Topographical Organization of the Pedunculopontine Nucleus

Martinez-Gonzalez, Cristina; Bolam, J. Paul; Mena‐Segovia, Juan

doi:10.3389/fnana.2011.00022

Cited by 208 publications

(202 citation statements)

References 118 publications

(186 reference statements)

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“…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.…”

Section: Discussionmentioning

confidence: 99%

“…The PPN has extensive connections with the basal ganglia 5,11 , receiving strong inhibitory inputs from both the globus pallidus internus and substantia nigra 41 . Thus, the reduction in PPN activity may be mediated by inhibitory input from the basal ganglia 41 .…”

Section: Discussionmentioning

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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Imagined gait modulates neuronal network dynamics in the human pedunculopontine nucleus

et al. 2014

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“…Besides being anatomically separated, each of these regions contains neurons with diverse transmitter phenotypes with excitatory long-range projection neurons –that are glutamatergic in CnF and both glutamatergic and cholinergic in PPN– intermingled with local inhibitory interneurons 11,12 . Electrical stimulation or lesion studies are therefore unable to distinguish the contribution from the various intermingled neuronal populations present in these areas 12,13 . Recently, optogenetic manipulations have showed that stimulation of glutamatergic neurons (GlutNs) in and around PPN induced locomotion in mice 14 .…”

Section: Introductionmentioning

confidence: 99%

Midbrain circuits that set locomotor speed and gait selection

Caggiano¹,

Leiras²,

Goñi-Erro³

et al. 2018

Nature

365

511

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Summary Locomotion is a fundamental motor function common to the animal kingdom. It is executed episodically and adapted to behavioural needs including exploration, requiring slow locomotion, and escaping behaviour, necessitating faster speeds. The control of these functions originates in brainstem structures although the neuronal substrate(s) supporting them are debated. Here, we show in mice that speed/gait selection are controlled by glutamatergic excitatory neurons (GlutNs) segregated in two distinct midbrain nuclei: the Cuneiform Nucleus (CnF) and the Pedunculopontine Nucleus (PPN). GlutNs in each of those two regions are sufficient for controlling slower alternating locomotor behavior but only GlutNs in the CnF are necessary for high-speed synchronous locomotion. Additionally, PPN- and CnF-GlutNs activation dynamics and their input and output connectivity matrices support explorative and escape locomotion, respectively. Our results identify dual regions in the midbrain that act in common to select context dependent locomotor behaviours.

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“…Stimulation of VTA dopaminergic neurons likely works by recruiting neural circuits that involve limbic cortices, nucleus accumbens, and pedunculopontine nucleus (6,9,18). The role of other wake-active neurons in the emergence from general anesthesia (6,19) remains to be clarified, including neurons using neurotransmitter acetylcholine, histamine, norepinephrine (20), serotonin and orexin.…”

mentioning

confidence: 99%

Dopamine in the ventral tegmental area facilitates emergence from general anesthesia

Leung

2017

Ann. Transl. Med.

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Topographical Organization of the Pedunculopontine Nucleus

Cited by 208 publications

References 118 publications

Imagined gait modulates neuronal network dynamics in the human pedunculopontine nucleus

Imagined gait modulates neuronal network dynamics in the human pedunculopontine nucleus

Midbrain circuits that set locomotor speed and gait selection

Dopamine in the ventral tegmental area facilitates emergence from general anesthesia

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