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
N1 - Funding Information:
We thank Dr Takashi Kitamura for advice on the statistical analyses. This work was supported in part by grants for Scientific Research on Priority Areas in “Molecular Brain Science” from the Ministry of Education, Culture, Sports, Science, and Technology of the Japanese Government to K. I.
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.
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U2 - 10.1016/j.neulet.2009.01.074
DO - 10.1016/j.neulet.2009.01.074
M3 - Article
C2 - 19348730
AN - SCOPUS:60849130953
SN - 0304-3940
VL - 452
SP - 232
EP - 237
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 3
ER -