Abstract

Objectives: It is supposed that the movement is controlled through the cortex-striatum-pallidum-thalamus-cortex circuitry in the basal ganglia and surgical interventions for the treatment of movement disorders are performed on this area. This study refers to stimulation effect of, the principal origin of this circuitry model and one of the most interesting areas of functional neurosurgery, the globus pallidus (GP), on the next step, which is the thalamus.

Materials and Methods: The study has been carried out on seven rats. All rats have been subjected to the same procedure using the stereotactic electrodes placed under anesthesia. In all the subjects, the spontaneous activities of the GP and the ventrobasal (VB) thalamus, respectively, and the GP’s response to the somatic motor (passive joint) and sensory (whisker movement) stimuli have been investigated. Also, in all the rats, 0.14 ms, 0.5 Hz, 1 volt single pulse electrical stimuli have been applied to the GP and responses evoked in the VB thalamus have been measured by a second electrode. The electrophysiological data have been analyzed off-line on a personal computer. The microscopic structural post-study carried out on the rat brains demonstrated the correct targeting of the electrodes for GP and VB thalamus according to Pellegrino atlas.

Results: When the findings were evaluated, it has been observed that the GP’s response was stronger to the motor stimuli. An early stimulus response has been formed in VB thalamus following the GP electrical stimulus and negative deviations of 150 ms average latency and -70 µV average amplitude have been detected immediately afterwards. Positive deviations of 50 µV average amplitude and 220 ms latency were recorded, superposed at the stage when the negative deviation turned into spontaneous activity. The integral calculations demonstrated that the negative deviation is 3 to 3.5 times more powerful.

Conclusion: The interpretation and measuring of the records demonstrated that the VB thalamus gives a powerful inhibitor response to the GP electrical stimulus. These findings verify that this inhibitor effect shown in the basal ganglia model investigated here eliminates the inhibitor effect known to be formed between the striatum and the GP, and the thalamus increases the cortex excitation as a result of this. This conclusion demonstrated once more the importance of the GP (which is the main output origin of the basal ganglia circuit) in the control of the movement.