日本研究人員日前宣布,，他們在利用小鼠進行的實驗中，弄清了腦內“消除恐懼感覺”的機制,，這一成果將有助開發(fā)治療創(chuàng)傷后應激障礙的藥物,。
腦內有眾多的神經(jīng)元，而突觸是神經(jīng)元的結合部,，負責傳遞視覺和聽覺等各種信息,。北海道大學教授渡邊雅彥等人在新一期美國《國家科學院學報》網(wǎng)絡版上發(fā)表論文說，他們發(fā)現(xiàn)了腦內傳遞大麻成分的突觸,，而這種大麻成分對消除恐懼和不安感覺和記憶有重要作用,。
研究人員發(fā)現(xiàn)，能夠傳遞大麻成分的突觸位于控制恐懼和不安等“負面情緒”的大腦基底核區(qū)域,。而大麻成分會推動突觸發(fā)揮作用,，使基底核活躍起來，從而消除恐懼感覺或記憶,。（生物谷Bioon.com）
生物谷推薦原文出處：
PNAS doi: 10.1073/pnas.1012875108
Unique inhibitory synapse with particularly rich endocannabinoid signaling machinery on pyramidal neurons in basal amygdaloid nucleus
Takayuki Yoshidaa,b,c, Motokazu Uchigashimaa, Miwako Yamasakia, Istvan Katonad, Maya Yamazakie, Kenji Sakimurae,f, Masanobu Kanoc,g, Mitsuhiro Yoshiokab, and Masahiko Watanabea,f,1
Abstract
2-Arachidonoylglycerol (2-AG) is the endocannabinoid that mediates retrograde suppression of synaptic transmission in the brain. 2-AG is synthesized in activated postsynaptic neurons by sn-1-specific diacylglycerol lipase (DGL), binds to presynaptic cannabinoid CB1 receptors, suppresses neurotransmitter release, and is degraded mainly by monoacylglycerol lipase (MGL). In the basolateral amygdala complex, it has been demonstrated that CB1 is particularly enriched in axon terminals of cholecystokinin (CCK)-positive GABAergic interneurons, induces short- and long-term depression at inhibitory synapses, and is involved in extinction of fear memory. Here, we clarified a unique molecular convergence of DGLα, CB1, and MGL at specific inhibitory synapses in the basal nucleus (BA), but not lateral nucleus, of the basolateral amygdala. The synapses, termed invaginating synapses, consisted of conventional symmetrical contact and unique perisynaptic invagination of nerve terminals into perikarya. At invaginating synapses, DGLα was preferentially recruited to concave somatic membrane of postsynaptic pyramidal neurons, whereas invaginating presynaptic terminals highly expressed CB1, MGL, and CCK. No such molecular convergence was seen for flat perisomatic synapses made by parvalbumin-positive interneurons. On the other hand, DGLα and CB1 were expressed weakly at axospinous excitatory synapses. Consistent with these morphological data, thresholds for DGLα-mediated depolarization-induced retrograde suppression were much lower for inhibitory synapses than for excitatory synapses in BA pyramidal neurons. Moreover, depolarization-induced suppression was readily saturated for inhibition, but never for excitation. These findings suggest that perisomatic inhibition by invaginating synapses is a key target of 2-AG-mediated control of the excitability of BA pyramidal neurons.
