened and closed by specific experience, and that there are multiple, overlapping sensitive periods that occur through-out development as functions come on line. It is also likely that experience-dependent behavioral or brain plasticity accrued during one sensitive period can serve as a scaffold on which later experience and plasticity can build. Based on current knowledge, there are a number of broad questions and challenges to be addressed in this domain, these include: generating new information about the neurobiological mediators of structural and functional changes; proposing models of brain development that will better predict when sensitive periods should occur and what functions are implicated; investigation of the interaction between experience during a sensitive period and pre-existing individual differences; and the relationship between experience during a sensitive period and on-going experience. The goal of this Research Topic is to bring together scientists in different fields whose work addresses these issues, including animal and human developmental neuroscience, language and cognitive development, education, developmental psychopathology and sensory neuroscience

Shaping the aging brain: role of auditory input patterns in the emergence of auditory cortical impairments

Age-related impairments in the primary auditory cortex (A1) include poor tuning selectivity, neural desynchronization and degraded responses to low-probability sounds. These changes have been largely attributed to reduced inhibition in the aged brain, and are thought to contribute to substantial hearing impairment in both humans and animals. Since many of these changes can be partially reversed with auditory training, it has been speculated that they might not be purely degenerative, but might rather represent negative plastic adjustments to noisy or distorted auditory signals reaching the brain. To test this hypothesis, we examined the impact of exposing young adult rats to 8 weeks of low-grade broadband noise on several aspects of A1 function and structure. We then characterized the same A1 elements in aging rats for comparison. We found that the impact of noise exposure on A1 tuning selectivity, temporal processing of auditory signal and responses to oddball tones was almost indistinguishable from the effect of natural aging. Moreover, noise exposure resulted in a reduction in the population of parvalbumin inhibitory interneurons and cortical myelin as previously documented in the aged group. Most of these changes reversed after returning the rats to a quiet environment. These results support the hypothesis that age-related changes in A1 have a strong activity-dependent component and indicate that the presence or absence of clear auditory input patterns might be a key factor in sustaining adult A1 function

Resting state networks in temporal lobe epilepsy

Temporal lobe epilepsy (TLE) is typically described as a neurologic disorder affecting a cerebral network comprising the hippocampus proper and several anatomically related extrahippocampal regions. A new level of complexity was recently added to the study of this disorder by the evidence that TLE also appears to chronically alter the activity of several brain-wide neural networks involved in the control of higher order brain functions and not traditionally linked to epilepsy. Recently developed brain imaging techniques such as functional magnetic resonance imaging (fMRI) analysis of resting state connectivity, have greatly contributed to these observations by allowing the precise characterization of several brain networks with distinct functional signatures in the resting brain, and therefore also known as resting state networks. These significant advances in imaging represent an opportunity to investigate the still elusive origins of the disabling cognitive and psychiatric manifestations of TLE, and could have important implications for its pathophysiology and, perhaps, its therapy. Herein we review recent studies in this field by focusing on resting state networks that have been implicated in the pathophysiology of psychiatric disorders and cognitive impairment in patients with epilepsy: the default mode network, the attention network, and the reward/emotion network

Adaptive Training Diminishes Distractibility in Aging across Species

Aging is associated with deficits in the ability to ignore distractions, which has not yet been remediated by any neurotherapeutic approach. Here, in parallel auditory experiments with older rats and humans, we evaluated a targeted cognitive training approach that adaptively manipulated distractor challenge. Training resulted in enhanced discrimination abilities in the setting of irrelevant information in both species that was driven by selectively diminished distraction-related errors. Neural responses to distractors in auditory cortex were selectively reduced in both species, mimicking the behavioral effects. Sensory receptive fields in trained rats exhibited improved spectral and spatial selectivity. Frontal theta measures of top-down engagement with distractors were selectively restrained in trained humans. Finally, training gains generalized to group and individual level benefits in aspects of working memory and sustained attention. Thus, we demonstrate converging cross-species evidence for training-induced selective plasticity of distractor processing at multiple neural scales, benefitting distractor suppression and cognitive control

Critical period window for spectral tuning defined in the primary auditory cortex (A1) in the rat

Experience-dependent plasticity during development results in the emergence of highly adapted representations of the external world in the adult brain. Previous studies have convincingly shown that the primary auditory cortex (A1)of the rat possesses a postnatal period of sensory input-driven plasticity but its precise timing ( onset, duration, end) has not been defined. In the present study, we examined the effects of pure-tone exposure on the auditory cortex of developing rat pups at different postnatal ages with a high temporal resolution. We found that pure-tone exposure resulted in profound, persistent alterations in sound representations in A1 only if the exposure occurred during a brief period extending from postnatal day 11 (P11) to P13. We also found that postnatal sound exposure in this epoch led to striking alterations in the cortical representation of sound intensity

Manipulation of BDNF signaling affects spectral selectivity.

<p>(A) Percentage of single and multi/flat-peaked receptive fields for each study group. The percentage of single-peaked receptive fields was significantly reduced in the anti-BDNF group compared to controls (F = 13.6, p = 0.003, ANOVA). (B) Response bandwidths above threshold (BW20) were significantly augmented in the anti-BDNF group compared to controls (F = 7.3, p = 0.007, ANOVA). Values are means ± SEM. * p<0.05.</p