Cellular substrates and laminar profile of sleep K-complex

Laboratoire de Neurophysiologie, Faculté de Médecine, Université Laval, Quebec, Canada.
Neuroscience (Impact Factor: 3.36). 03/1998; 82(3):671-86. DOI: 10.1016/S0306-4522(97)00319-9
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We describe the cellular mechanisms that underlie the generation of the K-complex, a major grapho-element of sleep electroencephalogram in humans. First we demonstrate the similarity between K-complexes recorded during natural sleep and under ketamine-xylazine anaesthesia in cats. Thereafter, we show by means of multi-site cellular and field potential recordings that K-complexes are rhythmic at frequencies of less than 1 Hz (mainly 0.5-0.9 Hz) and that they are synchronously distributed over the whole cortical surface as well as transferred to the thalamus. The surface K-complex reverses its polarity at a cortical depth of about 0.3 mm. At the cortical depth, the K-complex is made of a sharp and high-amplitude negative deflection that reflects cellular depolarization, often preceded by a smaller-amplitude, positive slow-wave reflecting cellular hyperpolarization. The sharp component of the K-complex may lead to a spindle sequence and/or to fast (mainly 20-50 Hz) oscillations. K-complexes appear spontaneously or triggered by cortical or thalamic stimulation, and they arise within cortical networks. We suggest that K-complexes, either in isolation or followed by a brief sequence of spindle waves, are the expression of the spontaneously occurring, cortically generated slow oscillation.

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Available from: Florin Amzica, Sep 23, 2014
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    • "Slow waves are local field potential and EEG signatures of cortical network transitions between high and low activity states: a depolarized UP state associated with neuronal spiking and a low-activity DOWN state with little firing or synaptic drive (Steriade et al., 1993a,b). The membrane potentials of pyramidal cells therefore display a characteristic bimodal distribution during slow waves, with the origin of UP/DOWN state transitions focused in the deep layers of the cortex (Amzica & Steriade, 1997b; Sanchez-Vives & McCormick, 2000; Chauvette et al., 2010; Beltramo et al., 2013). "
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    ABSTRACT: The neurophysiology of non-rapid eye movement sleep is characterized by the occurrence of neural network oscillations with distinct origins and frequencies, which act in concert to support sleep-dependent information processing. Thalamocortical circuits generate slow (0.25–4 Hz) oscillations reflecting synchronized temporal windows of cortical activity, whereas concurrent waxing and waning spindle oscillations (8–15 Hz) act to facilitate cortical plasticity. Meanwhile, fast (140–200 Hz) and brief (< 200 ms) hippocampal ripple oscillations are associated with the reactivation of neural assemblies recruited during prior wakefulness. The extent of the forebrain areas engaged by these oscillations, and the variety of cellular and synaptic mechanisms involved, make them sensitive assays of distributed network function. Each of these three oscillations makes crucial contributions to the offline memory consolidation processes supported by non-rapid eye movement sleep. Slow, spindle and ripple oscillations are therefore potential surrogates of cognitive function and may be used as diagnostic measures in a range of brain diseases. We review the evidence for disrupted slow, spindle and ripple oscillations in schizophrenia, linking pathophysiological mechanisms to the functional impact of these neurophysiological changes and drawing links with the cognitive symptoms that accompany this condition. Finally, we discuss potential therapies that may normalize the coordinated activity of these three oscillations in order to restore healthy cognitive function.
    European Journal of Neuroscience 04/2014; 39(7). DOI:10.1111/ejn.12533 · 3.18 Impact Factor
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    • "In agreement with other experimental studies, our findings show that acoustic stimulation during SWS evokes a specific electrophysiological response, consisting of a strong hyperpolarization after about 500 ms followed by a depolarization, which is maximal at about 900 ms (Amzica and Steriade, 1998; Plihal et al., 1996; Riedner et al., 2011). A strong hyperpolarization followed by a depolarization is characteristic for the SOs that are detected as such by our algorithm. "
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    ABSTRACT: Slow oscillations are electrical potential oscillations with a spectral peak frequency of ∼0.8 Hz, and hallmark the electroencephalogram during slow-wave sleep. Recent studies have indicated a causal contribution of slow oscillations to the consolidation of memories during slow-wave sleep, raising the question to what extent such oscillations can be induced by external stimulation. Here, we examined whether slow oscillations can be effectively induced by rhythmic acoustic stimulation. Human subjects were examined in three conditions: (i) with tones presented at a rate of 0.8 Hz ('0.8-Hz stimulation'); (ii) with tones presented at a random sequence ('random stimulation'); and (iii) with no tones presented in a control condition ('sham'). Stimulation started during wakefulness before sleep and continued for the first ∼90 min of sleep. Compared with the other two conditions, 0.8-Hz stimulation significantly delayed sleep onset. However, once sleep was established, 0.8-Hz stimulation significantly increased and entrained endogenous slow oscillation activity. Sleep after the 90-min period of stimulation did not differ between the conditions. Our data show that rhythmic acoustic stimulation can be used to effectively enhance slow oscillation activity. However, the effect depends on the brain state, requiring the presence of stable non-rapid eye movement sleep.
    Journal of Sleep Research 08/2012; 22(1). DOI:10.1111/j.1365-2869.2012.01039.x · 3.35 Impact Factor
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    • "UP states have been demonstrated to underlie the " slow oscillation " which is a neocortical rhythm (<1 Hz) that occurs during the deeper stages of slow wave sleep and anesthesia (Steriade et al., 1993c; Steriade, 1997; Amzica and Steriade, 1998). The slow oscillation during slow wave sleep has been proposed to be involved in long-term memory consolidation in neocortex (Marshall and Born, 2007; Crunelli and Hughes, 2010). "
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    ABSTRACT: Despite the pronounced neurological deficits associated with mental retardation and autism, the degree to which neocortical circuit function is altered remains unknown. Here, we study changes in neocortical network function in the form of persistent activity states in the mouse model of fragile X syndrome--the Fmr1 knock-out (KO). Persistent activity states, or UP states, in the neocortex underlie the slow oscillation which occurs predominantly during slow-wave sleep, but may also play a role during awake states. We show that spontaneously occurring UP states in the primary somatosensory cortex are 38-67% longer in Fmr1 KO slices. In vivo, UP states reoccur with a clear rhythmic component consistent with that of the slow oscillation and are similarly longer in the Fmr1 KO. Changes in neocortical excitatory circuitry likely play the major role in this alteration as supported by three findings: (1) longer UP states occur in slices of isolated neocortex, (2) pharmacologically isolated excitatory circuits in Fmr1 KO neocortical slices display prolonged bursting states, and (3) selective deletion of Fmr1 in cortical excitatory neurons is sufficient to cause prolonged UP states whereas deletion in inhibitory neurons has no effect. Excess signaling mediated by the group 1 glutamate metabotropic receptor, mGluR5, contributes to the longer UP states. Genetic reduction or pharmacological blockade of mGluR5 rescues the prolonged UP state phenotype. Our results reveal an alteration in network function in a mouse model of intellectual disability and autism which may impact both slow-wave sleep and information processing during waking states.
    The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 10/2011; 31(40):14223-34. DOI:10.1523/JNEUROSCI.3157-11.2011 · 6.34 Impact Factor
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