Origin and function of short-latency inputs to the neural substrates underlying the acoustic startle reflex

The acoustic startle reflex (ASR) is a survival mechanism of alarm, which rapidly alerts the organism to a sudden loud auditory stimulus. In rats, the primary ASR circuit encompasses three serially connected structures: cochlear root neurons (CRNs), neurons in the caudal pontine reticular nucleus (P...

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Main Authors:	Gómez-Nieto, Ricardo, Horta-Júnior, José de Anchieta C., Castellano, Orlando, Millian-Morell, Lymarie, Rubio, Maria E., López, Dolores E.
Format:	Online
Language:	English
Published:	Frontiers Media S.A. 2014
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110630/

id	pubmed-4110630
recordtype	oai_dc
spelling	pubmed-41106302014-08-12 Origin and function of short-latency inputs to the neural substrates underlying the acoustic startle reflex Gómez-Nieto, Ricardo Horta-Júnior, José de Anchieta C. Castellano, Orlando Millian-Morell, Lymarie Rubio, Maria E. López, Dolores E. Psychology The acoustic startle reflex (ASR) is a survival mechanism of alarm, which rapidly alerts the organism to a sudden loud auditory stimulus. In rats, the primary ASR circuit encompasses three serially connected structures: cochlear root neurons (CRNs), neurons in the caudal pontine reticular nucleus (PnC), and motoneurons in the medulla and spinal cord. It is well-established that both CRNs and PnC neurons receive short-latency auditory inputs to mediate the ASR. Here, we investigated the anatomical origin and functional role of these inputs using a multidisciplinary approach that combines morphological, electrophysiological and behavioral techniques. Anterograde tracer injections into the cochlea suggest that CRNs somata and dendrites receive inputs depending, respectively, on their basal or apical cochlear origin. Confocal colocalization experiments demonstrated that these cochlear inputs are immunopositive for the vesicular glutamate transporter 1 (VGLUT1). Using extracellular recordings in vivo followed by subsequent tracer injections, we investigated the response of PnC neurons after contra-, ipsi-, and bilateral acoustic stimulation and identified the source of their auditory afferents. Our results showed that the binaural firing rate of PnC neurons was higher than the monaural, exhibiting higher spike discharges with contralateral than ipsilateral acoustic stimulations. Our histological analysis confirmed the CRNs as the principal source of short-latency acoustic inputs, and indicated that other areas of the cochlear nucleus complex are not likely to innervate PnC. Behaviorally, we observed a strong reduction of ASR amplitude in monaural earplugged rats that corresponds with the binaural summation process shown in our electrophysiological findings. Our study contributes to understand better the role of neuronal mechanisms in auditory alerting behaviors and provides strong evidence that the CRNs-PnC pathway mediates fast neurotransmission and binaural summation of the ASR. Frontiers Media S.A. 2014-07-25 /pmc/articles/PMC4110630/ /pubmed/25120419 http://dx.doi.org/10.3389/fnins.2014.00216 Text en Copyright © 2014 Gómez-Nieto, Horta-Júnior, Castellano, Millian-Morell, Rubio and López. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Gómez-Nieto, Ricardo Horta-Júnior, José de Anchieta C. Castellano, Orlando Millian-Morell, Lymarie Rubio, Maria E. López, Dolores E.
spellingShingle	Gómez-Nieto, Ricardo Horta-Júnior, José de Anchieta C. Castellano, Orlando Millian-Morell, Lymarie Rubio, Maria E. López, Dolores E. Origin and function of short-latency inputs to the neural substrates underlying the acoustic startle reflex
author_facet	Gómez-Nieto, Ricardo Horta-Júnior, José de Anchieta C. Castellano, Orlando Millian-Morell, Lymarie Rubio, Maria E. López, Dolores E.
author_sort	Gómez-Nieto, Ricardo
title	Origin and function of short-latency inputs to the neural substrates underlying the acoustic startle reflex
title_short	Origin and function of short-latency inputs to the neural substrates underlying the acoustic startle reflex
title_full	Origin and function of short-latency inputs to the neural substrates underlying the acoustic startle reflex
title_fullStr	Origin and function of short-latency inputs to the neural substrates underlying the acoustic startle reflex
title_full_unstemmed	Origin and function of short-latency inputs to the neural substrates underlying the acoustic startle reflex
title_sort	origin and function of short-latency inputs to the neural substrates underlying the acoustic startle reflex
description	The acoustic startle reflex (ASR) is a survival mechanism of alarm, which rapidly alerts the organism to a sudden loud auditory stimulus. In rats, the primary ASR circuit encompasses three serially connected structures: cochlear root neurons (CRNs), neurons in the caudal pontine reticular nucleus (PnC), and motoneurons in the medulla and spinal cord. It is well-established that both CRNs and PnC neurons receive short-latency auditory inputs to mediate the ASR. Here, we investigated the anatomical origin and functional role of these inputs using a multidisciplinary approach that combines morphological, electrophysiological and behavioral techniques. Anterograde tracer injections into the cochlea suggest that CRNs somata and dendrites receive inputs depending, respectively, on their basal or apical cochlear origin. Confocal colocalization experiments demonstrated that these cochlear inputs are immunopositive for the vesicular glutamate transporter 1 (VGLUT1). Using extracellular recordings in vivo followed by subsequent tracer injections, we investigated the response of PnC neurons after contra-, ipsi-, and bilateral acoustic stimulation and identified the source of their auditory afferents. Our results showed that the binaural firing rate of PnC neurons was higher than the monaural, exhibiting higher spike discharges with contralateral than ipsilateral acoustic stimulations. Our histological analysis confirmed the CRNs as the principal source of short-latency acoustic inputs, and indicated that other areas of the cochlear nucleus complex are not likely to innervate PnC. Behaviorally, we observed a strong reduction of ASR amplitude in monaural earplugged rats that corresponds with the binaural summation process shown in our electrophysiological findings. Our study contributes to understand better the role of neuronal mechanisms in auditory alerting behaviors and provides strong evidence that the CRNs-PnC pathway mediates fast neurotransmission and binaural summation of the ASR.
publisher	Frontiers Media S.A.
publishDate	2014
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4110630/
_version_	1613117845914255360

Origin and function of short-latency inputs to the neural substrates underlying the acoustic startle reflex

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