The Amygdala: A Critical Modulator of Sensory Influence on Sleep

Morrison, Adrian R.; Sanford, Larry D.; Ross, Richard

doi:10.1159/000014652

Cited by 37 publications

(12 citation statements)

References 42 publications

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“…The current results clearly revealed a dose-dependent reduction after injections of MDZ into the amygdala. This effect may be due to direct projections from the amygdala to brainstem nuclei known to be involved in arousal and sleep control (Morrison et al, 2000;Sanford et al, 2002). With regard to the hippocampus, our results and past studies demonstrate that MDZ significantly inhibits locomotion in the open field at relatively high drug concentrations, that is, 20-30 nmol (Stefanski et al, 1993;Nazar et al, 1999).…”

Section: Discussionsupporting

confidence: 65%

Localized injections of midazolam into the amygdala and hippocampus induce differential changes in anxiolytic-like motor activity in mice

Heldt¹,

Ressler²

2006

Behavioural Pharmacology

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Various strains of mice display a reliable increase in motor activity in response to benzodiazepines given at low to moderate doses. This hyperactivity has been described as both an anxiolytic-associated increase in exploratory activity and a nonspecific stimulant effect controlled by central neural mechanisms separate from those involved in the anxiolytic-like effects. The purpose of the current study was to investigate the neural circuitry underlying the hyperactivity effects of benzodiazepines in mice. Specifically, we examined the relationship between anxiety and motor activity after bilateral intra-amygdala or intra-hippocampal microinjections of the nonselective full benzodiazepine receptor agonist midazolam in C57BL/6 mice. Behavioral measures of anxiety and motor activity in open field were examined in mice given localized injections of 0, 2, 8 or 32 nmol of midazolam directed into the amygdala or hippocampus. Midazolam injected into the amygdala at the low dose produced an anxiolytic-like effect, as reflected by an increase in central open field activity. Higher doses injected into the amygdala produced a motor-depressant action, indicative of a drug-induced sedative effect. Infusions into the hippocampus produced a biphasic effect on motor activity with the two lower doses of midazolam producing a motor-stimulant action and the high dose producing a motor-depressant effect. Hippocampus injections produced no anxiolytic-like effects. The current findings demonstrate that injections of midazolam produced a regional dissociation of the anxiety-related and motor-related parameters and provide evidence that the stimulant and anxiolytic effects of benzodiazepines are independent phenomena regulated by different central mechanisms.

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Section: Discussionsupporting

confidence: 65%

Localized injections of midazolam into the amygdala and hippocampus induce differential changes in anxiolytic-like motor activity in mice

Heldt¹,

Ressler²

2006

Behavioural Pharmacology

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“…From an evolutionary perspective, REM sleep is closely linked to the development of the mammalian nervous system, suggesting a relationship between REM sleep‐related processes and the enhancement of cortical plasticity (Maquet & Franck, 1997; Maquet et al ., 2000; Hobson & Pace‐Schott, 2002; Pace‐Schott & Hobson, 2002). Amygdala activation strengthens phasic REM sleep elements, which are hypothesized to play a role in plasticity changes on a neuronal level (Morrison et al ., 2000; Datta, 2000; Datta et al ., 2004). These proposed functions may be specifically enhanced during phasic REM sleep episodes as indicated by increased network activity.…”

Section: Discussionmentioning

confidence: 99%

Functional microstates within human REM sleep: first evidence from fMRI of a thalamocortical network specific for phasic REM periods

Wehrle

Kaufmann

Wetter

et al. 2007

Eur J of Neuroscience

201

138

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High thalamocortical neuronal activity characterizes both, wakefulness and rapid eye movement (REM) sleep, but apparently this network fulfills other roles than processing external information during REM sleep. To investigate thalamic and cortical reactivity during human REM sleep, we used functional magnetic resonance imaging with simultaneous polysomnographic recordings while applying acoustic stimulation. Our observations indicate two distinct functional substates within general REM sleep. Acoustic stimulation elicited a residual activation of the auditory cortex during tonic REM sleep background without rapid eye movements. By contrast, periods containing bursts of phasic activity such as rapid eye movements appear characterized by a lack of reactivity to sensory stimuli. We report a thalamocortical network including limbic and parahippocampal areas specifically active during phasic REM periods. Thus, REM sleep has to be subdivided into tonic REM sleep with residual alertness, and phasic REM sleep with the brain acting as a functionally isolated and closed intrinsic loop.

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“…The difference was particularly pronounced in the amygdala [53]. The amygdala plays a critical role in processing emotional stimuli and heavily interconnects with brainstem sleep circuits [54]. The tachykinin peptide family includes Substance P and it has been shown that substance Plike afferents from the central nucleus of the amygdala project to brain regions that might generate muscle atonia, e.g., the parvicellular reticular nuclei of the medulla [55].…”

Section: Narcolepsy In Human Beingsmentioning

confidence: 99%

Animal Models of Narcolepsy

Chen

Brown²,

Mckenna³

et al. 2009

CNSNDDT

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Narcolepsy is a debilitating sleep disorder with excessive daytime sleepiness and cataplexy as its two major symptoms. Although this disease was first described about one century ago, an animal model was not available until the 1970s. With the establishment of the Stanford canine narcolepsy colony, researchers were able to conduct multiple neurochemical studies to explore the pathophysiology of this disease. It was concluded that there was an imbalance between monoaminergic and cholinergic systems in canine narcolepsy. In 1999, two independent studies revealed that orexin neurotransmission deficiency was pivotal to the development of narcolepsy with cataplexy. This scientific leap fueled the generation of several genetically engineered mouse and rat models of narcolepsy. To facilitate further research, it is imperative that researchers reach a consensus concerning the evaluation of narcoleptic behavioral and EEG phenomenology in these models.

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The Amygdala: A Critical Modulator of Sensory Influence on Sleep

Cited by 37 publications

References 42 publications

Localized injections of midazolam into the amygdala and hippocampus induce differential changes in anxiolytic-like motor activity in mice

Localized injections of midazolam into the amygdala and hippocampus induce differential changes in anxiolytic-like motor activity in mice

Functional microstates within human REM sleep: first evidence from fMRI of a thalamocortical network specific for phasic REM periods

Animal Models of Narcolepsy

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