ABSTRACT
We present high-density EEG datasets of auditory steady-state responses (ASSRs) recorded from the cortex of freely moving mice with or without optogenetic stimulation of basal forebrain parvalbumin (BF-PV) neurons, known as a subcortical hub circuit for the global workspace. The dataset of ASSRs without BF-PV stimulation (dataset 1) contains raw 36-channel EEG epochs of ASSRs elicited by 10, 20, 30, 40, and 50 Hz click trains and time stamps of stimulations. The dataset of ASSRs with BF-PV stimulation (dataset 2) contains raw 36-channel EEG epochs of 40-Hz ASSRs during BF-PV stimulation with latencies of 0, 6.25, 12.5, and 18.75 ms and time stamps of stimulations. We provide the datasets and step-by-step tutorial analysis scripts written in Python, allowing for descriptions of the event-related potentials, spectrograms, and the topography of power. We complement this experimental dataset with simulation results using a time-dependent perturbation on coupled oscillators. This publicly available dataset will be beneficial to the experimental and computational neuroscientists.
Subject(s)
Acoustic Stimulation , Basal Forebrain/cytology , Electroencephalography , Neurons/physiology , Animals , Evoked Potentials , MiceABSTRACT
High-density electroencephalographic (hdEEG) recordings are widely used in human studies to determine spatio-temporal patterns of cortical electrical activity. How these patterns of activity are modulated by subcortical arousal systems is poorly understood. Here, we couple selective optogenetic stimulation of a defined subcortical cell-type, basal forebrain (BF) parvalbumin (PV) neurons, with hdEEG recordings in mice (Opto-hdEEG). Stimulation of BF PV projection neurons preferentially generated time-locked gamma oscillations in frontal cortices. BF PV gamma-frequency stimulation potently modulated an auditory sensory paradigm used to probe cortical function in neuropsychiatric disorders, the auditory steady-state response (ASSR). Phase-locked excitation of BF PV neurons in advance of 40 Hz auditory stimuli enhanced the power, precision and reliability of cortical responses, and the relationship between responses in frontal and auditory cortices. Furthermore, synchronization within a frontal hub and long-range cortical interactions were enhanced. Thus, phasic discharge of BF PV neurons changes cortical processing in a manner reminiscent of global workspace models of attention and consciousness.
Subject(s)
Auditory Perception/physiology , Basal Forebrain/physiology , Evoked Potentials, Auditory , Gamma Rhythm , Neurons/physiology , Acoustic Stimulation , Animals , Electroencephalography , Male , Mice , Mice, Transgenic , Neurons/metabolism , Optogenetics , Parvalbumins/metabolismABSTRACT
The thalamocortical network serves a role in both consciousness and sensorimotor processing. However, little is known regarding how changes in conscious states, via induction of and recovery from anesthesia, affect the processing of sensorimotor information in the thalamocortical network. To address this, we investigated the dynamics of causal interactions among sensorimotor rhythms (SMR; frequency range of 3-12Hz) across the thalamocortical network during transitions into and out of ketamine-induced unconsciousness. Two local field potentials from the ventral lateral and ventrobasal thalamic nuclei, as well as two intracranial electroencephalography signals from the primary sensory and primary motor regions, were recorded in 10 mice. Spectral Granger causality analysis revealed two distinct frequency-specific patterns in sensorimotor rhythms. For the low-frequency (3-6.5Hz) SMR, loss of consciousness evoked causal influences directed from the cortex to the thalamus. For the high-frequency (6.5-12Hz) SMR, causal influences from the primary sensory cortex to other regions during the conscious period were abruptly altered by loss of consciousness and gradually regenerated following recovery of consciousness. The results of the present study indicate that anesthesia alters the flow of sensorimotor information in the thalamocortical network and may provide evidence of the neural basis of loss and recovery of sensorimotor function associated with anesthesia.
