Neuronal avalanches in acute cortex slices. A, Light microscopic picture of the acute coronal brain slice and position of the microelectrode array. Cx, Cortex. B, Overplot of three different periods in which spontaneous, synchronized LFPs are visible. Three different periods (1-3) are shown (1 sec each) that reveal the occurrence of neuronal avalanches in three different, partially overlapping locations. For spatial location in the slice, see A. C, Raster plot of LFP activity in response to bath application of the NMDA receptor agonist NMDA and the D 1 receptor agonist SKF-38393. Note that synchronized events are visible across the array for 2000 sec after which the activity subsides. D, Individual event size distribution at t IEI avg from each acute slice experiment over plotted (n 9 acute slices). Black, Number of electrodes; gray, summed LFPs; broken line, power law with 3/2). E, Average event size distribution from data shown in D. Inset, Lifetime distributions of avalanches display a power law in initial portion with characteristic slope of 2 and exponential cutoff. Broken line, Power law with exponent of 2. 

Neuronal avalanches in acute cortex slices. A, Light microscopic picture of the acute coronal brain slice and position of the microelectrode array. Cx, Cortex. B, Overplot of three different periods in which spontaneous, synchronized LFPs are visible. Three different periods (1-3) are shown (1 sec each) that reveal the occurrence of neuronal avalanches in three different, partially overlapping locations. For spatial location in the slice, see A. C, Raster plot of LFP activity in response to bath application of the NMDA receptor agonist NMDA and the D 1 receptor agonist SKF-38393. Note that synchronized events are visible across the array for 2000 sec after which the activity subsides. D, Individual event size distribution at t IEI avg from each acute slice experiment over plotted (n 9 acute slices). Black, Number of electrodes; gray, summed LFPs; broken line, power law with 3/2). E, Average event size distribution from data shown in D. Inset, Lifetime distributions of avalanches display a power law in initial portion with characteristic slope of 2 and exponential cutoff. Broken line, Power law with exponent of 2. 

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Networks of living neurons exhibit diverse patterns of activity, including oscillations, synchrony, and waves. Recent work in physics has shown yet another mode of activity in systems composed of many nonlinear units interacting locally. For example, avalanches, earthquakes, and forest fires all propagate in systems organized into a critical state...

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... slice experiments. Coronal sections from adult rat brains (6 -8 weeks) were cut at 350 -400 m in chilled artificial CSF (ACSF) contain- ing the following (in mM): 124 NaCl, 0.3 NaH 2 PO 4 , 3.5 KCl, 1.2 CaCl 2 , 1 MgSO 4 , 26.2 NaHCO 3 , 10 D-glucose, and 50 M D,L-2-amino-5- phosphonovalerate (APV; Sigma, St. Louis, MO), saturated with 95% O 2 and 5% CO 2 (310 5 mOsm). Slices were stored submerged for 1-2 hr in ACSF without APV at room temperature before recording. For record- ing, slices were gently transferred onto the multielectrode array. The electrode array covered mostly supragranular layers of primary motor and somatosensory cortex. Electrode positions were reconstructed using pictures taken at the end of each recording session (see Fig. 6 A). Slices were submerged in ACSF without APV at 35.5 0.5°C saturated with 95% O 2 and 5% CO 2 and recordings were performed at a flow rate of 2 ...
