Excitatory effects of the primary auditory cortex on the sound-evoked responses in the ipsilateral anterior auditory field in rat. (11th October 2017)

• Record Type: Journal Article
• Authors: Zhang, Guangwei; Tao, Can; Zhou, Chang; Yan, Sumei; Wang, Zhaoqun; Zhou, Yi; Xiong, Ying
• Is Part Of: Neuroscience. Volume 361(2017)
• Page Start: 157
• Page End: 166
• Publication Date: 2017-10-11
• Subjects: A1 primary auditory cortex -- AAF anterior auditory field -- AAVs adeno-associated viruses -- CF characteristic frequency -- ChR2 channelrhodopsin -- eGFP enhanced green fluorescent protein -- eNpHR express halorhodopsin -- LFP local field potential -- PBS phosphate-buffered saline -- TRF tonal receptive field; multiunit recording -- parallel auditory pathway -- interaction -- terminal activation; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2017.08.019
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: Optogenetically activate A1 significantly increases the excitability of AAF. A1 suppression decreases spontaneous and tone-evoked responses in AAF. The excitatory effect of A1 on AAF is indirect. Abstract: In the neocortex, interaction and cooperation between different areas are important for information processing, which also applies to different areas within one sensory modality. In the temporal cortex of rodents and cats, both the primary auditory cortex (A1) and the anterior auditory field (AAF) have tonotopicity but with a mirrored frequency gradient. However, whether and how A1 modulates the responses in AAF is largely unknown. Here, we functionally identified the locations of A1 and AAF in rats and used an optogenetic approach to manipulate the activity of A1 in vivo. We found that activation of A1 axon terminals in AAF did not change AAF responses, but activating A1 neuronal cell bodies could increase the sound-evoked responses in AAF, as well as decrease the intensity threshold and broaden the frequency bandwidth, while suppressing A1 could cause the opposite effects. Our results suggested that A1 could modulate the general excitability of AAF through indirect pathways, which provides a potential relationship between these two parallel auditory ascending pathways.