Subject(s)
Anesthesia , Brain Waves/physiology , Recovery of Function/physiology , Somatosensory Cortex/physiology , Thalamus/physiology , Analgesics/pharmacology , Animals , Electroencephalography , Ketamine/pharmacology , Male , Mice , Mice, Inbred C57BL , Neural Pathways/physiology , Recovery of Function/drug effects , Somatosensory Cortex/drug effects , Thalamus/drug effects , Thalamus/physiopathology , Time Factors , Unconsciousness/physiopathologyABSTRACT
OBJECTIVES: In patients with schizophrenia, γ-band (30-70 Hz) auditory steady-state electroencephalogram responses (ASSR) are reduced in power and phase locking. Here, we examined whether γ-ASSR deficits are also present in a mouse model of schizophrenia, whose behavioural changes have shown schizophrenia-like endophenotypes. METHODS: Electroencephalogram in frontal cortex and local field potential in primary auditory cortex were recorded in phospholipase C ß1 (PLC-ß1) null mice during auditory binaural click trains at different rates (20-50 Hz), and compared with wild-type littermates. RESULTS: In mutant mice, the ASSR power was reduced at all tested rates. The phase locking in frontal cortex was reduced in the ß band (20 Hz) but not in the γ band, whereas the phase locking in auditory cortex was reduced in the γ band. The cortico-cortical connectivity between frontal and auditory cortex was significantly reduced in mutant mice. CONCLUSIONS: The tested mouse model of schizophrenia showed impaired electrophysiological responses to auditory steady state stimulation, suggesting that it could be useful for preclinical studies of schizophrenia".
Subject(s)
Auditory Cortex/physiopathology , Evoked Potentials, Auditory , Frontal Lobe/physiopathology , Schizophrenia/physiopathology , Acoustic Stimulation , Animals , Disease Models, Animal , Electroencephalography , Humans , Male , Mice , Mice, Inbred C57BL , Mice, KnockoutABSTRACT
STUDY OBJECTIVE: Sleep spindles in humans have been classified as slow anterior and fast posterior spindles; recent findings indicate that their profiles differ according to pharmacology, pathology, and function. However, little is known about the generation mechanisms within the thalamocortical system for different types of spindles. In this study, we aim to investigate the electrophysiological behaviors of the topographically distinctive spindles within the thalamocortical system by applying high-density EEG and simultaneous thalamic LFP recordings in mice. DESIGN: 32-channel extracranial EEG and 2-channel thalamic LFP were recorded simultaneously in freely behaving mice to acquire spindles during spontaneous sleep. SUBJECTS: Hybrid F1 male mice of C57BL/6J and 129S4/svJae. MEASUREMENTS AND RESULTS: Spindle events in each channel were detected by spindle detection algorithm, and then a cluster analysis was applied to classify the topographically distinctive spindles. All sleep spindles were successfully classified into 3 groups: anterior, posterior, and global spindles. Each spindle type showed distinct thalamocortical activity patterns regarding the extent of similarity, phase synchrony, and time lags between cortical and thalamic areas during spindle oscillation. We also found that sleep slow waves were likely to associate with all types of sleep spindles, but also that the ongoing cortical decruitment/ recruitment dynamics before the onset of spindles and their relationship with spindle generation were also variable, depending on the spindle types. CONCLUSION: Topographically specific sleep spindles show distinctive thalamocortical network behaviors.
Subject(s)
Sleep/physiology , Algorithms , Animals , Cerebral Cortex/physiology , Cluster Analysis , Electroencephalography , Male , Mice , Mice, Inbred C57BL , Thalamus/physiologyABSTRACT
The thalamocortical system plays a key role in the breakdown or emergence of consciousness, providing bottom-up information delivery from sensory afferents and integrating top-down intracortical and thalamocortical reciprocal signaling. A fundamental and so far unanswered question for cognitive neuroscience remains whether the thalamocortical switch for consciousness works in a discontinuous manner or not. To unveil the nature of thalamocortical system phase transition in conjunction with consciousness transition, ketamine/xylazine was administered unobtrusively to ten mice under a forced working test with motion tracker, and field potentials in the sensory and motor-related cortex and thalamic nuclei were concomitantly collected. Sensory and motor-related thalamocortical networks were found to behave continuously at anesthesia induction and emergence, as evidenced by a sigmoidal response function with respect to anesthetic concentration. Hyperpolarizing and depolarizing susceptibility diverged, and a non-discrete change of transitional probability occurred at transitional regimes, which are hallmarks of continuous phase transition. The hyperpolarization curve as a function of anesthetic concentration demonstrated a hysteresis loop, with a significantly higher anesthetic level for transition to the down state compared to transition to the up state. Together, our findings concerning the nature of phase transition in the thalamocortical system during consciousness transition further elucidate the underlying basis for the ambiguous borderlines between conscious and unconscious brains. Moreover, our novel analysis method can be applied to systematic and quantitative handling of subjective concepts in cognitive neuroscience.