作者: Erdong Chen , Jean-Francois Paré , Thomas Wichmann , Yoland Smith
DOI: 10.1007/S00429-016-1242-9
关键词: Basal ganglia 、 Voltage-dependent calcium channel 、 Neurotransmission 、 Inhibitory postsynaptic potential 、 Neuropil 、 Neuroscience 、 Thalamus 、 Biology 、 T-type calcium channel 、 Bursting
摘要: T-type calcium channels (Cav3) are key mediators of thalamic bursting activity, but also regulate single cells excitability, dendritic integration, synaptic strength and transmitter release. These functions strongly influenced by the subcellular subsynaptic localization Cav3 along somatodendritic domain cells. In Parkinson’s disease, dysfunction in basal ganglia-receiving nuclei likely contributes to pathological activity. this study, we analyzed cellular, subcellular, Cav3.1 channel ventral anterior (VA) centromedian/parafascicular (CM/Pf) nuclei, main targets ganglia output, normal parkinsonian monkeys. All displayed strong neuropil immunoreactivity, although intensity immunolabeling CM/Pf was significantly lower than VA. Ultrastructurally, 70–80 % Cav3.1-immunoreactive structures were shafts. Using immunogold labeling, commonly found perisynaptic asymmetric symmetric axo-dendritic synapses, suggesting a role regulating excitatory inhibitory neurotransmission. Significant labeling at non-synaptic sites plasma membrane neurons. There no difference overall pattern immunostaining between monkeys, that increased rebound state is not driven changes expression. Thus, located subserve neuronal bursting, glutamatergic non-glutamatergic transmission whole neurons primate thalamus.