Biology subjects

Castro, S.

Publications and source records attributed to Castro, S..

16 recordsLinked to original sources

bioRxiv2026

State-dependent top-down and bottom-up processes in gamma-band (~40 Hz) oscillations of the cat EEG

Cognitive processes rely on extensive thalamocortical and corticocortical recurrent interactions. The gamma frequency band ([~]40 Hz) of the electroencephalogram (EEG) emerges from these interactions. Importantly, cognitive processing depends on the interplay between bottom-up sensory inputs and top-down influences from higher-order cortical areas. However, the extent to which gamma-band oscillations are associated with directional patterns of functional interactions remains unclear. Therefore, the aim of this study was to investigate the directionality of gamma-band information flow during wakefulness (W) and sleep, under spontaneous conditions and in response to auditory stimulation. Cats were chronically implanted for polysomnographic recordings, with electrodes placed in multiple cortical and thalamic regions. Information-flow directionality was assessed using two complementary methods: (i) time-lag analysis of gamma-band amplitude envelopes between pairs of channels, and (ii) Granger Causality analysis of the same channel pairs. During quiet W gamma-band oscillations exhibited a predominantly top-down directional organization, from higher- to lower-order cortical areas, as well as from cortical regions to thalamic nuclei. Following auditory stimulation, a prominent gamma response emerged between 0.5 and 1.5 s after stimulus onset. Within this time window, distinct patterns of gamma-band information flow were observed depending on the nature of the stimulus. Specifically, a bottom-up directional predominance was observed for simple auditory stimuli (clicks), whereas top-down processing prevailed for complex variable stimuli. In contrast, no consistent directionality of information flow was observed during either NREM or REM sleep, regardless of whether auditory stimulation was present. These findings extend our understanding of gamma-band information-flow dynamics during wakefulness and sleep.

neuroscience↗

bioRxiv2025

Exploring the fog vegetation in the marginal Atacama Desert: common evolutionary history of species-rich genera and morphological convergence in Nolana and Heliotropium sect. Cochranea

The flora of the Atacama-Peru Desert (7{degrees}-30{degrees}S) is characterized by its remarkable diversity and adaptation in the driest place on Earth. It is composed of endemic and diverse genera, with most species having restricted geographic distributions. To infer its evolutionary history, the structure of a fog-dependent plant community in the Marginal Desert (27{degrees}-30{degrees}S) was characterized, with a special focus on congeners of Nolana and Heliotropium sect. Cochranea. Similarity profile analysis (SIMPROF) identified six plant assemblages differentially distributed along the altitudinal gradient. The congeners showed a pattern of niche segregation, with basal species N. rostrata and H. filifolium occupying the fog-influenced altitudinal range, while recently diverged species occurred outside its direct influence. To corroborate phylogenetic convergence, climatic zones were defined based on the presence of Nolana and Cochranea, and these were used to reconstruct ancestral areas and formulate a biogeographic hypothesis. The history of the Atacama Desert flora is marked by two periods: the formation of the hyperarid core (18{degrees}-27{degrees}S) during the late Miocene led to an initial divergence, leaving species isolated in different climatic zones. Then, beginning around 4 Mya, various wet phases promoted the northward geographic expansion of the flora inhabiting the Marginal Desert, with some genera reaching as far as Peru. Following geographic expansion, dry phases led to landscape-scale heterogeneity in water availability, promoting adaptive radiation. The ecological and phylogenetic affinities of N. rostrata and H. filifolium suggest that terete leaf morphology represents a case of evolutionary convergence associated with fog water capture.

plant biology↗

bioRxiv2024

Unique nigral and cortical pathways implicated by epigenomic and transcriptional analyses in a rotenone rat model of Parkinson's disease

