Sensory overamplification in layer 5 auditory corticofugal projection neurons following cochlear nerve synaptic damage

被引：63
作者：
Asokan, Meenakshi M. [1 ,2 ]
Williamson, Ross S. [1 ,3 ]
Hancock, Kenneth E. [1 ,3 ]
Polley, Daniel B. [1 ,2 ,3 ]
机构：
[1] Massachusetts Eye & Ear Infirm, Eaton Peabody Labs, Boston, MA 02114 USA
[2] Harvard Univ, Div Med Sci, Boston, MA 02114 USA
[3] Harvard Med Sch, Dept Otolaryngol, Boston, MA 02114 USA
来源：
NATURE COMMUNICATIONS | 2018年 / 9卷
关键词：
HEARING-LOSS; HOMEOSTATIC PLASTICITY; INFERIOR COLLICULUS; REGULAR-SPIKING; LONG-TERM; CORTEX; CONNECTIVITY; TINNITUS; CIRCUIT; EXCITABILITY;
D O I：
10.1038/s41467-018-04852-y
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Layer 5 (L5) cortical projection neurons innervate far-ranging brain areas to coordinate integrative sensory processing and adaptive behaviors. Here, we characterize a plasticity in L5 auditory cortex (ACtx) neurons that innervate the inferior colliculus (IC), thalamus, lateral amygdala and striatum. We track daily changes in sound processing using chronic widefield calcium imaging of L5 axon terminals on the dorsal cap of the IC in awake, adult mice. Sound level growth functions at the level of the auditory nerve and corticocollicular axon terminals are both strongly depressed hours after noise-induced damage of cochlear afferent synapses. Corticocollicular response gain rebounded above baseline levels by the following day and remained elevated for several weeks despite a persistent reduction in auditory nerve input. Sustained potentiation of excitatory ACtx projection neurons that innervate multiple limbic and subcortical auditory centers may underlie hyperexcitability and aberrant functional coupling of distributed brain networks in tinnitus and hyperacusis.
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页数：10
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