Electrophysiological Research About M1-CPu And Cpu-SNr Neural Pathway

Researches about biological behavior and cognition have already become a mainattention between neural-biology and computer and information science. Extracellularrecording technology allows us to extract the extracellular spikes of a single or even alarge number of neural populations. It provides us an excellent technology forresearch on movement-related neurons, nuclei and behavioral control pathways.In this experiment，adult SD rats were used as experimental materials. Then weused self-made tetrode or stereotrode ,and also through U.S. Plexon MAP 16-channeldata acquisition and processing system to record and extract the neural spikessequences of nucleus caudate putamen and substantia nigra par reticulate inanesthetized rats. We use extracellular recording method and also combined with thestimulation method of brain microinjection of sodium glutamate to excite the relatednuclei. Then with all of these methods we can research the role of nuclei in M1-CPuand CPu-SNr pathways，we hope that the research results can provide theoretical basisfor bio-robot control and guide.It was found that：（1）The majority of CPu neurons fired in a bursts model inanesthetized rats, the spike intervals centralized distributed during 4-10ms.（2）Ratsunder anesthesia，we injected the glutamate sodium to M1 region，while recordingextracellular discharging in the ipsilateral CPu region，the results were that：the firingrates of CPu neurons were 0.56±0.12Hz before glutamate sodium injection；thenduring the injection process，the firing rates came to 0.49±0.12Hz which had no asignificant difference compared with the frequency that before glutamate sodiuminjection（P=0.06＞0.05）；the firing rats came to 0.37±0.09Hz after stimulation within 0-30s，which had a extremely significant difference compared with the firingrates that before stimulation(P=0.00＜0.01)；after stimulation of 60-90s，the neuralfiring rates became 0.14±0.06Hz，which also had a extremely significant differencecompared with that before stimulation(P=0.00＜0.01).（3）Rats under anesthesia, weinjected the glutamate sodium to M1 region，while recording extracellular dischargingin the ipsilateral SNr region，the results were that: the firing rates of SNr neurons were7.02±2.12Hz before stimulation；then during the stimulation，the firing rates came to7.18±2.23 Hz which had no a significant difference compared with the frequency thatbefore stimulation (P=0.38＞0.05)；the firing rates came to 7.62±2.22Hz afterstimulation within 0-30s,which also have no a significant difference compared thefiring rates that before stimulation (P=0.06＞0.05). (4) Rats under anesthesia, weinjected the glutamate sodium to CPu region, while recording extracellulardischarging in the ipsilateral SNr region, results were that：the firing rates of SNrneurons were 7.17±1.12Hz；then the firing rates came to 2.28±0.91Hz during thestimulation，which had a extremely significant difference compared with that beforestimulation (P=0.00＜0.01)；after stimulation within 0-30s the neural firing rates cameto 6.13±1.36Hz，which had no a significant difference with that before stimulation（P=0.34＞0.05）.With the result above，we concluded that the inhibition of CPu neurons afterglutamate sodium stimulation within tens of seconds were probably form theextensive contracts among GABAergic neurons inside the CPu，but not form the M1region itself. CPu neurons could inhibit the SNr neurons extensively and deeply，thisinhibition came from the direct GABAergic projection to SNr neurons. But when westimulate the M1 with sodium glutamate，there were no significant change on thefiring rates of SNr neurons. A possible explanation is that the CPu neurons thataffected by excited M1 neurons were not the same as that were excited directly bysodium glutamate. But the real reason for this phenomenon remains to be discovered by further experiments.