How best to consider the structure and function of the pedunculopontine tegmental nucleus: Evidence from animal studies

Winn, Philip

doi:10.1016/j.jns.2006.05.036

Cited by 160 publications

(146 citation statements)

References 219 publications

(184 reference statements)

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“…The PPN is defined as a collection of neurons in the caudal mesencephalic tegmentum 12,13,23 extending caudally from the substantia nigra to the locus coeruleus 12,23 . Based on cell density, and neurochemical markers, the PPN is divided into the pars compacta (PPNc), located more caudally that contains a high density of cholinergic neurons, and pars dissipata (PPNd) which extends throughout the rostro-caudal axis of the nucleus 23,24 .…”

Section: Resultsmentioning

confidence: 99%

“…The PPN, located in the ponto-mesencephalic tegmentum is part of the mesencephalic locomotor region, and plays a role in the initiation and control of gait 12,13 . Stimulation of the PPN induces spontaneous locomotion, and lesions of the PPN result in gait deficits 14 .…”

Section: Discussionmentioning

confidence: 99%

“…The PPN is extensively connected with the basal ganglia and cerebellum, and thought to play a central role in the initiation and control of locomotion 12,13,32 and units were first tested for their response to passive movement of the lower limbs, involving flexion and extension of the ankle, knee and hip as occurs during locomotion 30,33 . In total, 76 narrow, and 10 wide-spike neurons were tested, and for narrow-spike units, 13 responded with an increase in discharge while 36 were inhibited.…”

Section: Neurons In the Ppn Respond To Limb Movement And Imagined Gaitmentioning

confidence: 99%

“…Among these, the mesencepalic locomotor region (MLR) in the brainstem plays a key role in the control of gait 9,10 . Within the MLR, the pedunculopontine nucleus (PPN), that is extensively connected with the basal ganglia 11 , has a central role in the initiation and maintenance of gait [12][13][14] and lesions of the PPN induce gait deficits 14 . Gait and postural disturbances in PD are accompanied by cell loss within the PPN [14][15][16] , but are partially relieved by deep brain stimulation (DBS) in the PPN [17][18][19] , supporting the central role of the PPN in locomotion.…”

Section: Introductionmentioning

confidence: 99%

“…Stimulation of the PPN induces spontaneous locomotion, and lesions of the PPN result in gait deficits 14 . Thus, the PPN has emerged as a target for deep brain stimulation to control freezing of gait and postural instability that appear in advanced Parkinson's disease 38 .The PPN contains a mixed population of cholinergic, glutamatergic and GABAergic neurons 11,13,23,29 . Electrophysiologically, at least three types of neuron have been identified 31,33,39 , however, there is little correlation between cells electrophysiological properties and their neurochemical identity.…”

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confidence: 99%

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Imagined gait modulates neuronal network dynamics in the human pedunculopontine nucleus

et al. 2014

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The pedunculopontine nucleus (PPN) is a part of the mesencephalic locomotor region and thought to play a key role in the initiation and maintenance of gait. Lesions of the PPN induce gait deficits, and the PPN has therefore emerged as a target for deep brain stimulation for the control of gait and postural disability. However, the role of the PPN gait control is not understood. Here, using extracellular single unit recordings in awake patients, we show that neurons in the PPN discharge as synchronous functional networks whose activity is phase locked to alpha oscillations. Neurons within the PPN respond to limb movement and imagined gait by dynamically changing network activity, and decreasing alpha phase locking. These results show that different synchronous networks are activated during initial motor planning and actual motion, and suggest that changes in gait initiation in PD may result from disrupted network activity in the PPN. IntroductionParkinson's disease (PD) is a progressive neurodegenerative disorder characterised by bradykinesia, rigidity and tremor, thought to result from loss of dopaminergic neurons 1 . Treatment of PD is symptomatic, with dopamine replacement with levodopa being the mainstay of treatment 2 . However, after an initial period of improvement, the beneficial effects of levodopa are overshadowed by side-effects such as dyskinesia and neuropsychiatric complications 3 . Moreover, in advanced PD, axial symptoms such as freezing of gait and postural difficulties become increasingly prevalent. Whereas the motor symptoms of PD are responsive to dopamine replacement, gait freezing and postural instability respond poorly. The pathophysiology of these gait disturbances is poorly understood, but their late onset and resistance to levodopa has led to the suggestion that they may result from pathology in nondopaminergic structures involved in locomotion 4,5 .Gait is controlled by genetically defined neuronal networks, the central pattern generators (CPGs), in the spinal cord 6,7 , which are in turn activated by supraspinal centres that initiate and control movement [6][7][8] . Among these, the mesencepalic locomotor region (MLR) in the brainstem plays a key role in the control of gait 9,10 . Within the MLR, the pedunculopontine nucleus (PPN), that is extensively connected with the basal ganglia 11 , has a central role in the initiation and maintenance of gait [12][13][14] and lesions of the PPN induce gait deficits 14 . Gait and postural disturbances in PD are accompanied by cell loss within the PPN [14][15][16] , but are partially relieved by deep brain stimulation (DBS) in the PPN [17][18][19] , supporting the central role of the PPN in locomotion.Much is understood about the development and function of spinal cord CPGs 20 . However, while CPG function is controlled by afferent projections from the MLR 9, 10 , little is understood about activity within the MLR, and its response to movement. In this study, using single unit recordings in awake patients, we describe the properties of neurons in t...

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