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Processing of Song Signals in the Cricket and its Hormonal Control
Authors
Gordon Atkins
John Stout
Publication date
1 December 1994
Publisher
Digital Commons @ Andrews University
Abstract
SYNOPSIS. Phonotaxis by female crickets to the calling song of males, is an important model for investigating the neural basis of auditory behavior. Recent advances make it possible to explain some components of this behavior and its hormonal control, at the level of identified neurons and molecular expression within those neurons. Tonotopically arranged afferents from the cricket\u27s ear, project to local and intersegmental prothoracic interneurons. Bilateral processing of signals and some temporal-pattern specific processing occurs in the prothoracic ganglion and influences acoustic information that is sent to the brain via ascending interneurons that are demonstrably involved in phonotaxis. High, low and band- pass interneurons in the brain continue temporal pattern processing which matches the selectivity of phonotaxis and may be filters for recognition of the calling song. Neurons descending from the brain and prothoracic ganglion, direct multimodal signals (including auditory) to more posterior regions, possibly the leg motor neurons that are responsible for phonotaxis. Age-related changes or artificially induced changes in Juvenile Hormone III levels regulate the threshold for phonotaxis in Acheta domesticus, by varying the threshold of LI, a prothoracic ascending interneuron that is necessary for phonotaxis to low intensity calling songs. Results from in situ hybridization suggest that this might be accomplished, in part, by controlling the levels of nicotinic acetylcholine receptor-like mRNA expressed in LI, presumably by increasing its neurotransmitter receptor density. L3 is a prothoracic ascending interneuron that exhibits bandselective response properties to the syllable period of the calling song. L3\u27s response is age and JHIII related, and is correlated to phonotactic selectivity. These changes in L3 might be accomplished, at least in part by JHIII regulating the expression of nicotinic acetylcholine receptor-like mRNA in L3 ©1994 American Society of Zoologists
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Last time updated on 13/11/2021