Central core modulation of spontaneous oscillations and sensory transmission in thalamocortical systems
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Active Dendrites and Local Field Potentials: Biophysical Mechanisms and Computational Explorations
2022, NeuroscienceCitation Excerpt :During NREM/slow wave sleep, cortical UP-DOWN states of alternating depolarization and hyperpolarization are observed that are associated with the generation of slow delta waves (∼1–4 Hz) and faster spindles (∼11–16 Hz) (Steriade and Timofeev, 2003; Fuentealba et al., 2004). Sleep spindles are generated by the interaction between the GABAergic neurons of the thalamic reticular nucleus and the thalamocortical nuclei, and are coupled to the cortical delta waves (Steriade, 1993c, b, a; Steriade et al., 1993c; Steriade et al., 1993b, a; Fernandez and Luthi, 2020). There is emerging evidence for a hippocampal-neocortical dialogue during NREM sleep through SPW-Rs, delta waves, and spindles, and for their role in learning, memory consolidation and interregional transfer of information (Buzsaki, 1996; Buzsaki and Peyrache, 2013; Buzsaki, 2015; Maingret et al., 2016; Seibt et al., 2016; Antony et al., 2019; Kim et al., 2019; Todorova and Zugaro, 2019; Karimi Abadchi et al., 2020; Peyrache and Seibt, 2020; Dickey et al., 2021).
Human subthalamic oscillatory dynamics following somatosensory stimulation
2018, Clinical NeurophysiologyCitation Excerpt :The post stimulation beta ERS has been suggested to serve as a selective deactivation process or “active inhibition” in the somatosensory cortex (Neuper and Pfurtscheller, 2001). Beta band activity has also been linked to enhanced alertness in thalamo-cortical systems, such that augmented beta oscillations suggest an activation of the somatosensory or motor cortex by motor preparation or focused attention (Steriade, 1993). Further evidence for attention related beta oscillations comes from the correlation of augmented sensorimotor beta power with attention focused on a motor event (Muthukumaraswamy and Singh, 2008) and an improvement in sensorimotor performance (Egner and Gruzelier, 2004; Vernon et al., 2003).
Attenuation of high-frequency (30-200 Hz) thalamocortical EEG rhythms as correlate of anaesthetic action: Evidence from dexmedetomidine
2017, British Journal of AnaesthesiaThe nonspecific thalamus: A place in a wedding bed for making memories last?
2015, Neuroscience and Biobehavioral ReviewsCitation Excerpt :The laterodorsal tegmental nucleus (LDTg) and the pedunculopontine tegmental nucleus (PPTg) provide cholinergic inputs to the thalamus, including the ILN, and to the cortex (e.g., Berendse and Groenewegen, 1991; Hallanger and Wainer, 1988; Herkenham, 1980; Rye et al., 1987;; rev Jones, 2004, Fig. 3B). The LDTg and PPTg are implicated in the switch from SWS to REM sleep or to wakefulness states by blocking spindle generation (e.g., Steriade, 1993; Steriade et al., 1990). Recent data showed that cells in the ARAS, particularly the PPTg neurons, exhibit both electrical coupling, mainly GABAergic, and gamma band activity, providing a new mechanism for sleep-wake control and consciousness maintenance (rev Urbano et al., 2012).
Cortical theta is increased while thalamocortical coherence is decreased in rat models of acute and chronic pain
2014, PainCitation Excerpt :Although electrophysiological techniques offer a good alternative, our understanding of the relationship between pain and network connectivity in the brain at the electrophysiological level is biased toward single-unit physiology under anesthesia, compared to multi-unit or population coding in the awake state [52]. Thalamocortical connections generate rhythmic activity referred to as oscillations, which are critical for the processing of sensory information [62]. Expectedly, painful sensory experiences modulate thalamocortical oscillations (oscillatory rhythms generated by reciprocal thalamocortical connections); however, the directionality of such modulation remains unresolved.
Cerebral mechanisms of general anesthesia
2014, Annales Francaises d'Anesthesie et de ReanimationCitation Excerpt :In the central nervous system, anesthetics target specific receptors that are drug-dependent [1]. A reasonable understanding of the pharmacological effects of anesthetics exists today [2], but very little is known regarding the neural mechanisms by which this receptor binding results in sedation and loss of consciousness. General anesthesia (GA) could be defined as a reversible drug-induced state leading to unconsciousness, amnesia, analgesia and immobility along with physiological stability [3].