权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Physiological roles of plasticity of inhibitory synaptic transmission

抑制性突触传递可塑性的生理作用

基本信息

批准号：
13680899
负责人：
OHNO-SHOSAKU Takako
金额：
$ 2.3万
依托单位：
Kanazawa University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2002
项目状态：
已结题

项目摘要

1. Recent studies have revealed that the activity of postsynaptic neurons can influence presynaptic functions via endocannabinoids that are released from postsynaptic neurons and act retrogradely on presynaptic terminals. In this study, we attempted to clarify physiological roles of endocannabinoid-mediated retrograde modulation of synaptic transmissions.2. We made paired whole-cell recordings from cultured hippocampal neurons prepared from newborn rats, and recorded evoked excitatory and inhibitory postsynaptic currents. Our results are summarized as follows. (1) Endocannabinoids can be released from postsynaptic neurons by depolarization or by activation of group I metabotropic glutamate receptors (mGluR) (Ohno-Shosaku et al., Eur J Neurosci 15, 2002). (2) Endocannabinoid release is also induced by activation of the M_1 and M_3 subtypes of muscarinic acetylcholine receptors (in preparation), (3) Postsynaptic depolarization and activation of group I mGluRs or M_1/M_3 receptors work in a cooperative manner to release endocannabinoids (Ohno-Shosaku et al., Eur J Neurosci, in press). (4) The released endocannabinoids act retrogradely onto presynaptic cannabinoid CB1 receptors and suppress the transmitter release from presynaptic terminals. (5) The cannabinoid-sensitivity of presynaptic terminals is high in a subpopulation (about 50 %) of inhibitory synapses, low in excitatory synapses, and almost absent in the rest of inhibitory synapses (Ohno-Shosaku et al., J Neurosci 22, 2002).3. These results suggest that endocannabinoids mediate target-specific retrograde signals, by which the postsynaptic neuronal activity influences the transmitter release from certain types of presynaptic terminals.

1.最近的研究表明，突触后神经元的活动可以通过突触后神经元释放的内源性大麻素影响突触前功能，并逆行作用于突触前末梢。在本研究中，我们试图阐明内源性大麻素介导的突触传递逆行调节的生理作用.我们从培养的新生大鼠海马神经元进行配对的全细胞记录，并记录诱发的兴奋性和抑制性突触后电流。我们的结果总结如下。(1)内源性大麻素可以通过去极化或激活I组代谢型谷氨酸受体（mGluR）从突触后神经元释放（Ohno-Shosaku等人，Eur J Neurosci 15，2002）。(2)内源性大麻素释放也通过激活毒蕈碱乙酰胆碱受体的M_1和M_3亚型（制备中）来诱导。（3）突触后去极化和I组mGluR或M_1/M_3受体的激活以协同方式起作用以释放内源性大麻素（Ohno-Shosaku et al.，Eur J Neurosci，出版中）。(4)释放的内源性大麻素逆行作用于突触前大麻素CB 1受体，并抑制突触前末梢的递质释放。(5)突触前末梢的大麻素敏感性在抑制性突触的亚群（约50%）中是高的，在兴奋性突触中是低的，并且在其余的抑制性突触中几乎不存在（Ohno-Shosaku等人，J Neurosci 22，2002）。这些结果表明，内源性大麻素介导的目标特异性逆行信号，突触后神经元活动影响某些类型的突触前末梢的递质释放。