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The Golgi apparatus is a central hub in the intracellular secretory pathway. By positioning in the specific intracellular region and transporting materials to spatially restricted compartments, the Golgi apparatus contributes to the cell polarity establishment and morphological specification in diverse cell types. In neurons, the Golgi apparatus mediates several essential steps of initial neural circuit formation during early brain development, such as axon-dendrite polarization, neuronal migration, primary dendrite specification, and dendritic arbor elaboration. Moreover, neuronal activity-dependent remodeling of the Golgi structure enables morphological changes in neurons, which provides the cellular basis of circuit reorganization during postnatal critical period. In this review, I summarize recent findings illustrating the unique Golgi positioning and its developmental dynamics in various types of neurons. I also discuss the upstream regulators for the Golgi positioning in neurons, and functional roles of the Golgi in neural circuit formation and reorganization. Elucidating how Golgi apparatus sculpts neuronal connectivity would deepen our understanding of the cellular/molecular basis of neural circuit development and plasticity.

Ischemic stroke triggers inflammation that promotes neuronal injury, leading to disruption of neural circuits and exacerbated neurological deficits in patients. Immune cells contribute to not only the acute inflammatory responses but also the chronic neural repair. During the post-stroke recovery, reparative immune cells support the neural circuit reorganization that occurs around the infarct region to connect broad brain areas. This review highlights the time-dependent changes of neuro-immune interactions and reorganization of neural circuits after ischemic brain injury. Understanding the molecular mechanisms involving immune cells in acute inflammation, subsequent neural repair, and neuronal circuit reorganization that compensate for the lost brain function is indispensable to establish treatment strategies for stroke patients.

Rhythmic brain activity is thought to reflect, and to help organize, spike activity in populations of neurons during on-going behavior. We report that during learning, a major transition occurs in task-related oscillatory activity in the ventromedial striatum, a striatal region related to motivation-dependent learning. Early on as rats learned a T-maze task, bursts of 70- to 90-Hz high-γ activity were prominent during T-maze runs, but these gradually receded as bursts of 15- to 28-Hz β-band activity became pronounced. Populations of simultaneously recorded neurons synchronized their spike firing similarly during both the high-γ–band and β-band bursts. Thus, the structure of spike firing was reorganized during learning in relation to different rhythms. Spiking was concentrated around the troughs of the β-oscillations for fast-spiking interneurons and around the peaks for projection neurons, indicating alternating periods of firing at different frequencies as learning progressed. Spike-field synchrony was primarily local during high-γ–bursts but was widespread during β-bursts. The learning-related shift in the probability of high-γ and β-bursting thus could reflect a transition from a mainly focal rhythmic inhibition during early phases of learning to a more distributed mode of rhythmic inhibition as learning continues and behavior becomes habitual. These dynamics could underlie changing functions of the ventromedial striatum during habit formation. More generally, our findings suggest that coordinated changes in the spatiotemporal relationships of local field potential oscillations and spike activity could be hallmarks of the learning process.

The plasticity of sensorimotor systems in mammals underlies the capacity for motor learning as well as the ability to relearn following injury. Spinal cord injury, which both deprives afferent input and interrupts efferent output, results in a disruption of cortical somatotopy. While changes in corticospinal axons proximal to the lesion are proposed to support the reorganization of cortical motor maps after spinal cord injury, intracortical horizontal connections are also likely to be critical substrates for rehabilitation-mediated recovery. Intrinsic connections have been shown to dictate the reorganization of cortical maps that occurs in response to skilled motor learning as well as after peripheral injury. Cortical networks incorporate changes in motor and sensory circuits at subcortical or spinal levels to induce map remodeling in the neocortex. This review focuses on the reorganization of cortical networks observed after injury and posits a role of intracortical circuits in recovery.

Descending neural pathways to the spinal cord plays vital roles in motor control. They are often damaged by brain injuries such as stroke and trauma, which lead to severe motor impairments. Due to the limited capacity for regeneration of neural circuits in the adult central nervous system, currently no essential treatments are available for complete recovery. Notably, accumulating evidence shows that residual circuits of the descending pathways are dynamically reorganized after injury and contribute to motor recovery. Furthermore, recent technological advances in cell-type classification and manipulation have highlighted the structural and functional diversity of these pathways. Here, we focus on three major descending pathways, namely, the corticospinal tract from the cerebral cortex, the rubrospinal tract from the red nucleus, and the reticulospinal tract from the reticular formation, and summarize the current knowledge of their structures and functions, especially in rodent models (mice and rats). We then review and discuss the process and patterns of reorganization induced in these pathways following injury, which compensate for lost connections for recovery. Understanding the basic structural and functional properties of each descending pathway and the principles of the induction and outcome of the rewired circuits will provide therapeutic insights to enhance interactive rewiring of the multiple descending pathways for motor recovery.

