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.
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"We studied vocal behavior during the first 4 weeks of life, a period in which the onset of dystonic symptoms in homozygote dt rats overlaps with a significant growth spurt (5 g at birth to about 25 g at P15) and at least three neurophysiological maturation processes. Pups begin to hear, and auditory experiences have long-lasting impacts on adult brain sound representation starting at P10 (e.g., Geal-Dor et al. 1993; de Villers-Sidani et al. 2007), adult respiratory patterns crystallizes between P10 and P15 (Paton and Richter 1995; Dutschmann et al. 2009), and the ingestive behavior transforms from suckling to mastication of hard food starting on P12 (Iriki et al. 1988; Westneat and Hall 1992). All four processes can affect vocal production, some in a predictable way (larger vocal organs likely lower pitch), whereas others are not fully understood. "
"The critical periods for LTP in visual and barrel cortex coincide with the critical periods for ocular dominance plasticity and barrel map plasticity , , , . In the auditory cortex, the critical period for frequency map plasticity is reported to be P11 to P13 for Sprague-Daley rats and P11 to P15 for C57B/6 mice , . However, other aspects of sensory representation can still be altered by experience after closure of the frequency map critical period , . "
[Show abstract][Hide abstract] ABSTRACT: Fragile X syndrome is a developmental disorder that affects sensory systems. A null mutation of the Fragile X Mental Retardation protein 1 (Fmr1) gene in mice has varied effects on developmental plasticity in different sensory systems, including normal barrel cortical plasticity, altered ocular dominance plasticity and grossly impaired auditory frequency map plasticity. The mutation also has different effects on long-term synaptic plasticity in somatosensory and visual cortical neurons, providing insights on how it may differentially affect the sensory systems. Here we present evidence that long-term potentiation (LTP) is impaired in the developing auditory cortex of the Fmr1 knockout (KO) mice. This impairment of synaptic plasticity is consistent with impaired frequency map plasticity in the Fmr1 KO mouse. Together, these results suggest a potential role of LTP in sensory map plasticity during early sensory development.
PLoS ONE 08/2014; 9(8):e104691. DOI:10.1371/journal.pone.0104691 · 3.23 Impact Factor
"Fixed material was sectioned on a freezing microtome at a 40 μm thickness in the coronal plane along the tonotopic axis of A1. The boundaries of the primary auditory cortex were functionally determined in a subset of animals of different ages with intracortical recordings as previously done (Bao et al., 2003; de Villers-Sidani et al., 2007) using the following criteria: (1) primary auditory neurons generally have a continuous, single-peaked, V-shaped receptive field, and (2) characteristic frequencies of the A1 neurons are tonotopically organized with high frequencies represented rostrally and low frequencies represented caudally. At the end of the recording session, the location of the electrode tracks was converted to coordinates in the Paxinos rat brain atlas. "
[Show abstract][Hide abstract] ABSTRACT: In both humans and rodents, decline in cognitive function is a hallmark of the aging process; the basis for this decrease has yet to be fully characterized. However, using aged rodent models, deficits in auditory processing have been associated with significant decreases in inhibitory signaling attributed to a loss of GABAergic interneurons. Not only are these interneurons crucial for pattern detection and other large-scale population dynamics, but they have also been linked to mechanisms mediating plasticity and learning, making them a prime candidate for study and modeling of modifications to cortical communication pathways in neurodegenerative diseases. Using the rat primary auditory cortex (A1) as a model, we probed the known markers of GABAergic interneurons with immunohistological methods, using antibodies against gamma aminobutyric acid (GABA), parvalbumin (PV), somatostatin (SOM), calretinin (CR), vasoactive intestinal peptide (VIP), choline acetyltransferase (ChAT), neuropeptide Y (NPY), and cholecystokinin (CCK) to document the changes observed in interneuron populations across the rat's lifespan. This analysis provided strong evidence that several but not all GABAergic neurons were affected by the aging process, showing most dramatic changes in expression of parvalbumin (PV) and somatostatin (SOM) expression. With this evidence, we show how understanding these trajectories of cell counts may be factored into a simple model to quantify changes in inhibitory signaling across the course of life, which may be applied as a framework for creating more advanced simulations of interneuronal implication in normal cerebral processing, normal aging, or pathological processes.
Frontiers in Neuroanatomy 06/2014; 8:40. DOI:10.3389/fnana.2014.00040 · 3.54 Impact Factor