Pesticide exposure is increasingly recognised as a potential environmental factor contributing to the onset of idiopathic Parkinsons disease, yet the molecular mechanisms underlying this connection remain unclear. This study aims to explore how pesticide exposure disrupts key brain regions involved in Parkinsons disease pathology by reshaping gene regulatory landscapes. Using the well-established rotenone rat model of the disease, we performed H3K27ac ChIP-sequencing to profile active regulatory elements in the substantia nigra and cortex. In this model, rotenone distributes uniformly throughout the brain, and the degree of complex I inhibition is equivalent in cortical and substantia nigra neurons. Despite the uniformity of complex I inhibition, we identified widespread epigenomic differences, with brain region specific acetylation patterns associated with rotenone exposure. We showed consistent changes in transcriptomic activity by RNA-sequencing. Our results indicate there is a strong immune response to rotenone localised to the substantia nigra and highlight an enrichment of immune-related motifs in this brain region, suggesting that the immune response is at least partially driven by gene regulatory mechanisms. We also noted an increase in C1q complement pathway activity in the substantia nigra. In contrast, we identified widespread dysregulation of synaptic function at the gene regulatory level in the cortex of these same rats. Our results highlight a role for gene regulatory mechanisms potentially mediating the effects of pesticide exposure, driving region-specific functional responses in the brain that may contribute to the pathology and selective vulnerability that characterise Parkinsons disease.

genomics↗

bioRxiv2024

15-Lipoxygenase-Mediated Lipid Peroxidation Regulates LRRK2 Kinase Activity

Mutations in leucine-rich repeat kinase 2 (LRRK2) that increase its kinase activity are strongly linked to genetic forms of Parkinsons disease (PD). However, the regulation of endogenous wild-type (WT) LRRK2 kinase activity remains poorly understood, despite its frequent elevation in idiopathic PD (iPD) patients. Various stressors such as mitochondrial dysfunction, lysosomal dyshomeostasis, or vesicle trafficking deficits can activate WT LRRK2 kinase, but the specific molecular mechanisms are not fully understood. We found that the production of 4-hydroxynonenal (4-HNE), a lipid hydroperoxidation end-product, is a common biochemical response to these diverse stimuli. 4-HNE forms post-translational adducts with Cys2024 and Cys2025 in the kinase activation loop of WT LRRK2, significantly increasing its kinase activity. Additionally, we discovered that the 4-HNE responsible for regulating LRRK2 is generated by the action of 15-lipoxygenase (15-LO), making 15-LO an upstream regulator of the pathogenic hyperactivation of LRRK2 kinase activity. Pharmacological inhibition or genetic ablation of 15-LO prevents 4-HNE post-translational modification of LRRK2 kinase and its subsequent pathogenic hyperactivation. Therefore, 15-LO inhibitors, or methods to lower 4-HNE levels, or the targeting of Cys2024/2025 could provide new therapeutic strategies to modulate LRRK2 kinase activity and treat PD.

neuroscience↗

bioRxiv2024

Compensating functional connectivity changesdue to structural connectivity damage viamodifications of local dynamics

Neurological pathologies as e.g. Alzheimers Disease or Multiple Sclerosis are often associated to neurodegenerative processes affecting the strength and the transmission speed of long-range inter-regional fiber tracts. Such degradation of Structural Connectivity impacts on large-scale brain dynamics and the associated Functional Connectivity, eventually perturbing network computations and cognitive performance. Functional Connectivity however is not bound to merely mirror Structural Connectivity, but rather reflects the complex coordinated dynamics of many regions. Here, using analytical characterizations of toy models and computational simulations connectome-base whole-brain models, we predict that suitable modulations of regional dynamics could precisely compensate for the effects of structural degradation, as if the original Structural Connectivity strengths and speeds of conduction were effectively restored. The required dynamical changes are widespread and aspecific (i.e. they do not need to be restricted to specific regions) so that they could be potentially implemented via neuromodulation or pharmacological therapy, globally shifting regional excitability and/or excitation/inhibition balance. Computational modelling and theory thus suggest that, in the future therapeutic interventions could be designed to "repair brain dynamics" rather than structure to boost functional connectivity without having to block or revert neurodegenerative processes. AUTHOR SUMMARYNeurological disorders affect Structural Connectivity, i.e. the wiring infrastructure interlinking distributed brain regions. Here we propose that the resulting disruptions in Functional Connectivity, i.e. inter-regional coordination and information sharing, could be compensated by modifying local dynamics so to effectively emulate the restoration of Structural Connectivity (but through a suitable "software patch" rather than by repairing the "hardware"). For simple toy models involving a few regions we can achieve an analytical understanding of how structural and dynamical changes jointly control Functional Connectivity. We then show that the concept of "effective connectome change" via modulation of dynamics robustly extend also to simulation of large-scale models embedding realistic whole-brain connectivity. We thus forecast that novel therapeutic strategies could be devised, targeting dynamics rather than neurodegenerative mechanisms.

neuroscience↗

bioRxiv2023

Can changes in ploidy drive the evolution to allogamy in a selfing species complex?

