Responsiveness of thalamic and cortical motor relays during arousal and various stages of sleep.

Steriade, Mircea; Iosif, G.; Apostol, V

doi:10.1152/jn.1969.32.2.251

Cited by 157 publications

(46 citation statements)

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“…This action of NO is compatible with physiological states of arousal where the activation of ascendent systems modifies the excitability of cortical cells and "wakens" the brain. 35 Further, these data are also consistent with reports that both pontine cholinergic stimulation 36 and brain NO 37 contribute to generation of electrocortical (EEG) arousal.…”

Section: Discussionsupporting

confidence: 87%

A Possible Role for Nitric Oxide at the Sleep/Wake Interface

Cudeiro

Rivadulla

Grieve³

2000

Sleep

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1. During periods of drowsiness and slow-wave sleep there is a relative synchrony of low-frequency rhythmic cortical and thalamic synaptic and neuronal activity, while during periods of waking and attentiveness, these rhythms are abolished and there is a marked increase in neuronal responsiveness to synaptic inputs 1,2 . These shifts are controlled by modulatory neurotransmitter systems arising from several brainstem and forebrain cell groups, of which cholinergic components play a key roles [3][4][5][6][7] .Recent evidence has shown that acetylcholine (ACh)-containing fibers arising from the peribrachial (PB) region of the brainstem and from the nucleus basalis of the forebrain (innervating the thalamus and the neocortex respectively) also contain nitric oxide synthase (NOS) the enzyme responsible for the production of nitric oxide (NO) 8,9 . This substance is now considered to be a widely spread nervous system neuromodulator, which, in stark contrast to traditional neurotransmitters, is a freely diffusible gaseous molecule. This offers a novel route of communication between neurons, possibly having a potent influence remote from its site of production. Its main mode of action is thought to be by stimulation of soluble guanylate cyclase, leading to an increase in intracellular cyclic GMP in target cells 10 . NO has been shown to increase the excitability of both thalamic and cortical neurons 11 and has also been shown to be involved with the modulation of sleep/wake states 12-14 , rapid eye movement sleep generation 15 and the circadian rhythms 16 . Here, using extracellular single recording of neurons in the dorsal thalamus and visual cortex of the anesthetized cat and simultaneous iontophoretic application of drugs acting upon the NO system, we have sought to determine the cooperative role of NO with ACh in controlling rhythmic neuronal activity. Specifically, we wish to demonstrate that NO fulfills, as does ACh, the main criteria necessary to be involved in a functional role in sleep/wake transition: increased neuronal responsiveness and modified rhythmic activity. MATERIALS AND METHODSExperiments were carried out on adult cats in the weight range 1.8-2.5kg. Animals were anesthetized with halothane (0.1-5%) in nitrous oxide (70%) and oxygen (30%), and paralyzed with gallamine triethiodide (10mg/kg/h). Briefly, EEG and ECG, expired CO 2 and temperature were monitored and maintained continuously, Abstract: Cholinergic neurotransmission is known to have important arousal/activating functions. The neurons responsible for those actions also release the atypical neuromodulator nitric oxide (NO), which has been shown in previous studies to be involved in the modulation of sleep/wake states. The present investigation, using an animal model (anesthetized cat) tests the hypothesis that NO cooperates with ACh in controlling rhythmic neuronal activity, which may play a role in sleep/wake transition. We have used extracellular singleunit recording of neurons in the dorsal thalamus and visual cortex with simultaneous iont...

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Section: Discussionsupporting

confidence: 87%

A Possible Role for Nitric Oxide at the Sleep/Wake Interface

Cudeiro

Rivadulla

Grieve³

2000

Sleep

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“…dependent on the behavioral state of vigilance. In the cortex, augmenting responses in motor and somatosensory thalamocortical systems are diminished during strong behavioral or brainstem-induced arousal (Steriade et al, 1969;Steriade and Morin, 1981;Castro-Alamancos and Connors 1996a). On the other hand, TC neurons display an enhanced responsiveness after a brief pulse train to the activating mesopontine cholinergic neurons , and this brainstem-thalamic potentiation may be prolonged up to 4 min (Paré et al, 1990).…”

Section: Genesis Of Intrathalamic Augmenting Responsesmentioning

confidence: 99%

Short-Term Plasticity during Intrathalamic Augmenting Responses in Decorticated Cats