Aim To investigate the directional and selective disconnection of the sensorimotor cortex (SMC) subregions in chronic stroke patients with hand dysfunction. Methods We mapped the resting‐state fMRI effective connectivity (EC) patterns for seven SMC subregions in each hemisphere of 65 chronic stroke patients and 40 healthy participants and correlated these patterns with paretic hand performance. Results Compared with controls, patients demonstrated disrupted EC in the ipsilesional primary motor cortex_4p, ipsilesional primary somatosensory cortex_2 (PSC_2), and contralesional PSC_3a. Moreover, we found that EC values of the contralesional PSC_1 to contralesional precuneus, the ipsilesional inferior temporal gyrus to ipsilesional PSC_1, and the ipsilesional PSC_1 to contralesional postcentral gyrus were correlated with paretic hand performance across all patients. We further divided patients into partially (PPH) and completely (CPH) paretic hand subgroups. Compared with CPH patients, PPH patients demonstrated decreased EC in the ipsilesional premotor_6 and ipsilesional PSC_1. Interestingly, we found that paretic hand performance was positively correlated with seven sensorimotor circuits in PPH patients, while it was negatively correlated with five sensorimotor circuits in CPH patients. Conclusion SMC neurocircuitry was selectively disrupted after chronic stroke and associated with diverse hand outcomes, which deepens the understanding of SMC reorganization. Stroke remains the primary reason for adult disability, and hand function recovery is vital for survivors to regain quality of life. Here, we found two functional reorganization patterns in chronic stroke patients with different hand outcomes. For stroke patients with a partially paretic hand (PPH), all motor‐related sensorimotor circuits were positive, while for stroke patients with a completely paretic hand (CPH), this relationship was reversed. Meanwhile, the effective couplings among the PSC_1, inferior temporal gyrus, precuneus, and postcentral gyrus were correlated with hand performance in all stroke patients. PMC, primary motor cortex; PSC, primary somatosensory cortex.

Spinal cord injury (SCI) destroys the sensorimotor pathway and blocks the information flow between the peripheral nerve and the brain, resulting in autonomic function loss. Numerous studies have explored the effects of obstructed information flow on brain structure and function and proved the extensive plasticity of the brain after SCI. Great progress has also been achieved in therapeutic strategies for SCI to restore the \"re-innervation\" of the cerebral cortex to the limbs to some extent. Although no thorough research has been conducted, the changes of brain structure and function caused by \"re-domination\" have been reported. This article is a review of the recent research progress on local structure, functional changes, and circuit reorganization of the cerebral cortex after SCI. Alterations of structure and electrical activity characteristics of brain neurons, features of brain functional reorganization, and regulation of brain functions by reconfigured information flow were also explored. The integration of brain function is the basis for the human body to exercise complex/fine movements and is intricately and widely regulated by information flow. Hence, its changes after SCI and treatments should be considered.

In this paper, we review the history of the concept of neuroplasticity as it relates to the understanding of neuropsychiatric disorders, using schizophrenia as a case in point. We briefly review the myriad meanings of the term neuroplasticity, and its neuroscientific basis. We then review the evidence for aberrant neuroplasticity and metaplasticity associated with schizophrenia as well as the risk for developing this illness, and discuss the implications of such understanding for prevention and therapeutic interventions. We argue that the failure and/or altered timing of plasticity of critical brain circuits might underlie cognitive and deficit symptoms, and may also lead to aberrant plastic reorganization in other circuits, leading to affective dysregulation and eventually psychosis. This “dysplastic” model of schizophrenia can suggest testable etiology and treatment-relevant questions for the future.

Neural network contributing to forelimb task performance in the frontal cortex is dynamically reorganized by the necessity for volitional control of action. Neurons in the posterior medial prefrontal cortex (pmPFC) exhibit clear activity modulation when monkeys volitionally select the correct response tactic from multiple choices, but such activity disappears if selection of a tactic is unnecessary. Prompted by these results, we studied how the requirement to select an appropriate tactic affects the neural representation of action in downstream cortical areas. Two monkeys performed a spatial arm-reaching task with either left or right targets. The task required the monkeys to reach either toward (concordant trials) or away from (discordant trials) an illuminated target. Under the dual-tactic condition, concordant and discordant trials were randomly intermixed, requiring the selection of a response tactic. Under the single-tactic condition, only concordant trials were presented, allowing the monkeys to use the same tactic. Neurons in the pmPFC exhibited clear activity related to task performance under the former condition, but such activity disappeared under the latter condition. In contrast, neurons related to task performance were present under both conditions in supplementary motor area (SMA) and presupplementary motor area (pre-SMA). However, the efficacy of action representation by SMA but not pre-SMA neurons dramatically improved under the single-tactic condition. These results suggest that selection of the appropriate response tactic reorganizes neural circuits in specific motor areas in the medial frontal cortex, in addition to the pmPFC.

Stimulating sensory afferents can increase corticospinal excitability. Intensive use of a particular part of the body can also induce reorganization of neural circuits (use-dependent plasticity) in the central nervous system (CNS). What happens in the CNS when the nerve stimulation is applied in concert with the use of particular muscle groups? The purpose of this study was to investigate short-term effects of electrical stimulation of the common peroneal (CP) nerve during walking on motor-evoked potentials (MEPs) in the ankle flexors and extensors in healthy subjects. Since the stimulation was applied during the swing phase of the step cycle when the ankle flexors are active, this is referred to as functional electrical stimulation (FES). The following questions were addressed: (1) can FES during walking increase corticospinal excitability more effectively than passively received repetitive nerve stimulation and (2) does walking itself improve the descending connection. FES was delivered using a foot drop stimulator that activates ankle dorsiflexors during the swing phase of the step cycle. MEPs in the tibialis anterior (TA) and soleus muscles were measured before, between, and after periods of walking with or without FES, using transcranial magnetic stimulation. After 30 min of walking with FES, the half-maximum peak-to-peak MEP (MEP(h)) in the TA increased in amplitude and this facilitatory effect lasted for at least 30 min. In contrast, walking had no effects on the TA MEP(h) without FES. The increase in the TA MEP(h) with FES (approximately 40%) was similar to that with repetitive CP nerve stimulation at rest. The soleus MEP(h) was also increased after walking with FES, but not without FES, which differs from the previous observation with CP nerve stimulation at rest. With FES, the TA silent period at MEP(h) was unchanged or slightly decreased, while it increased after walking without FES. Increased cortical excitability accompanied by unchanged cortical inhibition (no changes in the silent period with FES) suggests that FES did not simply increase general excitability of the cortex, but had specific effects on particular cortical neurons.