Neuronal activity (c-Fos) delineating interactions of the cerebral cortex and basal ganglia

Frontiers in Neuroanatomy

Jun eLu¹  Michael C Chen¹  Zhi-Li eHuang²  Mei-Hong eQiu³ 

[1] Beth Israel Deaconess Medical Center and Harvard Medical School;Fudan University;School of Basic Medical Science, Fudan University;

关键词: Arousal;    Atropine;    Basal Ganglia;    Cerebral Cortex;    Rats;    c-fos;   

DOI  :  10.3389/fnana.2014.00013

来源: DOAJ

【 摘 要 】

The cerebral cortex and basal ganglia (BG) form a neural circuit that is disrupted in disorders such as Parkinson’s disease. We found that neuronal activity (c-Fos) in the BG followed cortical activity, i.e., high in arousal state and low in sleep state. To determine if cortical activity is necessary for BG activity, we administered atropine to rats to induce a dissociative state resulting in slow-wave EEG but hyperactive motor behaviors. Atropine blocked c-Fos expression in the cortex and BG, despite high c-Fos expression in the sub-cortical arousal neuronal groups and thalamus, indicating that cortical activity is required for BG activation. To identify which glutamate receptors in the BG that mediate cortical inputs, we injected ketamine (NMDA receptor antagonist) and 6-cyano-nitroquinoxaline-2, 3-dione (CNQX, a non-NMDA receptor antagonist). Systemic ketamine and CNQX administration revealed that NMDA receptors mediated subthalamic nucleus (STN) input to internal globus pallidus (GPi) and substantia nigra pars reticulata (SNr), while non-NMDA receptor mediated cortical input to the STN. Both types of glutamate receptors were involved in mediating cortical input to the striatum. Dorsal striatal (caudoputamen, CPu) dopamine depletion by 6-hydroxydopamine resulted in reduced activity of the CPu, globus pallidus externa (GPe), and STN but increased activity of the GPi, SNr and putative layer V neurons in the motor cortex. Our results reveal that the cortical activity is necessary for BG activity and clarifies the pathways and properties of the BG-cortical network and their putative role in the pathophysiology of BG disorders.

【 授权许可】

Unknown