@article{MTMT:3318885, title = {Dual function of thalamic low-vigilance state oscillations: Rhythm-regulation and plasticity}, url = {https://m2.mtmt.hu/api/publication/3318885}, author = {Crunelli, V and Lőrincz, László Magor and Connelly, WM and David, F and Hughes, SW and Lambert, RC and Leresche, N and Errington, AC}, doi = {10.1038/nrn.2017.151}, journal-iso = {NAT REV NEUROSCI}, journal = {NATURE REVIEWS NEUROSCIENCE}, volume = {19}, unique-id = {3318885}, issn = {1471-003X}, abstract = {During inattentive wakefulness and non-rapid eye movement (NREM) sleep, the neocortex and thalamus cooperatively engage in rhythmic activities that are exquisitely reflected in the electroencephalogram as distinctive rhythms spanning a range of frequencies from <1 Hz slow waves to 13 Hz alpha waves. In the thalamus, these diverse activities emerge through the interaction of cell-intrinsic mechanisms and local and long-range synaptic inputs. One crucial feature, however, unifies thalamic oscillations of different frequencies: repetitive burst firing driven by voltage-dependent Ca(2+) spikes. Recent evidence reveals that thalamic Ca(2+) spikes are inextricably linked to global somatodendritic Ca(2+) transients and are essential for several forms of thalamic plasticity. Thus, we propose herein that alongside their rhythm-regulation function, thalamic oscillations of low-vigilance states have a plasticity function that, through modifications of synaptic strength and cellular excitability in local neuronal assemblies, can shape ongoing oscillations during inattention and NREM sleep and may potentially reconfigure thalamic networks for faithful information processing during attentive wakefulness.}, year = {2018}, eissn = {1471-0048}, pages = {107-118} } @article{MTMT:30759295, title = {The K-complex as a special reactive sleep slow wave - A theoretical update.}, url = {https://m2.mtmt.hu/api/publication/30759295}, author = {Halász, Péter}, doi = {10.1016/j.smrv.2015.09.004}, journal-iso = {SLEEP MED REV}, journal = {SLEEP MEDICINE REVIEWS}, volume = {29}, unique-id = {30759295}, issn = {1087-0792}, year = {2016}, eissn = {1532-2955}, pages = {34-40} } @article{MTMT:2889024, title = {A Distinct Class of Slow ( approximately 0.2-2 Hz) Intrinsically Bursting Layer 5 Pyramidal Neurons Determines UP/DOWN State Dynamics in the Neocortex}, url = {https://m2.mtmt.hu/api/publication/2889024}, author = {Lőrincz, László Magor and Gunner, D and Bao, Y and Connelly, WM and Isaac, JT and Hughes, SW and Crunelli, V}, doi = {10.1523/JNEUROSCI.3603-14.2015}, journal-iso = {J NEUROSCI}, journal = {JOURNAL OF NEUROSCIENCE}, volume = {35}, unique-id = {2889024}, issn = {0270-6474}, abstract = {During sleep and anesthesia, neocortical neurons exhibit rhythmic UP/DOWN membrane potential states. Although UP states are maintained by synaptic activity, the mechanisms that underlie the initiation and robust rhythmicity of UP states are unknown. Using a physiologically validated model of UP/DOWN state generation in mouse neocortical slices whereby the cholinergic tone present in vivo is reinstated, we show that the regular initiation of UP states is driven by an electrophysiologically distinct subset of morphologically identified layer 5 neurons, which exhibit intrinsic rhythmic low-frequency burst firing at approximately 0.2-2 Hz. This low-frequency bursting is resistant to block of glutamatergic and GABAergic transmission but is absent when slices are maintained in a low Ca(2+) medium (an alternative, widely used model of cortical UP/DOWN states), thus explaining the lack of rhythmic UP states and abnormally prolonged DOWN states in this condition. We also characterized the activity of various other pyramidal and nonpyramidal neurons during UP/DOWN states and found that an electrophysiologically distinct subset of layer 5 regular spiking pyramidal neurons fires earlier during the onset of network oscillations compared with all other types of neurons recorded. This study, therefore, identifies an important role for cell-type-specific neuronal activity in driving neocortical UP states.}, year = {2015}, eissn = {1529-2401}, pages = {5442-5458} } @article{MTMT:2506149, title = {Essential thalamic contribution to slow waves of natural sleep.}, url = {https://m2.mtmt.hu/api/publication/2506149}, author = {David, F and Schmiedt, JT and Taylor, HL and Orbán, Gergely and Di Giovanni, G and Uebele, VN and Renger, JJ and Lambert, RC and Leresche, N and Crunelli, V}, doi = {10.1523/JNEUROSCI.3169-13.2013}, journal-iso = {J NEUROSCI}, journal = {JOURNAL OF NEUROSCIENCE}, volume = {33}, unique-id = {2506149}, issn = {0270-6474}, abstract = {Slow waves represent one of the prominent EEG signatures of non-rapid eye movement (non-REM) sleep and are thought to play an important role in the cellular and network plasticity that occurs during this behavioral state. These slow waves of natural sleep are currently considered to be exclusively generated by intrinsic and synaptic mechanisms within neocortical territories, although a role for the thalamus in this key physiological rhythm has been suggested but never demonstrated. Combining neuronal ensemble recordings, microdialysis, and optogenetics, here we show that the block