O_LIThe evolution of mating systems in plants is central for understanding the rise of their diversity on Earth. The transition towards self-fertilization is a well-known example of convergent evolution although the opposite direction is expected to be forbidden according to evolutionary theories. We suggest that the ploidy level could promote changes in the reproductive strategies through its effect on traits related to pollination. C_LIO_LIWe performed controlled crosses on several populations from the polyploid Erysimum incanum species complex, described as predominantly selfing, to evaluate the inbreeding depression. Additionally, we measured mating traits such as floral size, herkogamy, anther exertion, the relative investment in male and female components (P:O ratio) and genetic diversity. C_LIO_LIWe described three ploidy levels in the complex - hexaploids were unknown until now. We found significant differences in the self-pollination success among ploidies and even among populations within the same ploidy. Inbreeding depression was present in higher ploidies, accompanied by bigger flowers with higher anther exposure, increased herkogamy and P:O and genetic diversity. C_LIO_LIThese findings suggest that ploidy could be promoting alternative reproductive strategies to selfing, driving mating system diversification within a selfing species, which has not been previously described in the wild. C_LI

plant biology↗

bioRxiv2023

Cortical high-frequency oscillations ({approx} 110 Hz) in cats are state-dependent and enhanced by a subanesthetic dose of ketamine

Ketamine is an NMDA receptor antagonist that has both antidepressant and anesthetic properties. At subanesthetic doses, ketamine can cause transient psychosis in humans, and is used to model psychosis in experimental animals. In rodents, subanesthetic doses of ketamine increase the power of high-frequency oscillations (HFO, 100-180 Hz) in the electroencephalogram and field potentials, a frequency band linked to cognitive functions. However, the effects of ketamine in higher mammals, with more translatable relevance, are poorly investigated. Here, we have examined cortical HFO during wakefulness, sleep, and after administering a sub-anesthetic dose of ketamine (15 mg/kg), utilizing the cat as an animal model. Four cats were implanted with cortical electrodes for chronic polysomnographic recordings. HFO power, connectivity, information flow directionality, and their relationships with respiratory activity were analyzed. During wakefulness, but not during sleep, we found that HFO were coupled with the inspiratory phase of the respiration. After ketamine administration, HFO were enhanced significantly and remained associated with the inspiratory phase. The analysis of the information flow after ketamine suggest that HFO originate from the olfactory bulb and stream towards the prefrontal cortex. Accordingly, occluding the nostrils significantly reduced HFO power in both the olfactory bulb and prefrontal cortex. In contrast, auditory stimulation did not affect HFO. In conclusion, spontaneous cortical HFO show certain state-dependent features in cats, and enhancement of this rhythm by ketamine may disrupt cortical information processing, which could contribute to some of the neuropsychiatric manifestations associated with ketamine. HighlightsO_LIKetamine is used to model psychosis in humans and experimental animals C_LIO_LISubanesthetic doses of ketamine increase the power of high-frequency oscillations C_LIO_LIHigh-frequency oscillations are coupled with the inspiratory phase of respiration C_LIO_LIThese oscillations originate in the olfactory bulb and stream to the neocortex C_LIO_LINostril occlusion lowers high-frequency activity in the olfactory bulb and neocortex C_LI Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=69 SRC="FIGDIR/small/543142v1_ufig1.gif" ALT="Figure 1"> View larger version (34K): org.highwire.dtl.DTLVardef@e386feorg.highwire.dtl.DTLVardef@1b3c06aorg.highwire.dtl.DTLVardef@1d93ecorg.highwire.dtl.DTLVardef@1daa161_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2022

Ploidy effects on the relationship between floral phenotype, reproductive investment and fitness exhibited by an autogamous species complex

