Agomelatine Is Unable to Attenuate Kainic Acid–Induced Deficits in Early Life Communicative Behavior

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Main Authors: Matthew S. Binder, Zachary J. Pranske, Samantha L. Hodges, Paige D. Womble, Eliesse M. Kwok, Saul I. Quintero, Andrew D. Kim, David A. Narvaiz, Joaquin N. Lugo
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Published: Wiley 2024
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author Matthew S. Binder
Zachary J. Pranske
Samantha L. Hodges
Paige D. Womble
Eliesse M. Kwok
Saul I. Quintero
Andrew D. Kim
David A. Narvaiz
Joaquin N. Lugo
author_facet Matthew S. Binder
Zachary J. Pranske
Samantha L. Hodges
Paige D. Womble
Eliesse M. Kwok
Saul I. Quintero
Andrew D. Kim
David A. Narvaiz
Joaquin N. Lugo
Matthew S. Binder
Zachary J. Pranske
Samantha L. Hodges
Paige D. Womble
Eliesse M. Kwok
Saul I. Quintero
Andrew D. Kim
David A. Narvaiz
Joaquin N. Lugo
collection Wiley Open Access
contents Agomelatine Is Unable to Attenuate Kainic Acid–Induced Deficits in Early Life Communicative Behavior Matthew S. Binder Zachary J. Pranske Samantha L. Hodges Paige D. Womble Eliesse M. Kwok Saul I. Quintero Andrew D. Kim David A. Narvaiz Joaquin N. Lugo Developmental Psychobiology ABSTRACTEarly life seizures are associated with a variety of behavioral comorbidities. Among the most prevalent of these are deficits in communication. Auditory communicative behaviors in mice, known as ultrasonic vocalizations (USVs), can be used to assess potential treatments. Agomelatine is a melatonin agonist that effectively reduces behavioral comorbidities of seizures in adults; however, its ability to attenuate seizure‐induced communicative deficits in neonates is unknown. To address this, we administered C57 mice either saline or kainic acid (KA) on postnatal day (PD) 10. The mice then received either agomelatine or saline 1‐h post‐status epilepticus. On PD 11, we assessed the quantity of USVs produced, the duration, peak frequency, fundamental frequency, and amplitude of the vocalizations, as well as the call type utilization. We found that KA increased vocal production and reduced USV variability relative to controls. KA also increased USV duration and amplitude and significantly altered the types of calls produced. Agomelatine did not attenuate any of the deficits. Our study is the first to assess agomelatine's efficacy to correct USVs and thus provides an important point of context to the literature, indicating that despite its high therapeutic efficacy to attenuate other behavioral comorbidities of seizures, agomelatine's ability to correct neonatal communicative deficits is limited. 10.1002/dev.22543 http://creativecommons.org/licenses/by/4.0/
doi_str_mv 10.1002/dev.22543
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id wiley_oa_10_1002_dev_22543
institution Wiley Open Access
license_str_mv http://creativecommons.org/licenses/by/4.0/
publishDate 2024
publisher Wiley
record_format wiley_oa
spellingShingle Agomelatine Is Unable to Attenuate Kainic Acid–Induced Deficits in Early Life Communicative Behavior
Matthew S. Binder
Zachary J. Pranske
Samantha L. Hodges
Paige D. Womble
Eliesse M. Kwok
Saul I. Quintero
Andrew D. Kim
David A. Narvaiz
Joaquin N. Lugo
Developmental Psychobiology
Agomelatine Is Unable to Attenuate Kainic Acid–Induced Deficits in Early Life Communicative Behavior Matthew S. Binder Zachary J. Pranske Samantha L. Hodges Paige D. Womble Eliesse M. Kwok Saul I. Quintero Andrew D. Kim David A. Narvaiz Joaquin N. Lugo Developmental Psychobiology ABSTRACTEarly life seizures are associated with a variety of behavioral comorbidities. Among the most prevalent of these are deficits in communication. Auditory communicative behaviors in mice, known as ultrasonic vocalizations (USVs), can be used to assess potential treatments. Agomelatine is a melatonin agonist that effectively reduces behavioral comorbidities of seizures in adults; however, its ability to attenuate seizure‐induced communicative deficits in neonates is unknown. To address this, we administered C57 mice either saline or kainic acid (KA) on postnatal day (PD) 10. The mice then received either agomelatine or saline 1‐h post‐status epilepticus. On PD 11, we assessed the quantity of USVs produced, the duration, peak frequency, fundamental frequency, and amplitude of the vocalizations, as well as the call type utilization. We found that KA increased vocal production and reduced USV variability relative to controls. KA also increased USV duration and amplitude and significantly altered the types of calls produced. Agomelatine did not attenuate any of the deficits. Our study is the first to assess agomelatine's efficacy to correct USVs and thus provides an important point of context to the literature, indicating that despite its high therapeutic efficacy to attenuate other behavioral comorbidities of seizures, agomelatine's ability to correct neonatal communicative deficits is limited. 10.1002/dev.22543 http://creativecommons.org/licenses/by/4.0/
title Agomelatine Is Unable to Attenuate Kainic Acid–Induced Deficits in Early Life Communicative Behavior
topic Developmental Psychobiology
url https://onlinelibrary.wiley.com/doi/10.1002/dev.22543