of the thalamic output to the neocortex markedly (up to 50%) decreases the frequency of slow waves recorded during non-REM sleep in freely moving, naturally sleeping-waking rats. A smaller volume of thalamic inactivation than during sleep is required for observing similar effects on EEG slow waves recorded during anesthesia, a condition in which both bursts and single action potentials of thalamocortical neurons are almost exclusively dependent on T-type calcium channels. Thalamic inactivation more strongly reduces spindles than slow waves during both anesthesia and natural sleep. Moreover, selective excitation of thalamocortical neurons strongly entrains EEG slow waves in a narrow frequency band (0.75-1.5 Hz) only when thalamic T-type calcium channels are functionally active. These results demonstrate that the thalamus finely tunes the frequency of slow waves during non-REM sleep and anesthesia, and thus provide the first conclusive evidence that a dynamic interplay of the neocortical and thalamic oscillators of slow waves is required for the full expression of this key physiological EEG rhythm.}, year = {2013}, eissn = {1529-2401}, pages = {19599-19610} } @article{MTMT:1536705, title = {Phase advancement and nucleus-specific timing of thalamocortical activity during slow cortical oscillation}, url = {https://m2.mtmt.hu/api/publication/1536705}, author = {Slézia, Andrea and Hangya, Balázs and Ulbert, István and Acsády, László}, doi = {10.1523/JNEUROSCI.3375-10.2011}, journal-iso = {J NEUROSCI}, journal = {JOURNAL OF NEUROSCIENCE}, volume = {31}, unique-id = {1536705}, issn = {0270-6474}, abstract = {The exact timing of cortical afferent activity is instrumental for the correct coding and retrieval of internal and external stimuli. Thalamocortical inputs represent the most significant subcortical pathway to the cortex, but the precise timing and temporal variability of thalamocortical activity is not known. To examine this question, we studied the phase of thalamic action potentials relative to cortical oscillations and established correlations among phase, the nuclear location of the thalamocortical neurons, and the frequency of cortical activity. The phase of thalamic action potentials depended on the exact frequency of the slow cortical oscillation both on long (minutes) and short (single wave) time scales. Faster waves were accompanied by phase advancement in both cases. Thalamocortical neurons located in different nuclei fired at significantly different phases of the slow waves but were active at a similar phase of spindle oscillations. Different thalamic nuclei displayed distinct burst patterns. Bursts with a higher number of action potentials displayed progressive phase advancement in a nucleus-specific manner. Thalamic neurons located along nuclear borders were characterized by mixed burst and phase properties. Our data demonstrate that the temporal relationship between cortical and thalamic activity is not fixed but displays dynamic changes during oscillatory activity. The timing depends on the precise location and exact activity of thalamocortical cells and the ongoing cortical network pattern. This variability of thalamic output and its coupling to cortical activity can enable thalamocortical neurons to actively participate in the coding and retrieval of cortical signals.}, keywords = {Animals; Male; RATS; Periodicity; Action Potentials; Rats, Wistar; Cerebral Cortex/*physiology; Neurons/physiology; Thalamus/*physiology}, year = {2011}, eissn = {1529-2401}, pages = {607-617}, orcid-numbers = {Slézia, Andrea/0000-0002-4528-3169; Ulbert, István/0000-0001-9941-9159} } @article{MTMT:1234812, title = {The human K-complex represents an isolated cortical down-state.}, url = {https://m2.mtmt.hu/api/publication/1234812}, author = {Cash, SS and Halgren, E and Dehghani, N and Rossetti, AO and Thesen, T and Wang, C and Devinsky, O and Kuzniecky, R and Doyle, W and Madsen, JR and Bromfield, E and Erőss, Loránd and Halász, Péter and Karmos, György and Csercsa, Richárd and Wittner, Lucia and Ulbert, István}, doi = {10.1126/science.1169626}, journal-iso = {SCIENCE}, journal = {SCIENCE}, volume = {324}, unique-id = {1234812}, issn = {0036-8075}, abstract = {The electroencephalogram (EEG) is a mainstay of clinical neurology and is tightly correlated with brain function, but the specific currents generating human EEG elements remain poorly specified because of a lack of microphysiological recordings. The largest event in healthy human EEGs is the K- complex (KC), which occurs in slow-wave sleep. Here, we show that KCs are generated in widespread cortical areas by outward dendritic currents in the middle and upper cortical layers, accompanied by decreased broadband EEG power and decreased neuronal firing, which demonstrate a steep decline in network activity. Thus, KCs are isolated "down-states," a fundamental cortico-thalamic processing mode already characterized in animals. This correspondence is compatible with proposed contributions of the KC to sleep preservation and memory consolidation.}, year = {2009}, eissn = {1095-9203}, pages = {1084-1087}, orcid-numbers = {Erőss, Loránd/0000-0002-5796-5546; Wittner, Lucia/0000-0001-6800-0953; Ulbert, István/0000-0001-9941-9159} }