European Journal of Neuroscience最新文献

The aim of the present study was to determine if anodal transcutaneous spinal direct current stimulation (tsDCS) affects corticospinal excitability (CSE) and voluntary activation (VA) of the quadriceps femoris muscle (QM). This was a double-blind, randomized study in which spine-shoulder anodal tsDCS (active electrode centered over T11–12, 2.5 mA, 20 min) was applied in a seated position. Transcranial magnetic stimulation (TMS) was used to measure motor evoked potentials (MEP) and construct stimulus–response curves in healthy participants (eight females and five males, Experiment 1). VA was measured via the interpolated twitch technique, whereby muscle twitches were evoked using electrical femoral nerve stimulation and TMS (seven females and six males, Experiment 2). Measurements were carried out before, directly, and 30 min after sham and anodal tsDCS (with ≥4 days between sessions). There was no interaction between stimulation × time on stimulus–response curve expressed by slope, stimulus intensity corresponding to 50% of the maximal MEP, and peak-to-peak amplitude of the maximal MEP. Maximal voluntary isometric contraction (MVIC) torque did not change and VA was not affected regardless of the QM torque level (25, 50, or 100% of MVIC). A single, twenty-minute session of spine-shoulder anodal tsDCS did not increase CSE and VA of QM during submaximal and maximal contraction. This suggests that neither excitability to a known input nor responsiveness of motoneurons to submaximal and maximal cortical drive were affected by anodal tsDCS.

Duarte-Campos, J.F., Vázquez-Moreno, C.N., Martínez-Marcial, M., Chavarría, A., Ramírez-Carreto, R. J., Velasco Velázquez, M. A., De La Fuente-Granada, M., & González-Arenas, A. (2024). Changes in neuroinflammatory markers and microglial density in the hippocampus and prefrontal cortex of the C58/J mouse model of autism. European Journal of Neuroscience, 59(1), 154–173. https://doi.org/10.1111/ejn.16204

In the paper by Duarte-Campos et al. (2024), there were some errors in Figures 2 and 4. Western blot images from Figure 2g were missing some labels. The order of the blots from top to bottom is iNOS, α-tubulin, ARG-1 and α-tubulin.

In Figure 4a,c,e, the immunofluorescence images did not have labels indicating which images correspond to B6/J or C58/J animals. In all cases, the panels from the top correspond to B6/J animals and the bottom ones to the C58/J animals.

The corrected Figures 2 and 4 are shown below.

We apologize for these errors.

Regulator of G protein signalling 14 (RGS14) is a multifunctional signalling protein that serves as a natural suppressor of synaptic plasticity in the mouse brain. Our previous studies showed that RGS14 is highly expressed in postsynaptic dendrites and spines of pyramidal neurons in hippocampal area CA2 of the developing mouse brain. However, our more recent work with monkey brain shows that RGS14 is found in multiple neuron populations throughout hippocampal area CA1 and CA2, caudate nucleus, putamen, globus pallidus, substantia nigra and amygdala. In the mouse brain, we also have observed RGS14 protein in discrete limbic regions linked to reward behaviour and addiction, including the central amygdala and the nucleus accumbens, but a comprehensive mapping of RGS14 protein expression in the adult mouse brain is lacking. Here, we report that RGS14 is more broadly expressed in mouse brain than previously known. Intense RGS14 staining is observed in specific neuron populations of the hippocampal formation, amygdala, septum, bed nucleus of stria terminalis and ventral striatum/nucleus accumbens. RGS14 is also observed in axon fibre tracts including the dorsal fornix, fimbria, stria terminalis and the ventrohippocampal commissure. Moderate RGS14 staining is observed in various other adjacent regions not previously reported. These findings show that RGS14 is expressed in brain regions that govern aspects of core cognitive functions such as sensory perception, emotion, memory, motivation and execution of actions and suggest that RGS14 may serve to suppress plasticity and filter inputs in these brain regions to set the overall tone on experience-to-action processes.

The suprachiasmatic nucleus is the circadian pacemaker of the mammalian brain. Suprachiasmatic nucleus neurons display synchronization of their firing frequency on a circadian timescale, which is required for the pacemaker function of the suprachiasmatic nucleus. However, the mechanisms by which suprachiasmatic nucleus neurons remain synchronized in vivo are poorly understood, although synaptic communication is considered indispensable. Suprachiasmatic nucleus neurons contain the neurotransmitter GABA and express GABA receptors. This has inspired the hypothesis that GABA signalling may play a central role in network synchronization, although this remains untested in vivo. Here, using local genetic deletion, we show that disruption of GABA synaptic transmission within the suprachiasmatic nucleus of adult mice results in the eventual deterioration of physiological and behavioural rhythmicity in vivo and concomitant cellular desynchrony in vitro. These findings suggest that intercellular GABA signalling is essential for behavioural rhythmicity and cellular synchrony of the suprachiasmatic nucleus neural network.

Concentric and eccentric contractions show different patterns of neural activity at both peripheral and cortical levels, which are thought to influence the perception of action properties such as the weight of objects moved by others. The aim of this study was to investigate how the type of muscle contraction influences weight estimation during action observation.

Forty-eight volunteers completed the Main experiment and the Control experiment. In the Main experiment, they performed a weight discrimination video task in which they watched videos of an actor moving two objects, a comparison, and a reference box, executing concentric or eccentric contractions and they had to indicate which box was the heaviest. Sensitivity analysis and psychometric functions were used to analyse the data. In the Control experiment, observers judged the actor's effort in moving the boxes.