PremiseThe relationships between reproductive investment, phenotype and fitness have been broadly studied in cross-pollinated plants in contrast to selfing species, which are considered less interesting in this area because they are supposed to be a dead-end in any evolutionary pathway. Still, selfing plants are unique systems to study these questions since the position of reproductive structures and traits related to flower size play an important role in female and male pollination success. MethodErysimum incanum s.l. is a selfing species complex exhibiting three levels of ploidy: diploids, tetraploids and hexaploids. This species complex shows traits typically associated with the selfing syndrome. Here, we used 1609 plants belonging to these three ploidies to characterize floral phenotype and spatial configuration of reproductive structures, reproductive investment (pollen and ovules production) and plant fitness. Then, we explored the relationship between all these variables using structural equation modelling across ploidy levels. Key ResultsAn increase in ploidy level leads to bigger flowers with more exerted stamens and a greater amount of pollen and ovules. In addition, hexaploid plants exhibit higher absolute values for herkogamy which is positively correlated with fitness. Phenotypic traits and pollen production are indirectly selected by the relationship among ovules and fitness, maintained across ploidies. ConclusionsChanges in floral phenotypes, reproductive investment and fitness with the ploidy level suggests that genome duplication can be a driver for the reproductive strategy transitions by modifying the investment in pollen and ovules and linking them with plant phenotype and fitness.

evolutionary biology↗

bioRxiv2021

Hybridization and introgression are prevalent in Southern European Erysimum (Brassicaceae) species

Background and AimsHybridization is a common and important force in plant evolution. One of its outcomes is introgression - the transfer of small genomic regions from one taxon to another by hybridization and repeated backcrossing. This process is believed to be common in glacial refugia, where range expansions and contractions can lead to cycles of sympatry and isolation, creating conditions for extensive hybridization and introgression. Polyploidization is another genome-wide process with a major influence on plant evolution. Both hybridization and polyploidization can have complex effects on plant evolution. However, these effects are often difficult to understand in recently evolved species complexes. MethodsWe combined flow cytometry, transcriptomic and genomic analyses, and pollen-tube growth assays to investigate the consequences of polyploidization, hybridization, and introgression on the recent evolution of several Erysimum (Brassicaceae) species from the South of the Iberian Peninsula, a well-known glacial refugium. This species complex differentiated in the last 2Myr, and its evolution has been hypothesized to be determined mainly by polyploidization, interspecific hybridization, and introgression. Key ResultsOur results support a scenario of widespread hybridization involving both extant and "ghost" taxa. Several taxa studied here, most notably those with purple corollas, are polyploids, likely of allopolyploid origin. Moreover, hybridization in this group might be an ongoing phenomenon, as prezygotic barriers appeared weak in many cases. ConclusionsThe evolution of Erysimum spp. has been determined by hybridization to a large extent. The adaptive value of such genomic exchanges remains unclear, but our results indicate the importance of hybridization for plant diversification across evolutionary scales.

evolutionary biology↗

bioRxiv2020

Protection from α-synuclein-induced dopaminergic neurodegeneration by overexpression of the mitochondrial import receptor TOM20 in the rat midbrain

Dopaminergic neurons of the substantia nigra are selectively vulnerable to mitochondrial dysfunction, which is hypothesized to be an early and fundamental pathogenic mechanism in Parkinsons disease (PD). Mitochondrial function depends on the successful import of nuclear-encoded proteins, many of which are transported through the TOM20-TOM22 outer mitochondrial membrane import receptor machinery. Recent data suggests that post-translational modifications of -synuclein promote its interaction with TOM20 at the outer mitochondrial membrane and thereby inhibit normal protein import, which leads to dysfunction and death of dopaminergic neurons. As such, preservation of mitochondrial import in the face of -synuclein accumulation might be a strategy to prevent dopaminergic neurodegeneration, however, this is difficult to assess using current in vivo models of PD. To this end, we established an exogenous co-expression system, utilizing AAV2 vectors to overexpress human -synuclein and TOM20, individually or together, in the adult Lewis rat substantia nigra in order to assess whether TOM20 overexpression attenuates -synuclein-induced dopaminergic neurodegeneration. Twelve weeks after viral injection, we observed that AAV2-TOM20 expression was sufficient to prevent loss of nigral dopaminergic neurons caused by AAV2-Syn overexpression. The observed TOM20-mediated dopaminergic neuron preservation appeared to be due, in part, to the rescued import of nuclear-encoded mitochondrial electron transport chain proteins that were inhibited by -synuclein overexpression. In addition, TOM20 overexpression rescued the import of the chaperone protein GRP75/mtHSP70/mortalin, a stress-response protein involved in -synuclein-induced injury. Collectively, these data indicate that TOM20 expression prevents -synuclein-induced mitochondrial dysfunction, which is sufficient to rescue dopaminergic neurons in the adult rat brain.

