日本研究人员日前宣布，他们在利用小鼠进行的实验中，弄清了脑内“消除恐惧感觉”的机制，这一成果将有助开发治疗创伤后应激障碍的药物。
脑内有众多的神经元，而突触是神经元的结合部，负责传递视觉和听觉等各种信息。北海道大学教授渡边雅彦等人在新一期美国《国家科学院学报》网络版上发表论文说，他们发现了脑内传递大麻成分的突触，而这种大麻成分对消除恐惧和不安感觉和记忆有重要作用。
研究人员发现，能够传递大麻成分的突触位于控制恐惧和不安等“负面情绪”的大脑基底核区域。而大麻成分会推动突触发挥作用，使基底核活跃起来，从而消除恐惧感觉或记忆。（生物谷Bioon.com）
生物谷推荐原文出处：
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.
