The firing activity of presumed cholinergic and non-cholinergic neurons of the pedunculopontine nucleus in 6-hydroxydopamine-lesioned rats: An in vivo electrophysiological study

Zhang, Qiao Jun; Liu, Jian; Wang, Yong; Wang, Shuang; Wu, Zihui; Yan, Wei; Hui, Yan Ping; Ali, Umar

doi:10.1016/j.brainres.2008.09.028

Cited by 19 publications

(21 citation statements)

References 48 publications

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“…The precise reasons for the reduced M1/4 receptor following a 6-OHDA lesion are not yet known. However, it has been documented that dopaminergic denervation in the striatal pathway resulted in hyperactivity of the cholinergic systems (Muma et al, 2001;Zhang et al, 2008). Therefore, we hypothesize that the possible mechanisms for the reduced M1/4 receptors involved in our study is due to enhanced striatal cholinergic neuron firing following dopamine denervation in the nigrostriatal pathway; however, we cannot exclude the possibility that the reduced M1/4 receptors in the observed brain areas may reflect the receptor hypo-innervations.…”

Section: Discussioncontrasting

confidence: 43%

Simvastatin reverses the downregulation of M1/4 receptor binding in 6-hydroxydopamine-induced parkinsonian rats: The association with improvements in long-term memory

et al. 2014

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. (2014). Simvastatin reverses the downregulation of M1/4 receptor binding in 6-hydroxydopamine-induced parkinsonian rats: the association with improvements in long-term memory. Neuroscience, 267 57-66.Simvastatin reverses the downregulation of M1/4 receptor binding in 6-hydroxydopamine-induced parkinsonian rats: the association with improvements in long-term memory AbstractBackground It is believed that muscarinic M1/4 receptors are closely correlated to the dopaminergic system and are strongly involved in the pathogenesis of Parkinson's disease (PD). In addition to regulating lipid metabolism and protection from stroke, statins have been used to regulate the declined cognition. We aimed to explore the regional changes in M1/4 receptors in the 6-hydroxydopamine (6-OHDA)-lesioned rat brain. Methods PD rat model was set up by injecting 6-OHDA into the unilateral medial forebrain bundle; while simvastatin (10 mg/kg/day) or saline was orally administrated for 3 weeks, respectively. Long-term memory was measured using the Morris water maze.[3H]pirenzepine binding autoradiography was applied to investigate the alterations of M1/4 receptors in the PD rat brains. Results 6-OHDA induced long-term memory deficits along with downregulation of M1/4 receptors in the hippocampus, the medial amygdala, the posteromedial cortical and the piriform cortex; simvastatin administration significantly ameliorated the impaired memory and reversed the downregulation of M1/4 receptors in the examined brain regions. Profound positive correlations were verified between the decline in long-term memory activity and the restoration of M1/4 receptors in different brain regions after simvastatin treatment. Conclusions/significance Our results provide strong evidence that M1/4 receptor modulation after simvastatin administration did, at least partially, contribute to the improvement in the long-term memory in 6-OHDA-induced PD rats. These results provide a possible mechanism for simvastatin treatment in psycho-neurological diseases such as PD via M1/4 receptors.

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Section: Discussioncontrasting

confidence: 43%

Simvastatin reverses the downregulation of M1/4 receptor binding in 6-hydroxydopamine-induced parkinsonian rats: The association with improvements in long-term memory

et al. 2014

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“…In support of this notion, one metabolic study [25] found that cholinergic neuronal activity is decreased in the PPN of PD primates, and this decrease could lead to reduced ACh release from the PPN to the VL. However, it is interesting to note that previous studies have reported overactivity of the neurons in the PPN of 6-OHDA rats [26]. In the current study, the ACh concentration in the VL was improved by PPN-LFS.…”

Section: Effects Of Ppn-dbs On Neurotransmittersmentioning

confidence: 65%

Low-frequency stimulation of the pedunculopontine nucleus affects gait and the neurotransmitter level in the ventrolateral thalamic nucleus in 6-OHDA Parkinsonian rats