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... neuronal propagation as described in the above para- graphs might be affected by the specific culture condition, we further examined propagation of synchronized, negative LFPs in mature, acute slices from rat primary motor and somatosensory cortex. Spontaneous activity was induced pharmacologically by increasing the NMDA-mediated sustained excitation in the cor- tical networks ( Seamans et al., 2001) through bath application of the glutamate receptor agonist NMDA and the dopamine D 1 - receptor agonist SKF-38393, which robustly induced spontane- ous LFP activity (Fig. 6). Similarly as in the organotypic cortex cultures, LFPs had a typical time course of a negative peak fol- lowed by a longer-lasting depolarization. Many electrodes initi- ated spontaneous LFPs in the acute slices, and neuronal ava- lanches typically encompassed a spatial extent of up to 10 -15 neighboring electrodes (Fig. 6 B). Spontaneous activity lasted on average for 1780 448 sec (n 9 acute slices) and correlation between LFPs declined sharply within 50 -80 msec, resulting in an IEI avg 3.73 0.467. At the closest integer of t 4 msec, this activity had a contiguity index of 28 9% and was composed of on average 505 420 avalanches (rate, 966 590 avalanches/ hr) (Fig. 6C). The event size distributions for spontaneous activ- ity in the acute slices clearly revealed the initial signature of the same power law as was described for the cultured networks (Fig. 6 D,E). The average initial slope values for acute slices were 1.50 0.08 for LFP (r 0.95; 10 -80 V) and 1.58 0.04 for electrode data (r 0.999; 1-8 electrodes). Thus, neuronal ava- lanches also exist in acute, mature cortex slices and display a characteristic exponent of 3/2. However, neuronal avalanches in acute slices are more compact and spatially restricted to fewer electrodes compared with the neuronal culture. This is indicated by the exponential cutoff of the power law (Fig. 6 E) and most likely reflects the severed long-range cortical connectivity in the acute slice. Finally, the lifetime distribution for neuronal avalanches in acute slices was also characterized by an initial slope close to 2 and an exponential cutoff, as was described for neuronal ava- lanches in organotypic cortex cultures (Fig. 6 E, ...
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... neuronal propagation as described in the above para- graphs might be affected by the specific culture condition, we further examined propagation of synchronized, negative LFPs in mature, acute slices from rat primary motor and somatosensory cortex. Spontaneous activity was induced pharmacologically by increasing the NMDA-mediated sustained excitation in the cor- tical networks ( Seamans et al., 2001) through bath application of the glutamate receptor agonist NMDA and the dopamine D 1 - receptor agonist SKF-38393, which robustly induced spontane- ous LFP activity (Fig. 6). Similarly as in the organotypic cortex cultures, LFPs had a typical time course of a negative peak fol- lowed by a longer-lasting depolarization. Many electrodes initi- ated spontaneous LFPs in the acute slices, and neuronal ava- lanches typically encompassed a spatial extent of up to 10 -15 neighboring electrodes (Fig. 6 B). Spontaneous activity lasted on average for 1780 448 sec (n 9 acute slices) and correlation between LFPs declined sharply within 50 -80 msec, resulting in an IEI avg 3.73 0.467. At the closest integer of t 4 msec, this activity had a contiguity index of 28 9% and was composed of on average 505 420 avalanches (rate, 966 590 avalanches/ hr) (Fig. 6C). The event size distributions for spontaneous activ- ity in the acute slices clearly revealed the initial signature of the same power law as was described for the cultured networks (Fig. 6 D,E). The average initial slope values for acute slices were 1.50 0.08 for LFP (r 0.95; 10 -80 V) and 1.58 0.04 for electrode data (r 0.999; 1-8 electrodes). Thus, neuronal ava- lanches also exist in acute, mature cortex slices and display a characteristic exponent of 3/2. However, neuronal avalanches in acute slices are more compact and spatially restricted to fewer electrodes compared with the neuronal culture. This is indicated by the exponential cutoff of the power law (Fig. 6 E) and most likely reflects the severed long-range cortical connectivity in the acute slice. Finally, the lifetime distribution for neuronal avalanches in acute slices was also characterized by an initial slope close to 2 and an exponential cutoff, as was described for neuronal ava- lanches in organotypic cortex cultures (Fig. 6 E, ...
