催產素除了參與在分娩以及泌乳的過程之外，近期的研究顯示其調控許多不同的行為。目前已知海馬迴中有催產素受體的表現，以及旁室核的催產素神經細胞可投射大量神經輸入至海馬迴，因此我們的目標將著重於探討催產素在海馬迴神經突觸可塑性及成年神經細胞新生所扮演之角色。對於影響突觸可塑性的研究，我們證明催產素可以在沒有生產經驗的母鼠及公鼠的海馬迴CA1腦片，促進經由一次高頻電刺激所產生之長期增益效應，其機制是透過以前未知的催產素受體及表皮生長因子受體所調控之路徑。在電生理及生化分析結果中，我們發現常見的催產素受體訊息傳遞路徑交互活化表皮生長因子下游路徑，並且刺激局部樹突內轉譯非典型PKC蛋白之亞型，PKMζ。這些結果證明催產素受體及表皮生長因子受體間的聯繫調控了對於海馬迴CA1突觸維持長期增益效應的重要因子-PKMζ的合成。除了對於神經突觸塑性之調控以外，我們也證明了內生性催產素可透過位於CA3錐狀細胞上之催產素受體調控成熟神經細胞新生，這是一種非本體細胞調控之機制。利用基因剔除小鼠移除興奮性細胞之催產素受體，不只減少新生神經細胞的存活數量，也延遲存活的新生細胞其形態及功能上的發育。此外，催產素受體剔除小鼠相較於正常小鼠在海馬迴相關的空間記憶行為方面也產生缺損。結合神經細胞逆向追蹤及免疫螢光染色技術發現，旁視核的催產素細胞確實可以直接投射於海馬迴之CA3區域。此外，催產素對於CA3表現催產素受體之錐狀細胞會造成膜電位去即化及增加動作電位發生之結果。利用腺病毒表現帶有連結抑制性蛋白之受體 (hM4Di)，再以CNO活化該受體使CA3錐狀細胞活性降低，會減少正常型老鼠神經細胞新生數量。反之，在催產素受體基因剔除小鼠給予CNO以活化連接興奮性蛋白受體(hM3Dq)，則可以恢復神經細胞新生的數量。整體而言，催產素透過表現於CA3錐狀細胞上之催產素受體影響成年神經細胞之新生作用。在此，我們透過電生理、生化實驗和行為學的研究，證實催產素對於調控海馬迴神經突觸塑性及成年神經細胞新生扮演了重要的角色。

In addition to involvement in parturition and lactation, oxytocin (OXT) has been shown to regulate a wide variety of behaviors. Given that OXT receptors (OXTR) are expressed in the hippocampus and oxytocin neurons of the paraventricular nucleus also send substantial projections to the hippocampus, we attempt to identify the role of oxytocin in the hippocampal synaptic plasticity and adult neurogenesis. In term of the effect on the synaptic plasticity, we demonstrate that OXT promotes the maintenance of long-term potentiation (LTP) induced by one train of tetanic stimulation in the CA1 region of hippocampal slices from both nulliparous female and male rats through a previously unknown mechanism involving OXTR-dependent and epidermal growth factor receptor (EGFR)-mediated pathway. Using electrophysiological and biochemical approaches, we show that the conventional OXTR-associated signaling pathway transactivates EGFR downstream signaling pathways and stimulates local dendritic translation of an atypical protein kinase C isoform, protein kinase Mζ (PKMζ). These results reveal a novel OXTR-to-EGFR communication to regulate the new synthesis of PKMζ, which functions to promote the maintenance of LTP at hippocampal CA1 synapses. Apart from regulation of synaptic plasticity, we also show that endogenous OXT signaling controls adult neurogenesis through a non-cell-autonomous mechanism by OXT receptors (OXTR) expressed in CA3 pyramidal neurons. Conditional deletion of OXTR (OXTR-/-) from excitatory neurons not only decreases the number of survival newborn neurons but also delays morphological and functional development of those survived newborn neurons. In the hippocampal dependent spatial memory task, OXTR-/- mice also show impairment when compared with wild type mice. Retrograde neuronal tracing combined with immunocytochemistry further comfirm that the OXT neurons in the paraventricular nucleus project directly to the CA3 region of the hippocampus. In addition, bath application of OXT elicited a membrane depolarization and increased action potential firing in OXTR-expressing CA3 pyramidal neurons. Using adenoviral-mediated expression of engineered Gi/o-coupled human M4 (hM4Di) receptors, we observe that activation of hM4Di receptors with clozapine-N-oxide (CNO) reduces CA3 pyramidal neuron activity and resultes in fewer newly DGCs in Floxed OXTR mice. Conversely, CNO-induced activation of Gq-coupled human M3 receptors restores adult neurogenesis in the DG of OXTR-/- mice. These results suggest that CA3 may regulate adult DG neurogenesis under basal conditions and OXT controls adult hippocampal neurogenesis via OXTR expressed in CA3 pyramidal neurons. Here, we combine electrophysiological, biochemical and behavioral studies to identify the important role of OXT in the regulation of hippocampal synaptic plasticity and adult neurogenesis.

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