Wen

Xiao

et al. 2015

Neuroscience Letters

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“…4h) and a narrower spike width (arrowhead in Fig. 4h) than cholinergic subtypes (Zhang et al 2008). We examined only these PPTg cells, which we speculate are glutamatergic, and found that 15/20 decreased with STN-HFS (population response shown in Fig.…”

Section: Stn-dbs and Concurrent Recordings Of Stn Pptg And Cerebellamentioning

confidence: 97%

“…h Identification of non-cholinergic neurons, which we presume are glutamatergic, was made using waveforms since non-cholinergic neurons typically have a narrower rising phase in spike waveform and significantly faster spiking frequency. The left waveform represents non-cholinergic neurons, whereas the wider waveform on the right is from a cholinergic PPTg neuron; the horizontal bracket indicates the positive rising phase of the spike waveform, which is measured in the lower right panel and Ginsberg 1992) or modulate mossy fibers originating from the pontine nuclei (Tsutsumi et al 2007) and these were identified by their spiking waveforms and frequencies which were more narrow and faster, respectively, than those of cholinergic neurons (Zhang et al 2008) (Fig. 4h).…”

Section: Stn-dbs and Concurrent Recordings Of Stn Pptg And Cerebellamentioning

confidence: 99%

Stimulation of the subthalamic nucleus engages the cerebellum for motor function in parkinsonian rats

et al. 2014

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Deep brain stimulation (DBS) is effective in managing motor symptoms of Parkinson's disease in well-selected individuals. Recently, research has shown that DBS in the basal ganglia (BG) can alter neural circuits beyond the traditional basal ganglia-thalamus-cortical (BG-TH-CX) loop. For instance, functional imaging showed alterations in cerebellar activity with DBS in the subthalamic nucleus (STN). However, these imaging studies revealed very little about how cell-specific cerebellar activity responds to STN stimulation or if these changes contribute to its efficacy. In this study, we assess whether STN-DBS provides efficacy in managing motor symptoms in Parkinson's disease by recruiting cerebellar activity. We do this by applying STN-DBS in hemiparkinsonian rats and simultaneously recording neuronal activity from the STN, brainstem and cerebellum. We found that STN neurons decreased spiking activity by 55% during DBS (P = 0.038), which coincided with a decrease in most pedunculopontine tegmental nucleus and Purkinje neurons by 29% (P < 0.001) and 28% (P = 0.003), respectively. In contrast, spike activity in the deep cerebellar nuclei increased 45% during DBS (P < 0.001), which was likely from reduced afferent activity of Purkinje cells. Then, we applied STN-DBS at sub-therapeutic current along with stimulation of the deep cerebellar nuclei and found similar improvement in forelimb akinesia as with therapeutic STN-DBS alone. This suggests that STN-DBS can engage cerebellar activity to improve parkinsonian motor symptoms. Our study is the first to describe how STN-DBS in Parkinson's disease alters cerebellar activity using electrophysiology in vivo and reveal a potential for stimulating the cerebellum to potentiate deep brain stimulation of the subthalamic nucleus.

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The firing activity of presumed cholinergic and non-cholinergic neurons of the pedunculopontine nucleus in 6-hydroxydopamine-lesioned rats: An in vivo electrophysiological study

Cited by 19 publications

References 48 publications

Simvastatin reverses the downregulation of M1/4 receptor binding in 6-hydroxydopamine-induced parkinsonian rats: The association with improvements in long-term memory

Simvastatin reverses the downregulation of M1/4 receptor binding in 6-hydroxydopamine-induced parkinsonian rats: The association with improvements in long-term memory

Low-frequency stimulation of the pedunculopontine nucleus affects gait and the neurotransmitter level in the ventrolateral thalamic nucleus in 6-OHDA Parkinsonian rats

Stimulation of the subthalamic nucleus engages the cerebellum for motor function in parkinsonian rats

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