The results of the Main experiment showed that the weight discrimination sensitivity was higher in the eccentric condition for the light boxes. Conversely, for the heaviest boxes, discrimination sensitivity was higher in the concentric condition. These results were confirmed by the psychometric function analysis. The control experiment showed that the perceived difference in effort between the comparison and reference stimuli was greater in the eccentric than in the concentric condition for light stimuli.

These results showed that the ability to evaluate the weight of the object involved in the observed action was influenced by the type of contraction and the amount of weight. The effort attributed to the actor influenced the observer's perception.

Individual neurons of the hypothalamic suprachiasmatic nuclei (SCN) contain an intracellular molecular clock that drives these neurons to exhibit day-night variation in excitability. The neuropeptide vasoactive intestinal polypeptide (VIP) and its cognate receptor, VPAC₂, are synthesized by SCN neurons and this intercellular VIP-VPAC₂ receptor signal facilitates coordination of SCN neuronal activity and timekeeping. How the loss of VPAC₂ receptor signalling affects the electrophysiological properties and states of SCN neurons as well as their responses to excitatory inputs is unclear. Here we used patch-clamp electrophysiology and made recordings of SCN neurons in brain slices prepared from transgenic animals that do not express VPAC₂ receptors (Vipr2^−/− mice) as well as animals that do (Vipr2^+/+ mice). We report that while Vipr2^+/+ neurons exhibit coordinated day-night variation in their electrical state, Vipr2^−/− neurons lack this and instead manifest a range of states during both day and night. Further, at the population level, Vipr2^+/+ neurons vary the membrane threshold potential at which they start to fire action potentials from day to night, while Vipr2^−/− neurons do not. We provide evidence that Vipr2^−/− neurons lack a component of voltage-gated sodium currents that contribute to SCN neuronal excitability. Moreover, we determine that this aberrant temporal control of neuronal state and excitability alters neuronal responses to a neurochemical mimic of the light-input pathway to the SCN. These results highlight the critical role VIP-VPAC₂ receptor signalling plays in the temporal expression of individual neuronal states as well as appropriate ensemble activity and input gating of the SCN neural network.

The suprachiasmatic nucleus (SCN) is the master clock that directly dictates behavioural rhythms to anticipate the earth's light/dark cycles. Although post-transcriptional regulators called microRNAs have been implicated in physiological SCN function, how the absence of the entire mature miRNome impacts SCN output has not yet been explored. To study the behavioural consequences of miRNA depletion in the SCN, we first generated a mouse model in which Dicer is inactivated in the SCN by crossing Syt10^Cre mice with Dicer^flox mice to study behavioural consequences of miRNA depletion in the SCN. Loss of all mature miRNAs in the SCN shortened the circadian period length by ~37 minutes at the tissue level and by ~45 minutes at the locomotor activity level. Moreover, knockout animals exhibited a reduction in the precision of the circadian rhythm with more variable activity onsets under both LD 12:12 and DD conditions. We also observed that knockouts with higher onset variations were inclined to develop ultradian rhythms under constant light. In a second mouse model, recombination of Dicer^flox via Cre delivery specifically in the SCN resulted in loss of behavioural rhythms in some animals depending on the injection efficiency. Together, our observations highlight the importance of microRNAs for a physiological SCN function and their pivotal role in robust circadian oscillations.

Parkinson's disease (PD) is primarily characterized by three histological hallmarks: dopaminergic neuronal degeneration, α-synuclein accumulation and iron deposition. Over the last years, neuroimaging, particularly magnetic resonance imaging (MRI) has provided invaluable insights into the mechanisms underlying the disease. However, no imaging method has yet been able to translate α-synuclein protein accumulation and spreading. Amongst the animal models mimicking the disease, the α-synuclein rat, generated through the injection of human α-synuclein, has been characterized in terms of behavioural and histological aspects but not thoroughly explored in MRI. The aim of this study is, therefore, to identify the radiological signature from several MRI sequences, while controlling for histological and behavioural characteristics. Rats were assessed for motor and cognitive functions over a 4-month period. During this time, three MRI sessions, including both morphological and functional sequences, were conducted. Histological studies evaluated the three main hallmarks of PD. The progressive dopaminergic neurodegeneration and the spread of human α-synuclein corresponded to the level of sensorimotor, attentional and learning deficits observed in this PD model. MRI analyses showed progressive structural abnormalities in the midbrain, diencephalon and several cortical structures, as well as a pattern of hyperconnectivity in the basal ganglia and cortical networks. The regions affected in imaging demonstrated the highest load of human α-synuclein. This model's structural and functional MRI changes could serve as indirect indicators of α-synuclein accumulation and its association with impaired non-motor functions.

Sickness sleep and rebound following sleep deprivation share humoral signals including the rise of cytokines, in particular interleukins. Nevertheless, they represent unique physiological states with unique brain firing patterns and involvement of specific circuitry. Here, we performed untargeted metabolomics of mouse cortex and hippocampus to uncover changes with sickness and rebound sleep as compared with normal daily sleep. We found that the three settings are biochemically unique with larger differences in the cortex than in the hippocampus. Both sickness and rebound sleep shared an increase in tryptophan. Surprisingly, these two sleep conditions showed opposite modulation of the methionine–homocysteine cycle and differences in terms of the energetic signature, with sickness impinging on glycolysis intermediates whilst rebound increased the triphosphorylated form of nucleotides. These findings indicate that rebound following sleep deprivation stimulates an energy rich setting in the brain that is devoid during sickness sleep.