Search bioRxiv⌕ Search

bioRxiv · 10.1101/2023.11.20.563492

Isolating Single Cycles of Neural Oscillations in Spiking Activity

Abstract

Neural oscillations are prominent features of brain activity, observable through frequency-specific power changes in electroencephalograms (EEG) and local field potentials (LFP). They also manifest as rhythmic coherence across brain regions. Although the identification of oscillations has primarily relied on EEG and LFP, the intrinsic relation between neural oscillations and neuronal spiking is noteworthy. We investigate the potential to detect individual cycles of neural rhythms solely through the spiking activity of neurons, leveraging recent advances in densely recording large populations of neurons within a local network. The numerous spikes from many neurons within a local network estimate the networks activity over time, enabling the identification of cyclic patterns. Here, we utilize a Long Short Term Memory (LSTM) network to effectively isolate and align individual cycles of neural oscillations from the spiking of a densely recorded population of neurons. We applied this network to robustly isolate specific cycles in different brain regions of mice across different time scales, from gamma to ultra-slow rhythms spanning durations of up to hundreds of seconds. These ultra-slow rhythms, which are usually cut off in the LFP, are also detected in behavioral measures of arousal, such as pupil size and mouse facial motion, and show delayed coherence with corresponding rhythms in the population spiking. We used the isolated neural cycles to investigate two questions: 1) With isolated gamma cycles driven by sensory input, we achieved a more precise alignment of the trials in sensory stimulation experiments in the primary visual cortex (V1) of mice. This alignment compensates for the biological variation in the transmission times of sensory signals from the retina to V1 across trials. As a result, we retrieve more accurate neural dynamics in response to sensory stimulation. 2) We used the distinct cycles in population spiking of simultaneously recorded regions to measure the correlated spiking across brain regions separately on different time scales. We observed that the delay in population spiking between brain regions varies according to brain regions and different time scales.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Sabri, E., Batista-Brito, R.. 2023-11-21. Isolating Single Cycles of Neural Oscillations in Spiking Activity. https://doi.org/10.1101/2023.11.20.563492

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Different hippocampal subfield volumes predict source memory performance and general cognitive ability in an adult lifespan sample

Modest positive associations between episodic memory performance and whole hippocampal and hippocampal subfield volumes have been reported in numerous prior studies. A smaller number of studies have reported associations between hippocampal volume and performance on tests of non-mnemonic cognition. The present study examined whether these associations were evident in a lifespan sample of cognitively healthy adults. Of particular interest was whether any identified associations were sensitive to age, and whether associations between subfield volumes and mnemonic and non-mnemonic performance were subfield dependent. We acquired high-resolution T1- and T2-weighted structural images from 163 adults (18-87 years of age). Participants also undertook a comprehensive neuropsychological test battery and an in-scanner test of source memory. Principal components analysis was employed to reduce the neuropsychological test scores to 5 cognitive components. Two components reflected memory performance while the other three reflected different aspects of non-mnemonic cognition. Hippocampal subfields (Cornu Ammonis (CA)1, CA2-3, dentate gyrus (DG) and subiculum) were segmented and measured with the Automated Segmentation of Hippocampus Subfields (ASHS) package. Source memory performance was selectively associated across participants with CA2-3 volume. By contrast, both mnemonic and non-mnemonic component scores derived from the test battery were associated exclusively with the volume of the DG. All associations were age-invariant. The findings indicate that different cognitive domains can be dissociated by virtue of their associations with different hippocampal subfields. Of importance, these associations appear to be life-long and hence are unlikely to reflect individual differences in age-related decline in structural integrity.

neuroscience↗

Cell type specific astrocytic feedback regulates excitation inhibition balance and cortical network dynamics

Astrocytes actively regulate synaptic transmission and neuronal excitability, yet their role in orchestrating macroscopic cortical network regimes and slow-wave oscillations remains an active area of reasearch. This study investigates how bidirectional neuron astrocyte interactions shape emergent population dynamics using a computational network model of excitatory and inhibitory neurons coupled to an astrocyte. The results identify astrocytic feedback topology, rather than astrocytic coupling strength alone, as a key determinant of emergent cortical network dynamics. By systematically dissecting pathway-specific connectivity, it has been shown that the neuronal population driving astrocytic activation and the neuronal population receiving gliotransmission jointly determine whether the network occupies asynchronous irregular (AI), synchronous irregular (SI), synchronous regular(SR), asynchronous regular(AR) or quiescent regimes.Directing gliotransmission selectively onto excitatory neurons consistently promotes population synchrony regardless of the population influencing astrocytic dynamics, whereas selective modulation of inhibitory interneurons induces network quiescence via strong suppression. Under dual-target gliotransmission, network synchrony is dictated by the population driving astrocytic dynamics: excitatory-only drive promotes synchrony, while combined or inhibitory-specific drive preserves asynchronous states. Furthermore, the model reveals that astrocytic signaling kinetics provide an additional temporal control mechanism that regulates the frequency and persistence of self sustained up states.

neuroscience↗

VCP inhibition prevents cone photoreceptor degeneration in the cpfl1 mouse model of achromatopsia

Achromatopsia (ACHM) is a rare autosomal recessive retinal disorder characterized by absent cone photoreceptor function from early life, leading to severe visual impairment. Mutations in genes involved in the cone phototransduction cascade frequently result in elevated cyclic guanosine monophosphate (cGMP) levels and activation of stress pathways, including endoplasmic reticulum (ER) stress and the unfolded protein response. Targeting common downstream mechanisms rather than individual mutations may provide a broadly applicable therapeutic strategy. Here, we investigated whether pharmacological inhibition of valosin-containing protein (VCP), a key regulator of ER and protein homeostasis, can prevent cone degeneration in the spontaneous cone photoreceptor function loss 1 (cpfl1) mouse model of ACHM. Organotypic culture of retinal explants from cpfl1 mice were treated with the selective VCP inhibitor ML240. Cone survival, cell death, opsin expression and localization were assessed by TUNEL assay, immunohistochemistry, and quantitative image analysis. ML240 treatment significantly increased cone density and improved cone opsin expression and trafficking to the outer segments (OSs) in cpfl1 explants compared to controls. Importantly, rhodopsin trafficking in rod photoreceptors was unaffected, indicating that VCP inhibition did not impair normal rod phototransduction. These findings demonstrate that VCP inhibition by ML240 effectively preserves cone photoreceptors and improves cone-specific functional markers in the cpfl1 model. Targeting VCP may represent a mutation-independent therapeutic strategy for preventing cone death in ACHM.

neuroscience↗