14 research outputs found

    Thalamocortical Inputs Show Post-Critical-Period Plasticity

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    SummaryExperience-dependent plasticity in the adult brain has clinical potential for functional rehabilitation following central and peripheral nerve injuries. Here, plasticity induced by unilateral infraorbital (IO) nerve resection in 4-week-old rats was mapped using MRI and synaptic mechanisms were elucidated by slice electrophysiology. Functional MRI demonstrates a cortical potentiation compared to thalamus 2 weeks after IO nerve resection. Tracing thalamocortical (TC) projections with manganese-enhanced MRI revealed circuit changes in the spared layer 4 (L4) barrel cortex. Brain slice electrophysiology revealed TC input strengthening onto L4 stellate cells due to an increase in postsynaptic strength and the number of functional synapses. This work shows that the TC input is a site for robust plasticity after the end of the previously defined critical period for this input. Thus, TC inputs may represent a major site for adult plasticity in contrast to the consensus that adult plasticity mainly occurs at cortico-cortical connections

    Functional networks and network perturbations in rodents

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    Synchronous low-frequency oscillation in the resting human brain has been found to form networks of functionally associated areas and hence has been widely used to map the functional connectivity of the brain using techniques such as resting-state functional MRI (rsfMRI). Interestingly, similar resting-state networks can also be detected in the anesthetized rodent brain, including the default mode-like network. This opens up opportunities for understanding the neurophysiological basis of the rsfMRI signal, the behavioral relevance of the network characteristics, connectomic deficits in diseases and treatment effects on brain connectivity using rodents, particularly transgenic mouse models. In this review, we will provide an overview on the resting-state networks in the rat and mouse brains, the effects of pharmacological agents, brain stimulation, structural connectivity, genetics on these networks, neuroplasticity after behavioral training and applications in models of neurological disease and psychiatric disorders. The influence of anesthesia, strain difference, and physiological variation on the rsfMRI-based connectivity measure will be discussed

    Cortical Plasticity and Behavioral Recovery Following Focal Lesion to Primary Motor Cortex in Adult Rats

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    Acquired brain injuries, such as ischemic stroke and traumatic brain injury, are the leading causes of physical disabilities. Previously, scientists have shown that damage of the primary motor cortex induced neural plasticity in the premotor area in human and non-human primate studies. Neural plasticity, particularly within the same hemisphere of the lesion (ipsilesional), is thought to contribute to and account for functional recovery. It is not yet known to what extent plasticity mediates recovery and how to take advantage of neural plasticity to maximize the functional outcome. Rodent models are most often used not only for studying the role of motor cortex in motor skill learning but also in neurodegenerative research. To further elucidate the role of adaptive plasticity in the ipsilesional hemisphere during the recovery of upper limb function, we aimed to establish the baseline neural changes after a focal cortical injury. Therefore, we took advantage of two separate cortical motor areas, in the Rattus norvegicus, from which the corticospinal tracts terminate in the motor nuclei of the cervical level spinal cord, controlling upper extremity musculature--the first, a more caudally located subregion of M1, often referred to as the caudal forelimb area (CFA), and the second, a more rostrally located non-primary area, referred to as the rostral forelimb area (RFA). The objective of this dissertation work was to characterize physiological changes in RFA during the complex and lengthy process of recovery using rat models of focal cortical trauma and cortical ischemia restricted to CFA. The results demonstrated that the post-injury cortical plasticity in RFA may play a role in functional recovery. Further, we showed differential effects of rehabilitative training on ipsilesional RFA plasticity after CFA ischemic injury. Extensive physiological changes were evident past rehabilitative training. Thus, neural plasticity in RFA appeared to be dependent both on post-lesion motor experience and time. The dissertation work supports the hypothesis that cortical plasticity within the spared RFA after restrictive damage to CFA mediates use-dependent physiological reorganization, which provides a substrate for sustaining rehabilitation-aided motor functional recovery
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