Context 4
... neuronal propagation as described in the above para- graphs might be affected by the specific culture condition, we further examined propagation of synchronized, negative LFPs in mature, acute slices from rat primary motor and somatosensory cortex. Spontaneous activity was induced pharmacologically by increasing the NMDA-mediated sustained excitation in the cor- tical networks ( Seamans et al., 2001) through bath application of the glutamate receptor agonist NMDA and the dopamine D 1 - receptor agonist SKF-38393, which robustly induced spontane- ous LFP activity (Fig. 6). Similarly as in the organotypic cortex cultures, LFPs had a typical time course of a negative peak fol- lowed by a longer-lasting depolarization. Many electrodes initi- ated spontaneous LFPs in the acute slices, and neuronal ava- lanches typically encompassed a spatial extent of up to 10 -15 neighboring electrodes (Fig. 6 B). Spontaneous activity lasted on average for 1780 448 sec (n 9 acute slices) and correlation between LFPs declined sharply within 50 -80 msec, resulting in an IEI avg 3.73 0.467. At the closest integer of t 4 msec, this activity had a contiguity index of 28 9% and was composed of on average 505 420 avalanches (rate, 966 590 avalanches/ hr) (Fig. 6C). The event size distributions for spontaneous activ- ity in the acute slices clearly revealed the initial signature of the same power law as was described for the cultured networks (Fig. 6 D,E). The average initial slope values for acute slices were 1.50 0.08 for LFP (r 0.95; 10 -80 V) and 1.58 0.04 for electrode data (r 0.999; 1-8 electrodes). Thus, neuronal ava- lanches also exist in acute, mature cortex slices and display a characteristic exponent of 3/2. However, neuronal avalanches in acute slices are more compact and spatially restricted to fewer electrodes compared with the neuronal culture. This is indicated by the exponential cutoff of the power law (Fig. 6 E) and most likely reflects the severed long-range cortical connectivity in the acute slice. Finally, the lifetime distribution for neuronal avalanches in acute slices was also characterized by an initial slope close to 2 and an exponential cutoff, as was described for neuronal ava- lanches in organotypic cortex cultures (Fig. 6 E, ...
Context 5
... neuronal propagation as described in the above para- graphs might be affected by the specific culture condition, we further examined propagation of synchronized, negative LFPs in mature, acute slices from rat primary motor and somatosensory cortex. Spontaneous activity was induced pharmacologically by increasing the NMDA-mediated sustained excitation in the cor- tical networks ( Seamans et al., 2001) through bath application of the glutamate receptor agonist NMDA and the dopamine D 1 - receptor agonist SKF-38393, which robustly induced spontane- ous LFP activity (Fig. 6). Similarly as in the organotypic cortex cultures, LFPs had a typical time course of a negative peak fol- lowed by a longer-lasting depolarization. Many electrodes initi- ated spontaneous LFPs in the acute slices, and neuronal ava- lanches typically encompassed a spatial extent of up to 10 -15 neighboring electrodes (Fig. 6 B). Spontaneous activity lasted on average for 1780 448 sec (n 9 acute slices) and correlation between LFPs declined sharply within 50 -80 msec, resulting in an IEI avg 3.73 0.467. At the closest integer of t 4 msec, this activity had a contiguity index of 28 9% and was composed of on average 505 420 avalanches (rate, 966 590 avalanches/ hr) (Fig. 6C). The event size distributions for spontaneous activ- ity in the acute slices clearly revealed the initial signature of the same power law as was described for the cultured networks (Fig. 6 D,E). The average initial slope values for acute slices were 1.50 0.08 for LFP (r 0.95; 10 -80 V) and 1.58 0.04 for electrode data (r 0.999; 1-8 electrodes). Thus, neuronal ava- lanches also exist in acute, mature cortex slices and display a characteristic exponent of 3/2. However, neuronal avalanches in acute slices are more compact and spatially restricted to fewer electrodes compared with the neuronal culture. This is indicated by the exponential cutoff of the power law (Fig. 6 E) and most likely reflects the severed long-range cortical connectivity in the acute slice. Finally, the lifetime distribution for neuronal avalanches in acute slices was also characterized by an initial slope close to 2 and an exponential cutoff, as was described for neuronal ava- lanches in organotypic cortex cultures (Fig. 6 E, ...
