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1.
Neuroscience Bulletin ; (6): 315-324, 2019.
Article in English | WPRIM | ID: wpr-775449

ABSTRACT

The thalamostriatal pathway is implicated in Parkinson's disease (PD); however, PD-related changes in the relationship between oscillatory activity in the centromedian-parafascicular complex (CM/Pf, or the Pf in rodents) and the dorsal striatum (DS) remain unclear. Therefore, we simultaneously recorded local field potentials (LFPs) in both the Pf and DS of hemiparkinsonian and control rats during epochs of rest or treadmill walking. The dopamine-lesioned rats showed increased LFP power in the beta band (12 Hz-35 Hz) in the Pf and DS during both epochs, but decreased LFP power in the delta (0.5 Hz-3 Hz) band in the Pf during rest epochs and in the DS during both epochs, compared to control rats. In addition, exaggerated low gamma (35 Hz-70 Hz) oscillations after dopamine loss were restricted to the Pf regardless of the behavioral state. Furthermore, enhanced synchronization of LFP oscillations was found between the Pf and DS after the dopamine lesion. Significant increases occurred in the mean coherence in both theta (3 Hz-7 Hz) and beta bands, and a significant increase was also noted in the phase coherence in the beta band between the Pf and DS during rest epochs. During the treadmill walking epochs, significant increases were found in both the alpha (7 Hz-12 Hz) and beta bands for two coherence measures. Collectively, dramatic changes in the relative LFP power and coherence in the thalamostriatal pathway may underlie the dysfunction of the basal ganglia-thalamocortical network circuits in PD, contributing to some of the motor and non-motor symptoms of the disease.


Subject(s)
Animals , Male , Brain Waves , Physiology , Corpus Striatum , Cortical Synchronization , Physiology , Dopaminergic Neurons , Physiology , Electrocorticography , Neural Pathways , Oxidopamine , Parkinsonian Disorders , Rats, Wistar , Thalamic Nuclei , Walking , Physiology
2.
Neuroscience Bulletin ; (6): 1067-1076, 2018.
Article in English | WPRIM | ID: wpr-775483

ABSTRACT

Restraint water-immersion stress (RWIS), a compound stress model, has been widely used to induce acute gastric ulceration in rats. A wealth of evidence suggests that the central nucleus of the amygdala (CEA) is a focal region for mediating the biological response to stress. Different stressors induce distinct alterations of neuronal activity in the CEA; however, few studies have reported the characteristics of CEA neuronal activity induced by RWIS. Therefore, we explored this issue using immunohistochemistry and in vivo extracellular single-unit recording. Our results showed that RWIS and restraint stress (RS) differentially changed the c-Fos expression and firing properties of neurons in the medial CEA. In addition, RWIS, but not RS, induced the activation of corticotropin-releasing hormone neurons in the CEA. These findings suggested that specific neuronal activation in the CEA is involved in the formation of RWIS-induced gastric ulcers. This study also provides a possible theoretical explanation for the different gastric dysfunctions induced by different stressors.


Subject(s)
Animals , Rats , Action Potentials , Physiology , Analysis of Variance , Central Amygdaloid Nucleus , Pathology , Corticotropin-Releasing Hormone , Metabolism , Disease Models, Animal , Gastric Mucosa , Pathology , Gene Expression Regulation , Physiology , Neurons , Physiology , Patch-Clamp Techniques , Proto-Oncogene Proteins c-fos , Metabolism , Rats, Wistar , Stress, Physiological , Physiology , Stress, Psychological
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