The postsynaptic inhibitory control of lumbar motoneurons during the atonia of active sleep: effect of strychnine on motoneuron properties

Soja, Peter J.; Rodríguez, Fernando López; Morales, F.R.; Chase, M H

doi:10.1523/jneurosci.11-09-02804.1991

Cited by 99 publications

(85 citation statements)

References 20 publications

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“…Using intracellular recording and microiontophoretic techniques, Chase and his colleagues found that IPSPs in both cranial and spinal motoneurons can be blocked by application of strychnine, a glycine antagonist, during natural (Chirwa et al, 1991;Soja et al, 1991) and pontine carbachol-induced (Kohlmeier et al, 1996;Yamuy et al, 1999) REM sleep in the cat. GABA has also been shown to inhibit motoneuron activity.…”

Section: Discussionmentioning

confidence: 99%

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

2003

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We hypothesized that cessation of brainstem monoaminergic systems and an activation of brainstem inhibitory systems are both involved in pontine inhibitory area (PIA) stimulation-induced muscle atonia. In our previous study (Lai et al., 2001), we found a decrease in norepinephrine and serotonin release in motoneuron pools during PIA stimulation-induced muscle tone suppression. We now demonstrate an increase in inhibitory amino acid release in motor nuclei during PIA stimulation in the decerebrate cat using in vivo microdialysis and HPLC analysis techniques. Microinjection of acetylcholine into the PIA elicited muscle atonia and simultaneously produced a significant increase in both glycine and GABA release in both the hypoglossal nucleus and the lumbar ventral horn. Glycine release increased by 74% in the hypoglossal nucleus and 50% in the spinal cord. GABA release increased by 31% in the hypoglossal nucleus and 64% in the spinal cord during atonia induced by cholinergic stimulation of the PIA. As with cholinergic stimulation, 300 msec train electrical stimulation of the PIA elicited a significant increase in glycine release in the hypoglossal nucleus and ventral horn. GABA release was significantly increased in the hypoglossal nucleus but not in the spinal cord during electrical stimulation of the PIA. Glutamate release in the motor nuclei was not significantly altered during atonia induced by electrical or acetylcholine stimulation of the PIA. We suggest that both glycine and GABA play important roles in the regulation of upper airway and postural muscle tone. A combination of decreased monoamine and increased inhibitory amino acid release in motoneuron pools causes PIA-induced atonia and may be involved in atonia linked to rapid eye-movement sleep.

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Section: Discussionmentioning

confidence: 99%

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

2003

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“…First, by means of intracellular recordings during PS, it has been shown that trigeminal, hypoglossal and spinal motoneurons are tonically hyperpolarized by large inhibitory postsynaptic potentials (IPSPs) during PS. Further when these recordings were combined with local iontophoretic application of strychnine (a specific antagonist of the inhibitory neurotransmitter, glycine), motoneurons hyperpolarization was strongly decreased indicating that they are tonically inhibited by glycinergic neurons during PS [12][13][14]. It has then been shown that the levels of glycine but also that of GABA increase within hypoglossal and spinal motor pools during PS-like atonia suggesting that GABA in addition to glycine might contribute to motoneurons hyperpolarization during PS [15].…”

Section: Paradoxical (Rem) Sleep Generating Neurons: the Switch From mentioning

confidence: 99%

Paradoxical (REM) sleep genesis by the brainstem is under hypothalamic control

Luppi

Olivier

Fort

2013

Current Opinion in Neurobiology

100

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“…Another key issue our data addresses is whether active sleep-specific suppression of the sciatic nerve-evoked responses in DSCT neurons can be adequately explained by withdrawal of afferent input, i.e., disfacilitation, that is secondary to motor atonia and the hyperpolarization of motoneurons (Chase et al 1989;Morales and Chase 1981;Soja et al 1991). Disfacilitation is unlikely to account for the reduced synaptic responses in this study because sciatic nerve stimulation bypasses peripheral sensory receptors.…”

Section: State-dependent Suppression Of Sciatic Nerveevoked Responsesmentioning

confidence: 86%

“…Lumbar motoneurons are known to be tonically hyperpolarized during non-eye movement periods of active sleep by a process of glycine-mediated postsynaptic inhibition (Chase et al 1989;Soja et al 1991). The amplitude of monosynaptic EPSPs intracellularly recorded from motoneurons decreases during non-eye movement periods of active sleep compared with quiet sleep.…”

