“…Interestingly, the relative LFP power in the lesioned rats was dramatically lower in all the low-frequency bands (from 0.5 Hz to 12 Hz) than in the control group (72.41 ± 3.90 vs 84.55 ± 3.15, P = 0.025). These results suggested that dopamine loss causes significant changes of LFP activity in the Pf in the lesioned hemisphere, confirming our previous findings [20]. Fig.…”
Section: Resultssupporting
confidence: 92%
“…We also found enhanced LFP power in the β band in the Pf, along with augmented low-γ band oscillatory activity in the dopamine-lesioned rats during two states, confirming our previous findings [20]. However, only the power in the β band was notably increased during the movement state in the study of Wang et al [20]. This inconsistency may be due to the different behavioral tasks used in the studies (food grabbing vs treadmill walking).…”
Section: Discussionsupporting
confidence: 91%
“…The SNpc sections were used to identify the lesions induced by 6-OHDA (data not shown). The detailed procedures and representative images of immunohistochemical staining were as described in our previous study [20]. The Pf and DS sections were mounted on glass slides, stained with cresyl violet, and visualized under a light microscope.…”
Section: Methodsmentioning
confidence: 99%
“…Alterations of firing rate and oscillatory activity in the CM/Pf have also been recorded in PD patients and anesthetized animal models of the disease [16–19]. Currently, only one study from our group has investigated these PD-related changes of neuronal activity in the CM/Pf in awake, behaving animals, revealing that these alterations are specifically related to ongoing activity during brain states (anesthetized versus awake state) and/or behavioral context (inattentive rest vs movement) [18, 20]. Therefore, exploring the effects of dopamine depletion on neuronal activity in the CM/Pf in different behavioral states remains of interest.…”
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.
“…Interestingly, the relative LFP power in the lesioned rats was dramatically lower in all the low-frequency bands (from 0.5 Hz to 12 Hz) than in the control group (72.41 ± 3.90 vs 84.55 ± 3.15, P = 0.025). These results suggested that dopamine loss causes significant changes of LFP activity in the Pf in the lesioned hemisphere, confirming our previous findings [20]. Fig.…”
Section: Resultssupporting
confidence: 92%
“…We also found enhanced LFP power in the β band in the Pf, along with augmented low-γ band oscillatory activity in the dopamine-lesioned rats during two states, confirming our previous findings [20]. However, only the power in the β band was notably increased during the movement state in the study of Wang et al [20]. This inconsistency may be due to the different behavioral tasks used in the studies (food grabbing vs treadmill walking).…”
Section: Discussionsupporting
confidence: 91%
“…The SNpc sections were used to identify the lesions induced by 6-OHDA (data not shown). The detailed procedures and representative images of immunohistochemical staining were as described in our previous study [20]. The Pf and DS sections were mounted on glass slides, stained with cresyl violet, and visualized under a light microscope.…”
Section: Methodsmentioning
confidence: 99%
“…Alterations of firing rate and oscillatory activity in the CM/Pf have also been recorded in PD patients and anesthetized animal models of the disease [16–19]. Currently, only one study from our group has investigated these PD-related changes of neuronal activity in the CM/Pf in awake, behaving animals, revealing that these alterations are specifically related to ongoing activity during brain states (anesthetized versus awake state) and/or behavioral context (inattentive rest vs movement) [18, 20]. Therefore, exploring the effects of dopamine depletion on neuronal activity in the CM/Pf in different behavioral states remains of interest.…”
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.
“…c-Fos immunohistochemistry has been used as a functional anatomical mapping tool to identify cells and serves as a marker of neuronal activation [ 18 , 19 ]. Neuronal activation can also be evaluated by the firing rate and firing pattern in extracellular recordings of neuronal spikes [ 20 , 21 ]. The firing rate, defined as the temporal average number of spikes, is used to evaluate neuronal activity and the firing pattern described by the coefficient of variance (CV) is used to evaluate neuronal discharge regularity.…”
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.
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