Biology subjects

Reboreda, A.

Publications and source records attributed to Reboreda, A..

5 recordsLinked to original sources

bioRxiv2026

Distinct regulation of intrinsic persistent firing by cholinergic, noradrenergic and dopaminergic neuromodulations in the mouse auditory cortex

Neuromodulators shape brain function by regulating neural activity in area- and state-dependent manners. While persistent firing (PF), a cellular correlate of short-term information retention, is strongly regulated by neuromodulation in executive and memory areas, such regulation in the sensory cortex remains less well understood. Here, using in vitro patch-clamp recordings, we investigated how cholinergic, noradrenergic, and dopaminergic systems regulate intrinsic PF in mouse auditory cortex (AC) neurons. We found that cholinergic and noradrenergic activation support PF, similar to observations in the prefrontal cortex (PFC) but unlike noradrenergic suppression seen in the hippocampus. In contrast, dopamine and D1 receptor activation showed no clear effect on AC PF, contrasting with their suppressive role in the PFC. Furthermore, PF was significantly stronger in corticocollicular than corticocallosal neurons. These findings reveal diverse monoamine regulation of intrinsic PF, offering a potential cellular basis for sensory information maintenance under conditions of stress and reward.

neuroscience↗

bioRxiv2025

Intrinsic persistent firing in CA1 encodes elapsed time across behaviorally relevant scales

The ability to encode and maintain temporal relationships is crucial for learning, predicting, and forming episodic memories. While hippocampal time cells and entorhinal temporal context cells are well-established in vivo, it remains unclear whether single neurons can sustain representations of elapsed time over multi-second intervals, independent of synaptic drive. Here, using whole-cell patchclamp recordings in rat hippocampal CA1 slices under synaptic blockade, we show that following a brief current pulse, many neurons exhibit exponentially decaying firing rates with a broad distribution of time constants extending to tens of seconds. This indicates that single neurons possess intrinsic mechanisms capable of covering behaviorally relevant temporal scales. These results highlight that single neurons can encode temporal information over more than an order of magnitude, providing a potential cellular substrate for temporal coding in the brain.

neuroscience↗

bioRxiv2025

Single neurons act as a memory buffer for space

Neurons are the fundamental units of cognitive processing. The prevailing view holds that neurons are input-output units that fire action potentials only upon receiving sufficient synaptic input. Here, we demonstrate that this may not be the sole operational mode of neurons in vivo during cognitive tasks, by showing that hippocampal place cells actively maintain firing and preserve spatial information through molecularly defined intrinsic mechanisms. Using in vitro and in vivo recordings coupled with molecular manipulation in mice, we reveal that hippocampal persistent firing during spatial working memory is supported by individual neurons via TRPC4 ion channels. Despite the general belief that persistent activity carries working memory content, we demonstrate that this firing maintains immediate spatial representations and is required for spatial working memory performance. These findings redefine neurons as active contributors to information retention, beyond their traditional role as passive input-output units, potentially reshaping our general understanding of computation in the brain.

neuroscience↗

bioRxiv2022

Grid cell disruption in a mouse model of early Alzheimer's disease reflects reduced integration of self-motion cues and increased influence of environmental geometry

Grid cell impairments and path integration deficits are sensitive markers of early Alzheimers disease (AD). Converging evidence from human and rodent studies suggest that disrupted grid coding underlies path integration deficits in preclinical individuals. However, it still remains unclear if disrupted early AD grid coding reflects increased noise across the network or a specific deficit in path integration, perhaps via an impairment in the integration of self-motion cues. Here, we report in the J20 transgenic amyloid beta mouse model of early AD that grid cells were spatially unstable towards the center of the square arena but not near the borders, had qualitatively different spatial components that aligned parallel to the borders of the environment, and exhibited impaired integration of distance travelled via reduced theta phase precession. Our results suggest that disrupted early AD grid coding reflects reduced integration of self-motion cues but not environmental landmarks, providing further evidence that grid cell impairments underlie specific path integration deficits in early AD.

neuroscience↗

bioRxiv2019

SGK1.1 activation causes early seizure termination via effects on M-current

Early termination of status epilepticus affords protection against brain damage and associated pathologies. Regulation of Kv7.2/7.3 potassium channels, underlying the neuronal M-current, is key for seizure control. This conductance is maintained during initiation of action potentials, affecting neuronal excitability and thus inhibiting epileptic discharges. The M-current is upregulated by the neuronal isoform of the serum and glucocorticoid-regulated kinase SGK1 (SGK1.1). We tested whether SGK1.1 is an anticonvulsant factor using the kainic acid (KA) model of acute seizures in a transgenic mouse model with expression of a constitutively active form of the kinase. Our results demonstrate that SGK1.1 confers robust protection against seizures associated to lower mortality levels, independently of sex or genetic background. SGK1.1-dependent protection results in reduced number, shorter duration, and early termination of EEG seizures. At the cellular level, it is associated to increased M-current amplitude mediated by Nedd4-2 phosphorylation, leading to decreased excitability of hippocampal CA1 neurons without alteration of basal synaptic transmission. Altogether, our results reveal that SGK1.1-mediated M-current upregulation in the hippocampus is a key component of seizure resistance in the KA epileptic paradigm, suggesting that regulation of this anticonvulsant pathway may improve adverse outcomes to status epilepticus, constituting a potential target for antiepileptic drugs.

neuroscience↗