neuroscience↗

bioRxiv2020

Electrocortical temporal complexity during wakefulness and sleep: an updated account

The states of sleep and wakefulness are critical physiological processes associated with different brain patterns of activity. The intracranial electroencephalogram allows us to measure these changes, thus, it is a critical tool for its study. Recently, we showed that the electrocortical temporal complexity decreased from wakefulness to sleep. Nevertheless, the origin of this complex activity remains a controversial topic due to the existence of possible artifacts contaminating the brain signals. In this work, we showed that complexity decreases during sleep, independently of the electrode configuration employed. This fact strongly suggests that the basis for the behavioral-state differences in complexity does not have an extracranial origin; i.e., generated from the brain.

neuroscience↗

bioRxiv2020

Cortical ignition dynamics is tightly linked to the core organisation of the human connectome

The capability of cortical regions to flexibly sustain an "ignited" state of activity has been discussed in relation to conscious perception or hierarchical information processing. Here, we investigate how the intrinsic propensity of different regions to get ignited is determined by the specific topological organisation of the structural connectome. More specifically, we simulated the resting-state dynamics of mean-field whole-brain models and assessed how dynamic multi-stability and ignition differ between a reference model embedding a realistic human connectome, and alternative models based on a variety of randomised connectome ensembles. We found that the strength of global excitation needed to first trigger ignition in a subset of regions is substantially smaller for the model embedding the empirical human connectome. Furthermore, when increasing the strength of excitation, the propagation of ignition outside of this initial core -which is able to self-sustain its high activity- is way more gradual than for any of the randomised connectomes, allowing for graded control of the number of ignited regions. We explain both these assets in terms of the exceptional weighed core-shell organisation of the empirical connectome, speculating that this topology of human structural connectivity may be attuned to support an enhanced ignition dynamic. Author summaryThe activity of the cortex in mammals constantly fluctuates in relation to cognitive tasks, but also during rest. The ability of brain regions to display ignition, a fast transition from low to high activity is central for the emergence of conscious perception and decision making. Here, using a biophysically inspired model of cortical activity, we show how the structural organization of human cortex supports and constrains the rise of this ignited dynamics in spontaneous cortical activity. We found that the weighted core-shell organization of the human connectome allows for a uniquely graded ignition. This graded ignition implies a smooth control of the ignition in cortical areas tuned by the global excitability. The smooth control cannot be replicated by surrogate connectomes, even though they conserve key local or global network properties. Indeed, the first trigger of ignition in the human cortex has the lowest global excitability and corresponds with the strongest interconnected areas, the ignition core. Finally, we suggest developmental and evolutionary constraints of the mesoscale organization that support this enhanced ignition dynamics in cortical activity.

neuroscience↗

bioRxiv2019

Programmable bacteria induce durable tumor regression and systemic antitumor immunity

SUMMARY PARAGRAPHSynthetic biology is driving a new era of medicine through the genetic programming of living cells1,2. This transformative approach allows for the creation of engineered systems that intelligently sense and respond to diverse environments, ultimately adding specificity and efficacy that extends beyond the capabilities of molecular-based therapeutics3-5. One particular focus area has been the engineering of bacteria as therapeutic delivery systems to selectively release therapeutic payloads in vivo6-8. Here, we engineered a non-pathogenic E. coli to specifically lyse within the tumor microenvironment and release an encoded nanobody antagonist of CD47 (CD47nb)9, an anti-phagocytic receptor commonly overexpressed in several human cancers10,11. We show that intratumoral delivery of CD47nb by tumor-colonizing bacteria increases activation of tumor-infiltrating T cells, stimulates rapid tumor regression, prevents metastasis, and leads to long-term survival in a syngeneic tumor model. Moreover, we report that local injection of CD47nb bacteria stimulates systemic antitumor immune responses that reduce the growth of untreated tumors - providing, to the best of our knowledge, the first demonstration of an abscopal effect induced by a bacteria cancer therapy. Thus, engineered bacteria may be used for safe and local delivery of immunotherapeutic payloads leading to systemic antitumor immunity.

