SAGE Journal Articles

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Journal Article 1: Foffani, G., Shumsky, J., Knudsen, E. B., Ganzer, P. D., & Moxon, K. A. (2016). Interactive effects between exercise and serotonergic pharmacotherapy on cortical reorganization after spinal cord injuryNeurorehabilitation and Neural Repair, 30(5), 479-489.
doi: 10.1177/1545968315600523.

Abstract: Background. In rat models of spinal cord injury, at least 3 different strategies can be used to promote long-term cortical reorganization: (1) active exercise above the level of the lesion; (2) passive exercise below the level of the lesion; and (3) serotonergic pharmacotherapy. Whether and how these potential therapeutic strategies – and their underlying mechanisms of action – interact remains unknown. Methods. In spinally transected adult rats, we compared the effects of active exercise above the level of the lesion (treadmill), passive exercise below the level of the lesion (bike), serotonergic pharmacotherapy (quipazine), and combinations of the above therapies (bike+quipazine, treadmill+quipazine, bike+treadmill+quipazine) on long-term cortical reorganization (9 weeks after the spinal transection). Cortical reorganization was measured as the percentage of cells recorded in the deafferented hindlimb cortex that responded to tactile stimulation of the contralateral forelimb. Results. Bike and quipazine are “competing” therapies for cortical reorganization, in the sense that quipazine limits the cortical reorganization induced by bike, whereas treadmill and quipazine are “collaborative” therapies, in the sense that the reorganization induced by quipazine combined with treadmill is greater than the reorganization induced by either quipazine or treadmill. Conclusions. These results uncover the interactive effects between active/passive exercise and serotonergic pharmacotherapy on cortical reorganization after spinal cord injury, emphasizing the importance of understanding the effects of therapeutic strategies in spinal cord injury (and in other forms of deafferentation) from an integrated system-level approach.

Journal Article 2: Bonini, L. (2017). The extended mirror neuron network: Anatomy, origin, and functions. Neuroscientist, 23(1), 56-67.
doi: 10.1177/1073858415626400.

Abstract: Mirror neurons (MNs) are a fascinating class of cells originally discovered in the ventral premotor cortex (PMv) and, subsequently, in the inferior parietal lobule (IPL) of the macaque, which become active during both the execution and observation of actions. In this review, I will first highlight the mounting evidence indicating that mirroring others’ actions engages a broad system of reciprocally connected cortical areas, which extends well beyond the classical IPLPMv circuit and might even include subcortical regions such as the basal ganglia. Then, I will present the most recent findings supporting the idea that the observation of one’s own actions, which might play a role in the ontogenetic origin and tuning of MNs, retains a particular relevance within the adult MN system. Finally, I will propose that both cortical and subcortical mechanisms do exist to decouple MN activity from the motor output, in order to render it exploitable for high-order perceptual, cognitive, and even social functions. The findings reviewed here provide an original framework for envisaging the main challenges and experimental directions of future neurophysiological and neuroanatomical studies of the monkey MN system.

Journal Article 3: Fontanesi, C., Kvint, S., Frazzitta, G., Bera, R., Ferrazzoli, D., Di Rocco, A., . . . Ghilardi, M. F. (2016).Intensive rehabilitation enhances lymphocyte BDNF-TrkB signaling in patients with Parkinson’s diseaseNeurorehabilitation and Repair, 30(5), 411-418.
doi: 10.1177/1545968315600272.

Abstract: Background. In a combined animal and human study, we have previously found that a 5-day treatment that enhances cortical plasticity also facilitates brain-derived neurotrophic factor (BDNF)-tyrosine receptor kinase B (TrkB) signaling and increases activated TrkB and N-methyl-d-aspartate receptor (NMDAR) association in both the cortex and the peripheral lymphocytes. Patients with Parkinson’s disease (PD), in general, show decreased cortical plasticity, as demonstrated by electrophysiological and behavioral studies. Here, we test the hypothesis that an exercise program that improves motor function and seems to slow down symptom progression can enhance BDNF-TrkB signaling in lymphocytes. Methods. A total of 16 patients with PD underwent a 4-week multidisciplinary intensive rehabilitation treatment (MIRT), which included aerobic training and physical and occupational therapy. Blood was collected before and after 2 and 4 weeks of MIRT. Lymphocytes were isolated to examine BDNF-TrkB signaling induced by incubation with recombinant human BDNF. TrkB signaling complexes, extracellular-signal-regulated kinase-2 and protein-kinase-B were immunoprecipitated; the content of immunocomplexes was determined by Western blotting. Results. After MIRT, all patients showed improvement in motor function. TrkB interaction with NMDAR and BDNF-TrkB signaling increased in peripheral lymphocytes at receptor, intracellular mediator, and downstream levels. The decrements in Unified Parkinson’s Disease Rating Scale II (UPDRSII) and total scores were significantly correlated with the increases in TrkB signaling at receptor, intracellular mediator, and NMDAR interaction levels. Conclusions. The significant correlation between reduced UPDRS scores and the changes in lymphocyte activity suggest that enhanced BDNF-TrkB signaling in lymphocyte and reduced severity of PD symptoms may be related.

Journal Article 4: Kucyi, A.,& Davis, K. D. (in press). The neural code for pain: From single-cell electrophysiology to the dynamic pain connectomeNeuroscientist.
doi: 10.1177/1073858416667716.

Abstract: Pain occurs in time. In naturalistic settings, pain perception is sometimes stable but often varies in intensity and quality over the course of seconds, minutes, and days. A principal aim in classic electrophysiology studies of pain was to uncover a neural code based on the temporal patterns of single neuron firing. In contrast, modern neuroimaging studies have placed emphasis on uncovering the spatial pattern of brain activity (or “map”) that may reflect the pain experience. However, in the emerging field of connectomics, communication within and among brain networks is characterized as intrinsically dynamic on multiple time scales. In this review, we revisit the single-cell electrophysiological evidence for a nociceptive neural code and consider how those findings relate to recent advances in understanding systems-level dynamic processes that suggest the existence of a “dynamic pain connectome” as a spatiotemporal physiological signature of pain. We explore how spontaneous activity fluctuations in this dynamic system shape, and are shaped by, acute and chronic pain experiences and individual differences in those experiences. Highlighting the temporal dimension of pain, we aim to move pain theory beyond the concept of a static neurosignature and toward an ethologically relevant account of naturalistic dynamics.