Gender differences in a Drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit.

A male Drosophila model of locomotor deficit induced by chronic pentylenetetrazole (PTZ), a proconvulsant used to model epileptogenesis in rodents, has recently been described. Antiepileptic drugs (AEDs) ameliorate development of this behavioral abnormality. Time-series of microarray profiling of he...

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Autores principales:	Abhay Sharma, Farhan Mohammad, Priyanka Singh
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2009
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ac6262a77b574fc7a411db67ee68c629
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spelling	oai:doaj.org-article:ac6262a77b574fc7a411db67ee68c6292021-11-25T06:27:39ZGender differences in a Drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit.1932-620310.1371/journal.pone.0008136https://doaj.org/article/ac6262a77b574fc7a411db67ee68c6292009-12-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19956579/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203A male Drosophila model of locomotor deficit induced by chronic pentylenetetrazole (PTZ), a proconvulsant used to model epileptogenesis in rodents, has recently been described. Antiepileptic drugs (AEDs) ameliorate development of this behavioral abnormality. Time-series of microarray profiling of heads of male flies treated with PTZ has shown epileptogenesis-like transcriptomic perturbation in the fly model. Gender differences are known to exist in neurological and psychiatric conditions including epileptogenesis. We describe here the effects of chronic PTZ in Drosophila females, and compare the results with the male model. As in males, chronic PTZ was found to cause a decreased climbing speed in females. In males, overrepresentation of Wnt, MAPK, TGF-beta, JAK-STAT, Cell communication, and Dorso-Ventral axis formation pathways in downregulated genes was previously described. Of these, female genes showed enrichment only for Dorso-Ventral axis formation. Surprisingly, the ribosomal pathway was uniquely overrepresented in genes downregulated in females. Gender differences thus exist in the Drosophila model. Gender neutral, the developmental pathway Dorso-Ventral axis formation may be considered as the candidate causal pathway in chronic pentylenetetrazole induced behavioral deficit. Prior evidence of developmental mechanisms in epileptogenesis may support potential usefulness of the fly model. Given this, gender specific pathways identified here may provide a lead for further understanding brain dimorphism in neuropsychiatric disorders.Abhay SharmaFarhan MohammadPriyanka SinghPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 4, Iss 12, p e8136 (2009)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Abhay Sharma Farhan Mohammad Priyanka Singh Gender differences in a Drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit.
description	A male Drosophila model of locomotor deficit induced by chronic pentylenetetrazole (PTZ), a proconvulsant used to model epileptogenesis in rodents, has recently been described. Antiepileptic drugs (AEDs) ameliorate development of this behavioral abnormality. Time-series of microarray profiling of heads of male flies treated with PTZ has shown epileptogenesis-like transcriptomic perturbation in the fly model. Gender differences are known to exist in neurological and psychiatric conditions including epileptogenesis. We describe here the effects of chronic PTZ in Drosophila females, and compare the results with the male model. As in males, chronic PTZ was found to cause a decreased climbing speed in females. In males, overrepresentation of Wnt, MAPK, TGF-beta, JAK-STAT, Cell communication, and Dorso-Ventral axis formation pathways in downregulated genes was previously described. Of these, female genes showed enrichment only for Dorso-Ventral axis formation. Surprisingly, the ribosomal pathway was uniquely overrepresented in genes downregulated in females. Gender differences thus exist in the Drosophila model. Gender neutral, the developmental pathway Dorso-Ventral axis formation may be considered as the candidate causal pathway in chronic pentylenetetrazole induced behavioral deficit. Prior evidence of developmental mechanisms in epileptogenesis may support potential usefulness of the fly model. Given this, gender specific pathways identified here may provide a lead for further understanding brain dimorphism in neuropsychiatric disorders.
format	article
author	Abhay Sharma Farhan Mohammad Priyanka Singh
author_facet	Abhay Sharma Farhan Mohammad Priyanka Singh
author_sort	Abhay Sharma
title	Gender differences in a Drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit.
title_short	Gender differences in a Drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit.
title_full	Gender differences in a Drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit.
title_fullStr	Gender differences in a Drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit.
title_full_unstemmed	Gender differences in a Drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit.
title_sort	gender differences in a drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit.
publisher	Public Library of Science (PLoS)
publishDate	2009
url	https://doaj.org/article/ac6262a77b574fc7a411db67ee68c629
work_keys_str_mv	AT abhaysharma genderdifferencesinadrosophilatranscriptomicmodelofchronicpentylenetetrazoleinducedbehavioraldeficit AT farhanmohammad genderdifferencesinadrosophilatranscriptomicmodelofchronicpentylenetetrazoleinducedbehavioraldeficit AT priyankasingh genderdifferencesinadrosophilatranscriptomicmodelofchronicpentylenetetrazoleinducedbehavioraldeficit
_version_	1718413701188419584

Gender differences in a Drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit.

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