Projection neurons from the central nucleus of the amygdala to the nucleus pontis oralis

Fung, Simon J.; Xi, Ming-Chu; Zhang, Jianhua; Torterolo, Pablo; Sampogna, Sharon; Morales, Francisco R.; Chase, Michael H.

doi:10.1002/jnr.22554

Cited by 26 publications

(17 citation statements)

References 47 publications

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“…The central nucleus of the amygdala sends excitatory projections to the SLD and inhibitory projections to the vlPAG/LPT (Boissard et al, 2003; Fung et al, 2011; Xi et al, 2011). Perhaps, strong, positive emotions activate these limbic pathways, increasing the likelihood of atonia.…”

Section: Neurobiology Of Cataplexymentioning

confidence: 99%

Narcolepsy: Neural Mechanisms of Sleepiness and Cataplexy

2012

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Narcolepsy is a common sleep disorder characterized by excessive daytime sleepiness and cataplexy - episodes of muscle weakness triggered by positive emotions. Over the last few years, researchers have discovered that narcolepsy results from a selective loss of neurons in the lateral hypothalamus that produce the orexin/hypocretin neuropeptides. While an autoimmune process is thought to underlie the loss of the orexin neurons this has not yet been conclusively demonstrated. Similarly, it is only partially understood how loss of the orexin neurons results in the various symptoms of narcolepsy. Studies in human patients and animal models of narcolepsy suggest that excessive sleepiness is due to behavioral state instability rather than disruption of sleep homeostasis or circadian rhythms. Cataplexy may result from the inappropriate activation during wakefulness of the pontine circuits that normally generate muscle atonia during REM sleep. This article reviews the clinical features and neurobiology of narcolepsy and outlines important areas in which progress might be achieved.

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Section: Neurobiology Of Cataplexymentioning

confidence: 99%

Narcolepsy: Neural Mechanisms of Sleepiness and Cataplexy

2012

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“…2008), basal forebrain (Rodrigo‐Angulo et al. 2008), amygdala (Fung et al. 2011), contralateral PnO (Liang and Marks 2009), and ventral lateral periaqueductal gray (Boissard et al.…”

Section: Limitations and Conclusionmentioning

confidence: 99%

“…2010). The PnO receives glutamatergic projections from the amygdala (Fung et al. 2011), the laterodorsal tegmental and pedunculopontine tegmental nuclei (Lai et al.…”

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confidence: 99%

Sleep duration varies as a function of glutamate and GABA in rat pontine reticular formation

Watson

Lydic

Baghdoyan

2011

Journal of Neurochemistry

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The oral part of the pontine reticular formation (PnO) is a component of the ascending reticular activating system and plays a role in the regulation of sleep and wakefulness. The PnO receives glutamatergic and GABAergic projections from many brain regions that regulate behavioral state. Indirect, pharmacological evidence has suggested that glutamatergic and GABAergic signaling within the PnO alters traits that characterize wakefulness and sleep. No previous studies have simultaneously measured endogenous glutamate and GABA from rat PnO in relation to sleep and wakefulness. The present study utilized in vivo microdialysis coupled on-line to capillary electrophoresis with laser-induced fluorescence to test the hypothesis that concentrations of glutamate and GABA in the PnO vary across the sleep/wake cycle. Concentrations of glutamate and GABA were significantly higher during wakefulness than during NREM sleep and REM sleep. Regression analysis revealed that decreases in glutamate and GABA accounted for a significant portion of the variance in the duration of NREM sleep and REM sleep episodes. These data provide novel support for the hypothesis that endogenous glutamate and GABA in the PnO contribute to the regulation of sleep duration.

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“…In rats, amygdala neurons encode positive stimulus associations (Paton et al, 2006), and amygdala-lesioned rats fail to approach stimuli of positive affective valence (Schoenbaum et al, 1998). Anatomically, the amygdala is well-positioned to influence muscle tone and REM sleep phenomena as the central nucleus of the amygdala in rats innervates regions in the pons that regulate REM sleep (Boissard et al, 2003, Fung et al, 2011). In addition, Gulyani and colleagues recorded from the amygdala of freely behaving narcoleptic dogs and found many neurons with increased activity during cataplexy (Gulyani et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Amygdala Lesions Reduce Cataplexy in Orexin Knock-Out Mice

Burgess

Oishi

Mochizuki

et al. 2013

Journal of Neuroscience

101

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Narcolepsy is characterized by excessive sleepiness and cataplexy, sudden episodes of muscle weakness during waking that are thought to be an intrusion of REM sleep muscle atonia into wakefulness. One of the most striking aspects of cataplexy is that it is often triggered by strong, generally positive emotions, but little is known about the neural pathways through which positive emotions trigger muscle atonia. We hypothesized that the amygdala is functionally important for cataplexy because the amygdala has a role in processing emotional stimuli and it contains neurons that are active during cataplexy. Using anterograde and retrograde tracing in mice, we found that GABAergic neurons in the central nucleus of the amygdala heavily innervate neurons that maintain waking muscle tone such as those in the ventrolateral periaqueductal grey, lateral pontine tegmentum, locus coeruleus, and dorsal raphe. We then found that bilateral, excitotoxic lesions of the amygdala markedly reduced cataplexy in orexin knockout mice, a model of narcolepsy. These lesions did not alter basic sleep/wake behavior, but substantially reduced the triggering of cataplexy. Lesions also reduced the cataplexy events triggered by conditions associated with high arousal and positive emotions (i.e., wheel running and chocolate). These observations demonstrate that the amygdala is a functionally important part of the circuitry underlying cataplexy and suggest that increased amygdala activity in response to emotional stimuli could directly trigger cataplexy by inhibiting brainstem regions that suppress muscle atonia.

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Projection neurons from the central nucleus of the amygdala to the nucleus pontis oralis

Cited by 26 publications

References 47 publications

Narcolepsy: Neural Mechanisms of Sleepiness and Cataplexy

Narcolepsy: Neural Mechanisms of Sleepiness and Cataplexy

Sleep duration varies as a function of glutamate and GABA in rat pontine reticular formation

Amygdala Lesions Reduce Cataplexy in Orexin Knock-Out Mice

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