eNeuro最新文献

Episodic timing refers to the one-shot, automatic encoding of temporal information in the brain, in the absence of attention to time. A previous magnetoencephalography (MEG) study showed that the relative burst time of spontaneous alpha oscillations (α) during quiet wakefulness was a selective predictor of retrospective duration estimation. This observation was interpreted as α embodying the "ticks" of an internal contextual clock. Herein, we replicate and extend these findings using electroencephalography (EEG), assess robustness to time-on-task effects, and test the generalizability in virtual reality (VR) environments. In three EEG experiments, 128 participants of either sex underwent 4 min eyes-open resting-state recordings followed by an unexpected retrospective duration estimation task. Experiment 1 tested participants before any tasks, Experiment 2 after 90 min of timing tasks, and Experiment 3 in VR environments of different sizes. We successfully replicated the original MEG findings in Experiment 1 but did not in Experiment 2. We explain the lack of replication through time-on-task effects (changes in α power and topography) and contextual changes yielding a cognitive strategy based on temporal expectation (supported by a fast passage of time). In Experiment 3, we did not find the expected duration underestimation in VR and did not replicate the correlation between α bursts and retrospective time estimates. Overall, while EEG captures the α burst marker of episodic timing, its reliability depends critically on experimental context. Our findings highlight the importance of controlling experimental context when using α bursts as a neural marker of episodic timing.

Mirror invariance is the cognitive tendency to perceive mirror-image objects as identical. Mirrored letters, however, are distinct orthographic units and must be identified as different despite having the same shape. Consistent with this phenomenon, a small, localized region in the ventral visual stream, the Visual Word Form Area (VWFA), exhibits repetition suppression to both identical and mirror pairs of objects but only to identical, not mirror, pairs of letters ( Pegado et al., 2011), a phenomenon named mirror invariance "breaking". The ability of congenitally blind individuals to "break" mirror invariance for pairs of mirrored Braille letters has been demonstrated behaviorally ( de Heering et al., 2018, Korczyk et al., 2024). However, its neural underpinnings have not yet been investigated. Here, in an fMRI repetition suppression paradigm, congenitally blind individuals (8 males and 10 females) recognized pairs of everyday objects and Braille letters in identical ("p" and "p"), mirror ("p" and "q"), and different ("p" and "z") orientations. We found repetition suppression for identical and mirror pairs of everyday objects in the parietal and ventral-lateral occipital cortex, indicating that mirror-invariant object recognition engages the ventral visual stream in tactile modality as well. However, repetition suppression for identical but not mirrored pairs of Braille letters was found not in the VWFA, but in broad areas of the left parietal cortex and the lateral occipital cortex. These results suggest that reading-related orthographic processes in blind individuals depend on different neural computations than those of the sighted.

There has been a long-term need for a low-cost, highly efficient, and high-fidelity epilepsy monitoring unit (EMU) suitable for synchronized multimodal home-cage monitoring of small-animal models of epilepsy and spreading depolarization. We present an accessible, scalable, highly space- and energy-efficient EMU capable of fulfilling chronic, continuous, synchronized, multiple-animal monitoring jobs. Each rig within the EMU can provide 16-channel high-fidelity, DC-sensitive biopotential recordings, head acceleration monitoring, voltammetry applications, and synchronized video recording on one freely moving rat. We present the overall EMU architecture design and subsystem details in each recording rig. We demonstrate long-term continuous in vivo recordings of spontaneous seizure and seizure-associated spreading depolarization from freely moving rats (male, 21; female, 6) prepared under the tetanus toxin model of temporal lobe epilepsy.