Context 6
... neuronal propagation as described in the above para- graphs might be affected by the specific culture condition, we further examined propagation of synchronized, negative LFPs in mature, acute slices from rat primary motor and somatosensory cortex. Spontaneous activity was induced pharmacologically by increasing the NMDA-mediated sustained excitation in the cor- tical networks ( Seamans et al., 2001) through bath application of the glutamate receptor agonist NMDA and the dopamine D 1 - receptor agonist SKF-38393, which robustly induced spontane- ous LFP activity (Fig. 6). Similarly as in the organotypic cortex cultures, LFPs had a typical time course of a negative peak fol- lowed by a longer-lasting depolarization. Many electrodes initi- ated spontaneous LFPs in the acute slices, and neuronal ava- lanches typically encompassed a spatial extent of up to 10 -15 neighboring electrodes (Fig. 6 B). Spontaneous activity lasted on average for 1780 448 sec (n 9 acute slices) and correlation between LFPs declined sharply within 50 -80 msec, resulting in an IEI avg 3.73 0.467. At the closest integer of t 4 msec, this activity had a contiguity index of 28 9% and was composed of on average 505 420 avalanches (rate, 966 590 avalanches/ hr) (Fig. 6C). The event size distributions for spontaneous activ- ity in the acute slices clearly revealed the initial signature of the same power law as was described for the cultured networks (Fig. 6 D,E). The average initial slope values for acute slices were 1.50 0.08 for LFP (r 0.95; 10 -80 V) and 1.58 0.04 for electrode data (r 0.999; 1-8 electrodes). Thus, neuronal ava- lanches also exist in acute, mature cortex slices and display a characteristic exponent of 3/2. However, neuronal avalanches in acute slices are more compact and spatially restricted to fewer electrodes compared with the neuronal culture. This is indicated by the exponential cutoff of the power law (Fig. 6 E) and most likely reflects the severed long-range cortical connectivity in the acute slice. Finally, the lifetime distribution for neuronal avalanches in acute slices was also characterized by an initial slope close to 2 and an exponential cutoff, as was described for neuronal ava- lanches in organotypic cortex cultures (Fig. 6 E, ...
Context 7
... neuronal propagation as described in the above para- graphs might be affected by the specific culture condition, we further examined propagation of synchronized, negative LFPs in mature, acute slices from rat primary motor and somatosensory cortex. Spontaneous activity was induced pharmacologically by increasing the NMDA-mediated sustained excitation in the cor- tical networks ( Seamans et al., 2001) through bath application of the glutamate receptor agonist NMDA and the dopamine D 1 - receptor agonist SKF-38393, which robustly induced spontane- ous LFP activity (Fig. 6). Similarly as in the organotypic cortex cultures, LFPs had a typical time course of a negative peak fol- lowed by a longer-lasting depolarization. Many electrodes initi- ated spontaneous LFPs in the acute slices, and neuronal ava- lanches typically encompassed a spatial extent of up to 10 -15 neighboring electrodes (Fig. 6 B). Spontaneous activity lasted on average for 1780 448 sec (n 9 acute slices) and correlation between LFPs declined sharply within 50 -80 msec, resulting in an IEI avg 3.73 0.467. At the closest integer of t 4 msec, this activity had a contiguity index of 28 9% and was composed of on average 505 420 avalanches (rate, 966 590 avalanches/ hr) (Fig. 6C). The event size distributions for spontaneous activ- ity in the acute slices clearly revealed the initial signature of the same power law as was described for the cultured networks (Fig. 6 D,E). The average initial slope values for acute slices were 1.50 0.08 for LFP (r 0.95; 10 -80 V) and 1.58 0.04 for electrode data (r 0.999; 1-8 electrodes). Thus, neuronal ava- lanches also exist in acute, mature cortex slices and display a characteristic exponent of 3/2. However, neuronal avalanches in acute slices are more compact and spatially restricted to fewer electrodes compared with the neuronal culture. This is indicated by the exponential cutoff of the power law (Fig. 6 E) and most likely reflects the severed long-range cortical connectivity in the acute slice. Finally, the lifetime distribution for neuronal avalanches in acute slices was also characterized by an initial slope close to 2 and an exponential cutoff, as was described for neuronal ava- lanches in organotypic cortex cultures (Fig. 6 E, ...

