Electrical stimulation of the cholinergic laterodorsal tegmental nucleus elicits scopolamine-sensitive excitatory postsynaptic potentials in medial pontine reticular formation neurons

Imon, Hitoshi; Ito, Keihachiro; Dauphin, L.; McCarley, Robert W.

doi:10.1016/0306-4522(96)00134-0

Cited by 43 publications

(11 citation statements)

References 22 publications

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“…These inputs, when stimulated, produce EPSPs in the pontine reticular formation neurons (Imon et al, 1996;Homma et al, 2002). Because of the stimulatory effect of UII on PPT neurons, it is likely that UII induces acetylcholine release in the pontine reticular formation and induces REM sleep.…”

Section: Discussionmentioning

confidence: 99%

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Huitrón‐Reséndiz

Kristensen²,

Sanchez‐Alavez³

et al. 2005

Journal of Neuroscience

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Urotensin II (UII) is a cyclic neuropeptide with strong vasoconstrictive activity in the peripheral vasculature. UII receptor mRNA is also expressed in the CNS, in particular in cholinergic neurons located in the mesopontine tegmental area, including the pedunculopontine tegmental (PPT) and lateral dorsal tegmental nuclei. This distribution suggests that the UII system is involved in functions regulated by acetylcholine, such as the sleep-wake cycle. Here, we tested the hypothesis that UII influences cholinergic PPT neuron activity and alters rapid eye movement (REM) sleep patterns in rats. Local administration of UII into the PPT nucleus increases REM sleep without inducing changes in the cortical blood flow. Intracerebroventricular injection of UII enhances both REM sleep and wakefulness and reduces slow-wave sleep 2. Intracerebroventricular, but not local, administration of UII increases cortical blood flow. Moreover, whole-cell recordings from rat-brain slices show that UII selectively excites cholinergic PPT neurons via an inward current and membrane depolarization that were accompanied by membrane conductance decreases. This effect does not depend on action potential generation or fast synaptic transmission because it persisted in the presence of TTX and antagonists of ionotropic glutamate, GABA, and glycine receptors. Collectively, these results suggest that UII plays a role in the regulation of REM sleep independently of its cerebrovascular actions by directly activating cholinergic brainstem neurons.

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Section: Discussionmentioning

confidence: 99%

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Huitrón‐Reséndiz

Kristensen²,

Sanchez‐Alavez³

et al. 2005

Journal of Neuroscience

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“…For example, the PPT/LDT functionally influence the pontine reticular formation (REM sleep and eye movements; Cornwall et al . 1990; Jones, 1991; Imon et al . 1996; Thakkar et al .…”

Section: Discussionmentioning

confidence: 99%

Action sequencing is impaired in D_1A‐deficient mutant mice

Cromwell

Berridge

Drago

et al. 1998

Eur J of Neuroscience

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The role of dopamine in the production of behaviour is multifarious in that it can influence different aspects of movement (e.g. movement initiation, sensorimotor integration, and movement sequencing). A characteristic of the dopamine system which seems to be critical for the expression of this diverse influence is its varied receptor population. Previous studies have shown that specific receptor subtype activation leads to specific behavioural responses or alterations of selective aspects of movement. It is known that one of the important influences of dopamine includes sequential co-ordination of 'syntactic' patterns of grooming movements because moderate loss of the dopaminergic nigrostriatal projections specifically disrupts these patterns without affecting grooming actions in a general fashion (Berridge, K.C. Psychobiology, 15, 336, 1989). The specific receptors of the dopamine family which play a key part in this co-ordination of movement sequences is not known. In the present study, we examined the serial order of particular syntactic sequences or chains of grooming actions in mice lacking D1A receptors to explore the relationship between this receptor subtype and movement sequencing. Mutant mice had shorter grooming bouts and a disruption of the organization of sequential patterns compared with wild-type littermate controls. Sequential disruption was reflected in the failure of D1A mutants to follow the syntactic pattern of grooming to completion. This sequential disruption deficit appeared to be specific, as mutant mice initiated more syntactic chains than wild-type controls even though they were less likely to complete them. These results support the hypothesis that D1A receptor activation plays a part in the sequencing of natural action. This conclusion has important implications for the understanding of the functional heterogeneity of dopamine receptor subtypes and of the aetiology of symptoms observed in patients with basal ganglia disease.

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“…Anatomical and electrophysiological experiments have confirmed the existence of many of the proposed interconnections of this model. Cholinergic modulation of reticular formation neurons: anatomical and electrical stimulation studies have demonstrated prominent cholinergic projections from the LDT and pedunculopontine tegmentum (PPT) to the reticular formation areas involved in REM sleep control (544, 861). Early in vitro intracellular recording studies in the PnO and PnC regions of the reticular formation revealed excitatory effects of cholinergic agonists mediated by nicotinic and muscarinic receptors in approximately two-thirds of reticular neurons (447, 1241), acting via nonselective cation channels and blockade of leak potassium, channels, respectively.…”

Section: Rem Sleepmentioning

confidence: 99%

Control of Sleep and Wakefulness

Brown

Basheer

Mckenna

et al. 2012

Physiological Reviews

1,164

1,105

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This review summarizes the brain mechanisms controlling sleep and wakefulness. Wakefulness promoting systems cause low-voltage, fast activity in the electroencephalogram (EEG). Multiple interacting neurotransmitter systems in the brain stem, hypothalamus, and basal forebrain converge onto common effector systems in the thalamus and cortex. Sleep results from the inhibition of wake-promoting systems by homeostatic sleep factors such as adenosine and nitric oxide and GABAergic neurons in the preoptic area of the hypothalamus, resulting in large-amplitude, slow EEG oscillations. Local, activity-dependent factors modulate the amplitude and frequency of cortical slow oscillations. Non-rapid-eye-movement (NREM) sleep results in conservation of brain energy and facilitates memory consolidation through the modulation of synaptic weights. Rapid-eye-movement (REM) sleep results from the interaction of brain stem cholinergic, aminergic, and GABAergic neurons which control the activity of glutamatergic reticular formation neurons leading to REM sleep phenomena such as muscle atonia, REMs, dreaming, and cortical activation. Strong activation of limbic regions during REM sleep suggests a role in regulation of emotion. Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function. Sleep disruption interferes with the normal restorative functions of NREM and REM sleep, resulting in disruptions of breathing and cardiovascular function, changes in emotional reactivity, and cognitive impairments in attention, memory, and decision making.

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Electrical stimulation of the cholinergic laterodorsal tegmental nucleus elicits scopolamine-sensitive excitatory postsynaptic potentials in medial pontine reticular formation neurons

Cited by 43 publications

References 22 publications

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Action sequencing is impaired in D_1A‐deficient mutant mice

Control of Sleep and Wakefulness

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Electrical stimulation of the cholinergic laterodorsal tegmental nucleus elicits scopolamine-sensitive excitatory postsynaptic potentials in medial pontine reticular formation neurons

Cited by 43 publications

References 22 publications

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Urotensin II Modulates Rapid Eye Movement Sleep through Activation of Brainstem Cholinergic Neurons

Action sequencing is impaired in D1A‐deficient mutant mice

Control of Sleep and Wakefulness

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Product

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Action sequencing is impaired in D_1A‐deficient mutant mice