The growing therapeutic promise of repeated, low-dose ketamine treatment across various psychopathologies-including depression and drug addiction-warrants clarity on its potential addictive properties and their associated mechanisms in both sexes. Accordingly, the present work examined the effects of intermittent low-dose ketamine in male and female rats on behavioral sensitization to the locomotor-activating effects of ketamine, as well as associated molecular profiles in dopamine D1- and D2-receptor-expressing medium spiny neurons (D1- and D2-MSNs) of the nucleus accumbens (NAc). Following intra-NAc infusion of a Cre-inducible RiboTag virus, locomotor activity was measured in adult Drd1a-iCre and Drd2-iCre male and female rats in either diestrus or proestrus following repeated administration of ketamine (0, 10, or 20 mg/kg, i.p.) to evaluate the development of locomotor sensitization. Female-but not male-rats developed sensitization to the locomotor-activating effects of ketamine, occurring more rapidly in proestrus than in diestrus females at the lower dose tested. To examine enduring context- and cell-type-specific changes in translating mRNAs associated with sensitization to ketamine, RNA sequencing was performed on polyribosome-bound mRNA of D1- and D2-MSNs isolated from the NAc of sensitized females in a drug-free state. A greater number of differentially expressed genes were observed selectively in D1-MSNs of ketamine-treated proestrus versus diestrus females, which were broadly related to regulation of transcription and epitranscriptional modification. These findings provide novel evidence of cell-type-specific and estrous cycle-dependent molecular profiles responsive to intermittent ketamine treatment in female rats and identify posttranscriptional mechanisms with relevance to ketamine's effects on behavioral plasticity.

The nigrostriatal and mesoaccumbal dopamine systems are thought to contribute to changes in behavior and learning during adolescence, yet it is unclear how the rise in gonadal hormones at puberty impacts the function of these systems. We studied the impact of prepubertal gonadectomy (GDX) on later evoked dopamine release in male Mus spicilegus, a mouse whose adolescent life history has been carefully characterized in the wild and laboratory. To examine how puberty impacts dopamine neuron function in M. spicilegus males, we removed the gonads prepubertally at postnatal day (P)25 and then examined evoked dopamine release in the dorsomedial, dorsolateral (DLS), and nucleus accumbens core regions of striatal slices at P60-70 (late adolescence/early adulthood). To measure dopamine release, we used near-infrared catecholamine nanosensors which enable study of spatial distribution of dopamine release. We found that prepubertal GDX led to a significantly reduced density of dopamine release sites and reduced dopamine release at each site in the DLS nigrostriatal system compared with sham controls. In contrast, mesoaccumbal dopamine release was comparable between sham and gonadectomized groups. Our data suggest that during adolescence, the development of the nigrostriatal dopamine system is significantly affected by the rise in gonadal hormones in males, while the mesoaccumbal system shows no detectable sensitivity at this time point. These data are consistent with molecular studies in rodents that suggest nigrostriatal neurons are sensitive to androgens at puberty and extend our understanding of how gonadal hormones could impact the spatial distribution and release potential of dopamine terminals in the striatum.

Speech in everyday life is often masked by background noise, making comprehension effortful. Characterizing brain activity patterns when individuals listen to masked speech can help clarify the mechanisms underlying such effort. In the current study, we used functional magnetic resonance imaging (fMRI) in humans of either sex to investigate how neural signatures of story listening change in the presence of masking noise. We show that, as speech masking increases, spatial and temporal activation patterns in auditory regions become more idiosyncratic to each listener. In contrast, spatial activity patterns in brain networks linked to effort (e.g., cingulo-opercular network) are more similar across listeners when speech is highly masked and less intelligible, suggesting shared neural processes. Moreover, at times during stories when one meaningful event ended and another began, neural activation increased in frontal, parietal, and medial cortices. This event-boundary response appeared little affected by background noise, suggesting that listeners process meaningful units and, in turn, the gist of naturalistic, continuous speech even when it is masked somewhat by background noise. The current data may indicate that people stay engaged and cognitive processes associated with naturalistic speech processing remain intact under moderate levels of noise, whereas auditory processing becomes more idiosyncratic to each listener.

The chemokine CXCL12 plays critical roles in the development of the hippocampus dentate gyrus during both embryogenesis and adulthood. While multiple cell types in the hippocampus express Cxcl12, their individual contributions to the dentate gyrus development and function remain unclear. Here, using Cxcl12 reporter mice of both sexes, we characterize Cxcl12 expression in Cajal-Retzius (CR) cells-neurons that guide dentate gyrus morphogenesis and influence hippocampal circuitry. We show that CR cells prominently express Cxcl12 during early postnatal development, although both the number and proportion of Cxcl12-expressing CR cells decline significantly in adulthood. Notably, partial deletion of Cxcl12 from hippocampal CR cells in male and female mice does not result in detectable changes in dentate gyrus architecture, adult neurogenesis, or specific behaviors. These findings suggest that CR cell-derived CXCL12 may be less critical for dentate gyrus development than previously assumed and underscore the complexity and potential redundancy of CXCL12 signaling in the hippocampus.