Experimental Brain Research最新文献

The concurrent effects of volitional breathing on motor-related brain regions have been documented in several studies, but it remains uncertain whether its after-effects influence neural processes involved in motor preparation. This study investigated whether a brief slow-paced breathing intervention alters the dynamics of the Bereitschaftspotential (BP) preceding voluntary movement. Thirty healthy participants were randomly assigned to a slow-paced breathing (SB) group (n = 15), who performed 5 min of 0.1-Hz breathing, or to a resting breathing (RB) group (n = 15). Before and after the intervention, participants executed self-paced isometric right index finger abductions while electroencephalography, electromyography, force output, end-tidal carbon dioxide (ETCO₂), and alertness were recorded. ETCO₂ was also monitored during the intervention. BP amplitudes were quantified for the early component associated with the supplementary motor area (Cz and Fz; - 800 to - 500 ms) and the late component associated with the primary motor cortex (C3; - 300 to 0 ms). Mixed-design ANOVAs revealed significant Group × Phase interactions for both early and late BP components (p < 0.01), with increased negativity after the intervention only in the SB group. Normalized electromyographic activity and force output remained unchanged, and subjective alertness showed a small overall decline that did not differ between groups. Within the SB group, lower absolute ETCO₂ levels during the intervention were associated with a more negative early BP amplitude after the intervention (ρ = 0.521, p = 0.049), whereas no correlation was found for the late BP. These findings suggest that a short session of SB enhances preparatory cortical activity, reflected in increased early and late BP components. Early BP enhancement was linked to lower ETCO₂ levels during the breathing task, indicating modulation of supplementary motor area excitability. SB may offer a simple, noninvasive means to alter cortical preparatory states.

Spinal dysfunction at the occipito-atlantal (C0-C1) joint complex in conjunction with other spinal regions induces maladaptive plasticity from processing altered neck sensory input, yielding poor head and neck proprioception. Past work found that the One-to-Zero (OTZ) system, which manipulated the C0-C1 joint prior to other regions of joint dysfunction, improves cervical kinesthesia likely by impacting the proprioceptors that are densely located around the C0-C1joint. The aim of the current study was to determine the impact of OTZ on cervical kinesthesia, as compared to no treatment. A pragmatic, parallel group RCT conducted at a private practice randomized 72 participants (ages 18 to 65), into treatment (T) (n = 36) or control (C) (n = 36) groups. T received OTZ treatment until initial symptoms improved by 80%. Neck ranges of motion (ROM), and cervical kinesthesia (head to neutral (HtoN) and head to target (HtoT) at 50 and 65% of maximum head rotation were measured with eyes closed at baseline and after T (two to six weeks) or C period (2 weeks). Three trials per side were performed for all head repositioning tests, with trial error used to calculate repositioning errors. Significant time by group interactions were found for the primary outcome measure of HtoT-50%: Absolute, constant and variable error improved to a greater extent for T. HtoN: Constant error on the right side improved for C, while variable error improved more for T on both right and left sides. Secondary outcomes- significant time by group interactions were found for: Range of motion (neck extension, lateral flexion, and rotation); Visual analog pain ratings and Neck disability which all improved more for T. Selective improvements in neck kinesthesia in association with improved mobility suggest that the OTZ system normalizes proprioceptive afferent feedback resulting in short-term improvements in neck proprioception.

Visual perception enables goal-directed movement control by mapping sensory input onto motor representations. While neural mechanisms of visuomotor integration have been extensively studied, the temporal dynamics of this process during real and mentally simulated movements remain poorly understood, particularly regarding stimulus-driven versus response-driven motor cortex contributions. We used transcranial magnetic stimulation (TMS) and electroencephalography (EEG) to investigate cortical activity during physical and imagined hand movements in a stimulus-response task. Single-pulse TMS was delivered to the primary motor cortex at 100, 200, and 400 ms following visual stimulus presentation to probe corticospinal excitability. Motor cortex facilitation during early preparation was found to be stimulus-locked rather than motor response-locked, indicating that visual cues drive initial motor cortex activation. Both motor execution (ME) and kinesthetic motor imagery (kMI) showed similar facilitation dynamics during this early stage, supporting functional equivalence during preparatory processing. However, ME and kMI diverged at later response stages: ME showed elevated excitability whereas in kMI it returned to baseline. EEG analyses confirmed this dissociation at later stages. Notably, kMI did not produce significant hemispheric lateralization, whereas ME generated robust lateralized readiness potentials whose duration correlated with pre-response motor excitability and behavioral performance. These findings challenge conventional response-driven conceptualizations of motor imagery and highlight stimulus-driven mechanisms in visuomotor processing during both overt and imagined movements.

Postoperative cognitive dysfunction is a type of cognitive impairment that occurs after surgery. Here, this experiment investigated the role of PLCG1 in sevoflurane-induced model and the molecular mechanisms underlying its regulation of ferroptosis. Single-cell RNA sequencing data and bioinformatic analyses were performed using GEO datasets (GSE196239). Mice were exposed to 2.3% sevoflurane for 2 h daily for 3 consecutive days. PLCG1 expression was up-regulation in patients exposed to sevoflurane. Specifically, blood samples from these patients exhibited elevated levels of PLCG1 mRNA. Consistently, in a mouse model of sevoflurane exposure, both mRNA and protein levels of PLCG1 were significantlyincreased in brain tissue. Single-cell RNA sequencing analysis revealed that PLCG1 was predominantly expressed in astrocytes (marked by AQP4, GFAP, LUZP2, and SLC25A28) and neurons (marked by B3GAT2, ENO2, GNG2, and SLC1A1) in sevoflurane-exposed patients. In contrast, PLCG1 expression was undetectable in B cells (CD74, CD79B, CD80, CD86), T cells (CD4, CD8B, CD69, CD247), or macrophages (CD36, CD68, CD83, CD163). In conclusion, PLCG1 drives neuronal ferroptosis in the context of sevoflurane exposure by enhancing mitochondrial oxidative stress and facilitating LAMP2A ubiquitination, thereby impairing the LAMP2A/HSPA8 pathway. These findings position PLCG1 as a promising biomarker and potential therapeutic target for monitoring and mitigating sevoflurane-induced neurotoxicity. In conclusion, PLCG1 drives neuronal in the context of sevoflurane exposure by enhancing mitochondrial oxidative stress and facilitating LAMP2A Ubiquitination, thereby impairing the LAMP2A/HSPA8 pathway. These findings position PLCG1 as a promising biomarker and potential therapeutic target for monitoring and mitigating sevoflurane-induced neurotoxicity.