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Articles, Neurobiology of Disease

Homeostatic Responses Fail to Correct Defective Amygdala Inhibitory Circuit Maturation in Fragile X Syndrome

Rebecca L. Vislay, Brandon S. Martin, Jose Luis Olmos-Serrano, Sebila Kratovac, David L. Nelson, Joshua G. Corbin and Molly M. Huntsman
Journal of Neuroscience 24 April 2013, 33 (17) 7548-7558; DOI: https://doi.org/10.1523/JNEUROSCI.2764-12.2013
Rebecca L. Vislay
1Center for Neuroscience Research, Children's National Medical Center, Washington, DC 20010,
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Brandon S. Martin
1Center for Neuroscience Research, Children's National Medical Center, Washington, DC 20010,
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Jose Luis Olmos-Serrano
1Center for Neuroscience Research, Children's National Medical Center, Washington, DC 20010,
2Department of Anatomy and Neurobiology, Boston University School of Medicine, Boston, Massachusetts 02118,
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Sebila Kratovac
1Center for Neuroscience Research, Children's National Medical Center, Washington, DC 20010,
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David L. Nelson
3Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, and
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Joshua G. Corbin
1Center for Neuroscience Research, Children's National Medical Center, Washington, DC 20010,
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Molly M. Huntsman
4Department of Pharmaceutical Sciences, Skaggs School of Pharmacy, Department of Pediatrics, School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045
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Abstract

Fragile X syndrome (FXS) is a debilitating neurodevelopmental disorder thought to arise from disrupted synaptic communication in several key brain regions, including the amygdala, a central processing center for information with emotional and social relevance. Recent studies reveal defects in both excitatory and inhibitory neurotransmission in mature amygdala circuits in Fmr1−/y mutants, the animal model of FXS. However, whether these defects are the result of altered synaptic development or simply faulty mature circuits remains unknown. Using a combination of electrophysiological and genetic approaches, we show the development of both presynaptic and postsynaptic components of inhibitory neurotransmission in the FXS amygdala is dynamically altered during critical stages of neural circuit formation. Surprisingly, we observe that there is a homeostatic correction of defective inhibition, which, despite transiently restoring inhibitory synaptic efficacy to levels at or beyond those of control, ultimately fails to be maintained. Using inhibitory interneuron-specific conditional knock-out and rescue mice, we further reveal that fragile X mental retardation protein function in amygdala inhibitory microcircuits can be segregated into distinct presynaptic and postsynaptic components. Collectively, these studies reveal a previously unrecognized complexity of disrupted neuronal development in FXS and therefore have direct implications for establishing novel temporal and region-specific targeted therapies to ameliorate core amygdala-based behavioral symptoms.

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The Journal of Neuroscience: 33 (17)
Journal of Neuroscience
Vol. 33, Issue 17
24 Apr 2013
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Homeostatic Responses Fail to Correct Defective Amygdala Inhibitory Circuit Maturation in Fragile X Syndrome
Rebecca L. Vislay, Brandon S. Martin, Jose Luis Olmos-Serrano, Sebila Kratovac, David L. Nelson, Joshua G. Corbin, Molly M. Huntsman
Journal of Neuroscience 24 April 2013, 33 (17) 7548-7558; DOI: 10.1523/JNEUROSCI.2764-12.2013

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Homeostatic Responses Fail to Correct Defective Amygdala Inhibitory Circuit Maturation in Fragile X Syndrome
Rebecca L. Vislay, Brandon S. Martin, Jose Luis Olmos-Serrano, Sebila Kratovac, David L. Nelson, Joshua G. Corbin, Molly M. Huntsman
Journal of Neuroscience 24 April 2013, 33 (17) 7548-7558; DOI: 10.1523/JNEUROSCI.2764-12.2013
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