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Plasticity of 5‐HT 1A receptor‐mediated signaling during early postnatal brain development
Author(s) -
Mehta Mukti,
Ahmed Zagloul,
Fernando Suraj Shawn,
CanoSanchez Patricia,
Adayev Tatyana,
Ziemnicka Dorota,
Wieraszko Andrzej,
Banerjee Probal
Publication year - 2007
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.04448.x
Subject(s) - dentate gyrus , neuroscience , biology , hippocampus , hippocampal formation , protein kinase c , neurotransmission , receptor , postsynaptic potential , synaptic plasticity , kinase , signal transduction , microbiology and biotechnology , biochemistry
The presence of serotonin 1A receptor (5‐HT 1A ‐R) in the hippocampus, amygdala, and most regions of the frontal cortex is essential between postnatal day‐5–21 (P5–21) for the expression of normal anxiety levels in adult mice. Thus, the 5‐HT 1A ‐R plays a crucial role in this time window of brain development. We show that the 5‐HT 1A ‐R‐mediated stimulation of extracellular signal‐regulated kinases 1 and 2 (Erk1/2) in the hippocampus undergoes a transition between P6 and P15. At P6, a protein kinase C (PKC) isozyme is required for the 5‐HT 1A ‐R ⇒Erk1/2 cascade, which causes increased cell division in the dentate gyrus. By contrast, at P15, PKCα participates downstream of Erk1/2 to augment synaptic transmission through the Schaffer Collateral pathway but does not cause increased cell division. Our data demonstrate that the 5‐HT 1A ‐R ⇒Erk1/2 cascade uses PKC isozymes differentially, first boosting the cell division to form new hippocampal neurons at P6 and then undergoing a plastic change in mechanism to strengthen synaptic connections in the hippocampus at P15.