Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, New Jersey 07102, USA.
Nat Commun. 2017 Jun 12;8:15860. doi: 10.1038/ncomms15860.
Recent discoveries of striatal GABAergic interneurons require a new conceptualization of the organization of intrastriatal circuitry and their cortical and thalamic inputs. We investigated thalamic inputs to the two populations of striatal neuropeptide Y (NPY) interneurons, plateau low threshold spike (PLTS) and NPY-neurogliaform (NGF) cells. Optogenetic activation of parafascicular inputs evokes suprathreshold monosynaptic glutamatergic excitation in NGF interneurons and a disynaptic, nicotinic excitation through cholinergic interneurons. In contrast, the predominant response of PLTS interneurons is a disynaptic inhibition dependent on thalamic activation of striatal tyrosine hydroxylase interneurons (THINs). In contrast, THINs do not innervate NGF or fast spiking interneurons, showing significant specificity in THINs outputs. Chemospecific ablation of THINs impairs prepulse inhibition of the acoustic startle response suggesting an important behavioural role of this disynaptic pathway. Our findings demonstrate that the impact of the parafascicular nucleus on striatal activity and some related behaviour critically depend on synaptic interactions within interneuronal circuits.
最近对纹状体 GABA 能中间神经元的发现需要对纹状体内电路及其皮质和丘脑输入的组织进行新的概念化。我们研究了两种纹状体细胞外肽 Y (NPY) 中间神经元，即高原低阈值棘波 (PLTS) 和 NPY-神经胶质 (NGF) 细胞的丘脑输入。束旁核输入的光遗传学激活在 NGF 中间神经元中引发超阈值单突触谷氨酸能兴奋，并通过胆碱能中间神经元引发双突触烟碱兴奋。相比之下，PLTS 中间神经元的主要反应是依赖于纹状体酪氨酸羟化酶中间神经元 (THINs) 的丘脑激活的双突触抑制。相反，THINs 不会支配 NGF 或快速放电中间神经元，表明 THINs 输出具有显著的特异性。化学特异性消融 THINs 会损害声惊反射的前脉冲抑制，表明这种双突触途径在行为中有重要作用。我们的发现表明，束旁核对纹状体活动和一些相关行为的影响严重依赖于中间神经元回路内的突触相互作用。