Section: State-dependent Suppression Of Sciatic Nerveevoked Responsesmentioning

confidence: 99%

“…Ineffective muscular atonia mechanisms and/or excess facilitatory drives onto motoneurons are thought to underlie the varying degrees of sensorimotor activation in RBD (Chase and Morales 1990;Schenck and Mahowald 2002). Taken together, impaired glycine and GABA-mediated inhibi-tion that normally occurs in motor (Chase et al 1989;Soja et al 1991) and ascending sensory pathways such as Clarke's column DSCT neurons (Soja et al 1993(Soja et al , 1996(Soja et al , 2001aTaepavarapruk et al 2002) may contribute to these clinical syndromes. Future electrophysiological studies are warranted to investigate the state-dependent regulation of GABAergic (and glycinergic) pathways inhibiting sensory inflow to higher brain centers under natural conditions and conditions emulating RLS and RBD.…”

Section: Functional Significance Of State-dependent Inhibition Of Dscmentioning

confidence: 99%

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State-Dependent GABAergic Inhibition of Sciatic Nerve-Evoked Responses of Dorsal Spinocerebellar Tract Neurons

Taepavarapruk

McErlane

Chan

et al. 2004

Journal of Neurophysiology

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. State-dependent GABAergic inhibition of sciatic nerve-evoked responses of dorsal spinocerebellar tract neurons. J Neurophysiol 92: 1479 -1490, 2004. First published April 21, 2004 10.1152/jn.01108.2003. Peripheral nerve-evoked potentials recorded in the cerebellum 35 yr ago inferred that sensory transmission via the dorsal spinocerebellar tract (DSCT) is reduced occasionally and only during eye movements of active sleep compared with wakefulness or quiet sleep. A reduction or withdrawal of primary afferent input and/or ongoing inhibition of individual lumbar DSCT neurons may underlie this occurrence. This study distinguished between these possibilities by examining whether peripheral nerveevoked responses recorded from individual DSCT neurons are suppressed specifically during active sleep, and if so, whether GABA mediates this phenomenon. Synaptic responses to threshold stimuli applied to the sciatic nerve were characterized by a single spike response at short latency and/or a longer latency burst of action potentials. During the state of quiet wakefulness, response magnitude did not differ from that observed during quiet sleep. During active sleep, short and long latency responses were suppressed by 26 and 14%, respectively, and returned to pre-active sleep levels following awakening from active sleep. Sciatic nerve-evoked early and late responses were further analyzed in a paired fashion around computertagged eye movement events that hallmark the state of active sleep. Response magnitude was suppressed by 14.4 and 11.5%, respectively, during eye movement events of active sleep. The GABA A antagonist bicuculline, applied juxtacellularly by microiontophoresis, abolished response suppression during non-eye movement periods and eye movement events of active sleep. In conclusion, synaptic transmission via DSCT neurons is inhibited by GABA tonically during non-eye movement periods and phasically during eye movement events of active sleep. I N T R O D U C T I O NRecent chronic unit recording studies of individual upper lumbar sensory projection neurons comprising the dorsal spinocerebellar tract (DSCT) have indicated that these cells are subjected to inhibition specifically during the behavioral state of active sleep as opposed to other states, such as wakefulness or quiet sleep (Soja et al. 1996(Soja et al. , 2001aTaepavarapruk et al. 2002). In particular, the spontaneous and glutamate-evoked responses of DSCT neurons are markedly reduced during active sleep and are mediated by the "fast" inhibitory amino acid neurotransmitters GABA and glycine. Evoked potential studies conducted in the 1960s revealed that peripheral nerveevoked responses recorded in the cerebellum were indeed suppressed only during intense eye movements of active sleep (Carli et al. 1966(Carli et al. , 1967a. These findings suggest that the magnitude of low-threshold, peripherally evoked responses of DSCT neurons may also depend on behavioral state.In this study, we investigated this issue for the first time by applying low-intensity stimuli to...

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The postsynaptic inhibitory control of lumbar motoneurons during the atonia of active sleep: effect of strychnine on motoneuron properties

Cited by 99 publications

References 20 publications

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

Changes in Inhibitory Amino Acid Release Linked to Pontine-Induced Atonia: AnIn VivoMicrodialysis Study

Paradoxical (REM) sleep genesis by the brainstem is under hypothalamic control

State-Dependent GABAergic Inhibition of Sciatic Nerve-Evoked Responses of Dorsal Spinocerebellar Tract Neurons

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