synthetic biology↗

bioRxiv2019

Engineered probiotics for local tumor delivery of checkpoint blockade nanobodies

Immunotherapies such as checkpoint inhibitors have revolutionized cancer therapy yet lead to a multitude of immune-related adverse events, suggesting the need for more targeted delivery systems. Due to their preferential colonization of tumors and advances in engineering capabilities from synthetic biology, microbes are a natural platform for the local delivery of cancer therapeutics. Here, we present an engineered probiotic bacteria system for the controlled production and release of novel immune checkpoint targeting nanobodies from within tumors. Specifically, we engineered genetic lysis circuit variants to effectively release nanobodies and safely control bacteria populations. To maximize therapeutic efficacy of the system, we used computational modeling coupled with experimental validation of circuit dynamics and found that lower copy number variants provide optimal nanobody release. Thus, we subsequently integrated the lysis circuit operon into the genome of a probiotic E. coli Nissle 1917, and confirmed lysis dynamics in a syngeneic mouse model using in vivo bioluminescent imaging. Expressing a nanobody against PD-L1 in this strain demonstrated enhanced efficacy compared to a plasmid-based lysing variant, and similar efficacy to a clinically relevant monoclonal antibody against PD-L1. Expanding upon this therapeutic platform, we produced a nanobody against cytotoxic T-lymphocyte associated protein -4 (CTLA-4), which reduced growth rate or completely cleared tumors when combined with a probiotically-expressed PD-L1 nanobody in multiple syngeneic mouse models. Together, these results demonstrate that our engineered probiotic system combines innovations in synthetic biology and immunotherapy to improve upon the delivery of checkpoint inhibitors. SENTENCE SUMMARYWe designed a probiotic platform to locally deliver checkpoint blockade nanobodies to tumors using a controlled lysing mechanism for therapeutic release.

synthetic biology↗

bioRxiv2018

Rapid screening of engineered microbial therapies in a 3-D multicellular model

Synthetic biology is transforming therapeutic paradigms by engineering living cells and microbes to intelligently sense and respond to diseases including inflammation1,2, infections3-5, metabolic disorders6,7, and cancer8,9. However, the ability to rapidly engineer new therapies far outpaces the throughput of animal-based testing regimes, creating a major bottleneck for clinical translation10,11. In vitro approaches to address this challenge have been limited in scalability and broad-applicability. Here, we present a bacteria-in-spheroid co-culture (BSCC) platform that simultaneously tests host species, therapeutic payloads and synthetic gene circuits of engineered bacteria within multicellular spheroids over a timescale of weeks. Long-term monitoring of bacterial dynamics and disease progression enables quantitative comparison of critical therapeutic parameters such as efficacy and biocontainment. Specifically, we screen S. typhimurium strains expressing and delivering a library of antitumor therapeutic molecules via several synthetic gene circuits. We identify novel candidates exhibiting significant tumor reduction and demonstrate high similarity in their efficacies using a syngeneic mouse model. Lastly, we show that our platform can be expanded to dynamically profile diverse microbial species including L. monocytogenes, P. mirabilis, and E. coli in various host cell types. This high-throughput framework may serve to accelerate synthetic biology for clinical applications and understanding the host-microbe interactions in disease sites.

synthetic biology↗

bioRxiv2017

Is chaos making a difference? Synchronization transitions in chaotic and non-chaotic neuronal networks

Chaotic dynamics of neural oscillations has been shown at the single neuron and network levels, both in experimental data and numerical simulations. Theoretical studies over the last twenty years have demonstrated an underlying role of chaos in neural systems. Nevertheless, whether chaotic neural oscillators make a significant contribution to relevant network behavior and whether the dynamical richness of neural networks are sensitive to the dynamics of isolated neurons, still remain open questions. We investigated transition dynamics of a medium-sized heterogeneous neural network of neurons connected by electrical coupling in a small world topology. We make use of an oscillatory neuron model (HB+Ih) that exhibits either chaotic or non-chaotic behavior at different combinations of conductance parameters. Measuring order parameter as a measure of synchrony, we find that the heterogeneity of firing rate and types of firing patterns make a greater contribution than chaos to the steepness of synchronization transition curve. We also show that chaotic dynamics of the isolated neurons do not always make a visible difference in process of network synchronization transitions. Moreover, the macroscopic chaos is observed regardless of the dynamics nature of the neurons. However, performing a Functional Connectivity Dynamics analysis, we show that chaotic nodes can promote what is known as the multi-stable behavior, where the network dynamically switches between a number of different semi-synchronized, metastable states.

biophysics↗