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Transient or partial synchronization can be used to do computations, although a fully synchronized network is sometimes related to the onset of epileptic seizures. Here, we propose a homeostatic mechanism that is capable of maintaining a neuronal network at the edge of a synchronization transition, thereby avoiding the harmful consequences of a fully synchronized network. We model neurons by maps since they are dynamically richer than integrate-and-fire models and more computationally efficient than conductance-based approaches. We first describe the synchronization phase transition of a dense network of neurons with different tonic spiking frequencies coupled by gap junctions. We show that at the transition critical point, inputs optimally reverberate through the network activity through transient synchronization. Then, we introduce a local homeostatic dynamic in the synaptic coupling and show that it produces a robust self-organization toward the edge of this phase transition. We discuss the potential biological consequences of this self-organization process, such as its relation to the Brain Criticality hypothesis, its input processing capacity, and how its malfunction could lead to pathological synchronization and the onset of seizure-like activity.
... In preparation for the discussion of the field-theoretical model of cortical dynamics, we draw on empirical evidence supporting the decisive role of neurotransmitters in triggering phase transitions. To start with, the propagation of synchronized activity in cortical networks is shown to manifest as neuronal avalanches with sizes and lifetimes obeying power law scaling, which is indicative of a system operating in the critical regime (Beggs and Plenz, 2003;Lombardi et al., 2014;Arviv et al., 2019;Plenz et al., 2021). These avalanches reflect the collective organization of cortical activity (Arviv et al., 2019), a key finding being that this organization is driven by the neurotransmitters glutamate and gamma-aminobutyric acid (GABA), as well as the presence of neuromodulators, such as dopamine, serotonin, and acetylcholine (Stewart and Plenz, 2006;Plenz et al., 2021). ...
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Empirical evidence indicates that conscious states, distinguished by the presence of phenomenal qualities, are closely linked to synchronized neural activity patterns whose dynamical characteristics can be attributed to self-organized criticality and phase transitions. These findings imply that insight into the mechanism by which the brain controls phase transitions will provide a deeper understanding of the fundamental mechanism by which the brain manages to transcend the threshold of consciousness. This article aims to show that the initiation of phase transitions and the formation of synchronized activity patterns is due to the coupling of the brain to the zero-point field (ZPF), which plays a central role in quantum electrodynamics (QED). The ZPF stands for the presence of ubiquitous vacuum fluctuations of the electromagnetic field, represented by a spectrum of normal modes. With reference to QED-based model calculations, the details of the coupling mechanism are revealed, suggesting that critical brain dynamics is governed by the resonant interaction of the ZPF with the most abundant neurotransmitter glutamate. The pyramidal neurons in the cortical microcolumns turn out to be ideally suited to control this interaction. A direct consequence of resonant glutamate-ZPF coupling is the amplification of specific ZPF modes, which leads us to conclude that the ZPF is the key to the understanding of consciousness and that the distinctive feature of neurophysiological processes associated with conscious experience consists in modulating the ZPF. Postulating that the ZPF is an inherently sentient field and assuming that the spectrum of phenomenal qualities is represented by the normal modes of the ZPF, the significance of resonant glutamate-ZPF interaction for the formation of conscious states becomes apparent in that the amplification of specific ZPF modes is inextricably linked with the excitation of specific phenomenal qualities. This theory of consciousness, according to which phenomenal states arise through resonant amplification of zero-point modes, is given the acronym TRAZE. An experimental setup is specified that can be used to test a corollary of the theory, namely, the prediction that normally occurring conscious perceptions are absent under experimental conditions in which resonant glutamate-ZPF coupling is disrupted.