Steriade

Timofeev

1997

J. Neurosci.

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The intrathalamic mechanisms of frequency-dependent augmenting responses were investigated in decorticated cats by means of intracellular recordings from thalamocortical ( TC) neurons in ventrolateral (VL) nucleus, including simultaneous impalements from two TC neurons. Pulse trains (10 Hz) applied to VL nucleus elicited two types of augmenting responses: (1) in 68% of cells, the incremental responses occurred on a progressive depolarization associated with the decrease in IPSPs produced by preceding stimuli in the train; (2) in the remaining cells, progressively growing low-threshold (LT ) responses resulted from the enhancement of Cl Ϫ -dependent IPSPs, giving rise to postinhibitory rebound bursts, followed by a selfsustained sequence of spindle waves. Although in some TC cells the augmenting responses developed from LT responses once the latter reached a given level of depolarization, other neurons displayed augmenting responses immediately after the early antidromic spike that depolarized the neuron to the required level, without an intermediate step of LT rebound. Repeated pulse trains led to a progressive and persistent increase in slow depolarizing responses of TC cells, as well as to a persistent and prolonged decrease in the amplitudes of the IPSPs. On the basis of parallel experiments, we propose that the two types of augmentation in TC cells are a result of contrasting responses of thalamic reticular neurons evoked by repetitive thalamic stimuli: decremental responses, which may account for disinhibition leading to depolarizing responses in TC cells, and incremental responses, explaining the progressive hyperpolarization of TC cells. These data demonstrate that frequency-dependent changes in neuronal excitability are present in the thalamus of a decorticated hemisphere and suggest that short-term plasticity processes in the gateway to the cerebral cortex may decisively influence cortical excitability during repetitive responses.

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“…First, application of acetylcholine (ACh) to pyramidal neurons of the cerebral cortex and basolateral amygdaloid nucleus elicits a slow muscarinic depolarization associated with a decrease in membrane conductance (Krnjevic et al, 1971;McCormick and Prince, 1986;Womble and Moises, 1992;Washburn and Moises, 1992). Second, cortical levels of ACh increase during behavioral states characterized by a desynchronized electroencephalogram (EEG) and increased cellular responsiveness (Steriade et al, 1969(Steriade et al, , 1974 such as waking and rapid-eye-movement sleep or following stimulation of the brainstem reticular formation (Kanai and Szerb, 1965;Collier and Mitchell, 1967;Jasper and Tessier, 1971). Third, excitotoxic lesions of the basal forebrain result in EEG synchronization (Buzsaki et al, 1988).…”

Section: Functional Implicationsmentioning

confidence: 99%

GABAergic projection from the intercalated cell masses of the amygdala to the basal forebrain in cats

Paré

Smith

1994

J of Comparative Neurology

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The intercalated cell masses (ICMs) are dense clusters of small GABAergic cells interposed between the basolateral and centromedial nuclear groups of the amygdala. Until now, the ICMs have been largely ignored in anatomical studies of the amygdaloid complex. Thus, this study was undertaken to identify some of their targets by means of tract-tracing methods combined with immunohistochemical techniques. Wheat-germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) was injected into numerous cortical areas and dorsal thalamic nuclei, in the anterior commissure and/or stria terminalis nuclei, and in the caudate nucleus, as well as into lateral and preoptic hypothalamic areas. Very few retrogradely labeled cells were seen in the ICMs following these injections. In contrast, massive retrograde labeling was found in the rostral groups of ICMs after WGA-HRP injections involving the substantia innominata and horizontal limb of the diagonal band. Furthermore, these retrogradely labeled intercalated cells were also GABA-immunoreactive. Results of iontophoretic injections of Phaseolus vulgaris-leucoagglutinin (PHA-L) in the rostral ICMs confirmed that they contribute a massive projection to the entire extent of the substantia innominata and horizontal limb of the diagonal band. Electron microscopic observations of ultrathin sections prepared for postembedding GABA or glutamate immunocytochemistry revealed that the ICM terminals labeled with PHA-L displayed GABA, but not glutamate immunoreactivity, and formed symmetric synapses with dendritic profiles. The present findings constitute the first direct demonstration of an amygdalofugal GABAergic projection to the basal forebrain. Considering that the basal forebrain contains a group of cholinergic and GABAergic neurons collectively projecting to the entire cortical mantle, this GABAergic projection of the ICMs could allow the amygdaloid complex to influence the activity of widespread cortical regions to which it is not directly connected, at least in the cat.

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Responsiveness of thalamic and cortical motor relays during arousal and various stages of sleep.

Cited by 157 publications

References 0 publications

A Possible Role for Nitric Oxide at the Sleep/Wake Interface

A Possible Role for Nitric Oxide at the Sleep/Wake Interface

Short-Term Plasticity during Intrathalamic Augmenting Responses in Decorticated Cats

GABAergic projection from the intercalated cell masses of the amygdala to the basal forebrain in cats

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