title: Striatal dopamine release in a schizophrenia mouse model measured by electrochemical amperometry in vivo.
abstract: Schizophrenia is a severely devastating mental disorder, the pathological process of which is proposed to be associated with the dysfunction of dopaminergic transmission. Our previous results have demonstrated slower kinetics of transmitter release (glutamate release in hippocampus and norepinephrine release in adrenal slice) in a schizophrenia model, dysbindin null-sandy mice. However, whether dopaminergic transmission in the nigrostriatal pathway contributes to the pathology of dysbindin-/- mice remains unknown. Here, we have provided a step-by-step protocol to be applied in the in vivo amperometric recording of dopamine (DA) release from the mouse striatum evoked by an action potential (AP) pattern. With this protocol, AP pattern-dependent DA release was recorded from dysbindin-/- mice striatum in vivo. On combining amperometric recording in slices and electrophysiology, we found that in dysbindin-/- mice, (1) presynaptically, AP-pattern dependent dopamine overflow and uptake were intact in vivo; (2) the recycling of the dopamine vesicle pool remained unchanged. (3) Postsynaptically, the excitability of medium spiny neuron (MSN) was also normal, as revealed by patch-clamp recordings in striatal slices. Taken together, in contrast to reduced norepinephrine release in adrenal chromaffin cells, the dopaminergic transmission remains unchanged in the nigrostriatal pathway in dysbindin-/- mice, providing a new insight into the functions of the schizophrenia susceptibility gene dysbindin.
authors: State Key Laboratory of Biomembrane and Membrane Biotechnology and Beijing Key Laboratory of Cardiometabolic Molecular Medicine, Institute of Molecular Medicine and PKU-IDG/McGovern Institute for Brain Research and Peking-Tsinghua Center for Life Sciences, Peking University, Beijing 100871, China. zzhou@pku.edu.cn changhewang@pku.edu.cn xjkang@pku.edu.cn.
authors: Huadong
authors: H
authors: Xu
authors: Panli
authors: P
authors: Zuo
authors: Shirong
authors: S
authors: Wang
authors: Li
authors: L
authors: Zhou
authors: Xiaoxuan
authors: X
authors: Sun
authors: Meiqin
authors: M
authors: Hu
authors: Bin
authors: B
authors: Liu
authors: Qihui
authors: Q
authors: Wu
authors: Haiqiang
authors: H
authors: Dou
authors: Bing
authors: B
authors: Liu
authors: Feipeng
authors: F
authors: Zhu
authors: Sasa
authors: S
authors: Teng
authors: Xiaoyu
authors: X
authors: Zhang
authors: Li
authors: L
authors: Wang
authors: Qing
authors: Q
authors: Li
authors: Mu
authors: M
authors: Jin
authors: Xinjiang
authors: X
authors: Kang
authors: Wei
authors: W
authors: Xiong
authors: Changhe
authors: C
authors: Wang
authors: Zhuan
authors: Z
authors: Zhou
mesh_terms: D000818:Animals; D001692:Biological Transport; D004195:Disease Models, Animal; D004298:Dopamine / Q000378:metabolism*; D000074765:Dysbindin; D049029:Dystrophin-Associated Proteins / Q000172:deficiency; D004558:Electric Stimulation; D004563:Electrochemistry / Q000379:methods*; D055724:Electrophysiological Phenomena; D051379:Mice; D008810:Mice, Inbred C57BL; D017072:Neostriatum / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D012559:Schizophrenia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology
chemical_list: C498992:Dtnbp1 protein, mouse; D000074765:Dysbindin; D049029:Dystrophin-Associated Proteins; D004298:Dopamine