Neuron type-selective effects of activin on development of the hippocampus

Mariko Sekiguchi, Fumihiko Hayashi, Kunihiro Tsuchida, Kaoru Inokuchi

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Activin is a member of the transforming growth factor-β superfamily and affects the viability of hippocampal neurons during postnatal neurogenesis. We used primary hippocampal neuron to study the actions of activin on developing neurons. Continuous treatment of hippocampal cultures with activin suppressed the emergence of GAD67+ neurons, which are a subtype of GABAergic interneurons, and increased the percentage of Prox1+ neurons, which are dentate granule cells. The effects of activin were abolished by co-treatment with follistatin, which is a direct inhibitor of activin. In contrast, follistatin treatment alone increased the percentage of GAD67+ neurons and decreased the percentage of Prox1+ neurons. These results indicate that changes in activin signaling during postnatal neural development alter the composition of the neural circuitry and suggest that alterations in the ratio of excitatory to inhibitory neurons may be responsible for changes in the spontaneous and evoked-reactivity of these neurons to other neural inputs.

Original languageEnglish
Pages (from-to)232-237
Number of pages6
JournalNeuroscience Letters
Volume452
Issue number3
DOIs
Publication statusPublished - 20-03-2009

Fingerprint

Activins
Hippocampus
Neurons
Follistatin
Neurogenesis
Transforming Growth Factors
Interneurons

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Sekiguchi, Mariko ; Hayashi, Fumihiko ; Tsuchida, Kunihiro ; Inokuchi, Kaoru. / Neuron type-selective effects of activin on development of the hippocampus. In: Neuroscience Letters. 2009 ; Vol. 452, No. 3. pp. 232-237.
@article{b3d2349006e34721b4ff6908d8e989c7,
title = "Neuron type-selective effects of activin on development of the hippocampus",
abstract = "Activin is a member of the transforming growth factor-β superfamily and affects the viability of hippocampal neurons during postnatal neurogenesis. We used primary hippocampal neuron to study the actions of activin on developing neurons. Continuous treatment of hippocampal cultures with activin suppressed the emergence of GAD67+ neurons, which are a subtype of GABAergic interneurons, and increased the percentage of Prox1+ neurons, which are dentate granule cells. The effects of activin were abolished by co-treatment with follistatin, which is a direct inhibitor of activin. In contrast, follistatin treatment alone increased the percentage of GAD67+ neurons and decreased the percentage of Prox1+ neurons. These results indicate that changes in activin signaling during postnatal neural development alter the composition of the neural circuitry and suggest that alterations in the ratio of excitatory to inhibitory neurons may be responsible for changes in the spontaneous and evoked-reactivity of these neurons to other neural inputs.",
author = "Mariko Sekiguchi and Fumihiko Hayashi and Kunihiro Tsuchida and Kaoru Inokuchi",
year = "2009",
month = "3",
day = "20",
doi = "10.1016/j.neulet.2009.01.074",
language = "English",
volume = "452",
pages = "232--237",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "3",

}

Neuron type-selective effects of activin on development of the hippocampus. / Sekiguchi, Mariko; Hayashi, Fumihiko; Tsuchida, Kunihiro; Inokuchi, Kaoru.

In: Neuroscience Letters, Vol. 452, No. 3, 20.03.2009, p. 232-237.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Neuron type-selective effects of activin on development of the hippocampus

AU - Sekiguchi, Mariko

AU - Hayashi, Fumihiko

AU - Tsuchida, Kunihiro

AU - Inokuchi, Kaoru

PY - 2009/3/20

Y1 - 2009/3/20

N2 - Activin is a member of the transforming growth factor-β superfamily and affects the viability of hippocampal neurons during postnatal neurogenesis. We used primary hippocampal neuron to study the actions of activin on developing neurons. Continuous treatment of hippocampal cultures with activin suppressed the emergence of GAD67+ neurons, which are a subtype of GABAergic interneurons, and increased the percentage of Prox1+ neurons, which are dentate granule cells. The effects of activin were abolished by co-treatment with follistatin, which is a direct inhibitor of activin. In contrast, follistatin treatment alone increased the percentage of GAD67+ neurons and decreased the percentage of Prox1+ neurons. These results indicate that changes in activin signaling during postnatal neural development alter the composition of the neural circuitry and suggest that alterations in the ratio of excitatory to inhibitory neurons may be responsible for changes in the spontaneous and evoked-reactivity of these neurons to other neural inputs.

AB - Activin is a member of the transforming growth factor-β superfamily and affects the viability of hippocampal neurons during postnatal neurogenesis. We used primary hippocampal neuron to study the actions of activin on developing neurons. Continuous treatment of hippocampal cultures with activin suppressed the emergence of GAD67+ neurons, which are a subtype of GABAergic interneurons, and increased the percentage of Prox1+ neurons, which are dentate granule cells. The effects of activin were abolished by co-treatment with follistatin, which is a direct inhibitor of activin. In contrast, follistatin treatment alone increased the percentage of GAD67+ neurons and decreased the percentage of Prox1+ neurons. These results indicate that changes in activin signaling during postnatal neural development alter the composition of the neural circuitry and suggest that alterations in the ratio of excitatory to inhibitory neurons may be responsible for changes in the spontaneous and evoked-reactivity of these neurons to other neural inputs.

UR - http://www.scopus.com/inward/record.url?scp=60849130953&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=60849130953&partnerID=8YFLogxK

U2 - 10.1016/j.neulet.2009.01.074

DO - 10.1016/j.neulet.2009.01.074

M3 - Article

C2 - 19348730

AN - SCOPUS:60849130953

VL - 452

SP - 232

EP - 237

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 3

ER -