Excitation and Inhibition Jointly Regulate Cortical Reorganization in Adult Rats

Benali, Alia; Weiler, E; Benali, Youssef; Dinse, Hubert R.; Eysel, Ulf T.

doi:10.1523/jneurosci.1952-08.2008

Cited by 55 publications

(41 citation statements)

References 77 publications

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“…Cortical application of bicuculline has allowed us to demonstrate that GABAergic transmission is critically placed to maintain the form of cortical motor representations (Jacobs and Donoghue, 1991;Benali et al, 2008) and to modulate the functional link between cortical points (Schneider et al 2002). In the present study, cortical application of bicuculline at a subconvulsive concentration (Stojic et al, 2000) resulted in global increase of M1 excitability.…”

Section: Neurobiological Mechanisms Underlying M1 Changesmentioning

confidence: 52%

Progressive Motor Cortex Functional Reorganization Following 6-Hydroxydopamine Lesioning in Rats

Viaro¹,

Morari²,

Franchi³

2011

J. Neurosci.

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Many studies have attempted to correlate changes of motor cortex activity with progression of Parkinson's disease, although results have been controversial. In the present study we used intracortical microstimulation (ICMS) combined with behavioral testing in 6-hydroxydopamine hemilesioned rats to evaluate the impact of dopamine depletion on movement representations in primary motor cortex (M1) and motor behavior. ICMS allows for motor-effective stimulation of corticofugal neurons in motor areas so as to obtain topographic movements representations based on movement type, area size, and threshold currents. Rats received unilateral 6-hydroxydopamine in the nigrostriatal bundle, causing motor impairment. Changes in M1 were time dependent and bilateral, although stronger in the lesioned than the intact hemisphere. Representation size and threshold current were maximally impaired at 15 d, although inhibition was still detectable at 60 -120 d after lesion. Proximal forelimb movements emerged at the expense of the distal ones. Movement lateralization was lost mainly at 30 d after lesion. Systemic L-3,4-dihydroxyphenylalanine partially attenuated motor impairment and cortical changes, particularly in the caudal forelimb area, and completely rescued distal forelimb movements. Local application of the GABA A antagonist bicuculline partially restored cortical changes, particularly in the rostral forelimb area. The local anesthetic lidocaine injected into the M1 of the intact hemisphere restored movement lateralization in the lesioned hemisphere. This study provides evidence for motor cortex remodeling after unilateral dopamine denervation, suggesting that cortical changes were associated with dopamine denervation, pathogenic intracortical GABA inhibition, and altered interhemispheric activity.

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Section: Neurobiological Mechanisms Underlying M1 Changesmentioning

confidence: 52%

Progressive Motor Cortex Functional Reorganization Following 6-Hydroxydopamine Lesioning in Rats

Viaro¹,

Morari²,

Franchi³

2011

J. Neurosci.

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“…However, more chronic effects on cell function were not determined, and it remains possible that alterations in the balance of excitation and inhibition conjointly regulate the cortical map in a particular spatial arrangement, in a manner similar to that observed after cortical plasticity induced by intracortical microstimulation. 46 In this interpretation, enhanced c-Fos cell activity that we observed after cABC infusion would occur in glutamatergic neurones, limited by inhibitory zones of increased cell numbers containing GABA. This would seem to concur with previous in vitro work showing increased L-glutamate trafficking and plasticity at synapses after digestion of the surrounding PNNs.…”

Section: And (E) Gap43mentioning

confidence: 68%

Chondroitinase Enhances Cortical Map Plasticity and Increases Functionally Active Sprouting Axons after Brain Injury

Harris

Nogueira

Verley

et al. 2013

Journal of Neurotrauma

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The beneficial effect of interventions with chondroitinase ABC enzyme to reduce axon growth-inhibitory chondroitin sulphate side chains after central nervous system injuries has been mainly attributed to enhanced axonal sprouting. After traumatic brain injury (TBI), it is unknown whether newly sprouting axons that occur as a result of interventional strategies are able to functionally contribute to existing circuitry, and it is uncertain whether maladaptive sprouting occurs to increase the well-known risk for seizure activity after TBI. Here, we show that after a controlled cortical impact injury in rats, chondroitinase infusion into injured cortex at 30 min and 3 days reduced c-Fos + cell staining resulting from the injury alone at 1 week postinjury, indicating that at baseline, abnormal spontaneous activity is likely to be reduced, not increased, with this type of intervention. c-Fos + cell staining elicited by neural activity from stimulation of the affected forelimb 1 week after injury was significantly enhanced by chondroitinase, indicating a widespread effect on cortical map plasticity. Underlying this map plasticity was a larger contribution of neuronal, rather than glial cells and an absence of c-Fos + cells surrounded by perineuronal nets that were normally present in stimulated naïve rats. After injury, chondroitin sulfate proteoglycan digestion produced the expected increase in growth-associated protein 43-positive axons and perikarya, of which a significantly greater number were double labeled for c-Fos after intervention with chondroitinase, compared to vehicle. These data indicate that chondroitinase produces significant gains in cortical map plasticity after TBI, and that either axonal sprouting and/or changes in perineuronal nets may underlie this effect. Chondroitinase dampens, rather than increases nonspecific c-Fos activity after brain injury, and induction of axonal sprouting is not maladaptive because greater numbers are functionally active and provide a significant contribution to forelimb circuitry after brain injury.

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“…This finding was surprising, as H 3 antagonists including GSK189254 are known to activate the intermediate early gene c-fos in both the prefrontal and somatosensory cortex Southam et al, 2009), and cortical reorganization of sensory information is accompanied by increased glutamatergic drive and c-fos activation (Benali et al, 2008). In contrast, chronic treatment (40 days) with the 5-HT 6 receptor antagonists SB-271046 and SB-399885 markedly increase NCAM PSA expression in the entorhinal and perirhinal cortex , an effect that may relate to their ability to increase glutamate outflow (Dawson et al, 2001), as a similar action is not observed with GSK189254 (Medhurst et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

H3 Receptor Antagonism Enhances NCAM PSA-Mediated Plasticity and Improves Memory Consolidation in Odor Discrimination and Delayed Match-to-Position Paradigms

Foley

Prendergast

Barry

et al. 2009

Neuropsychopharmacol

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To further understand the procognitive actions of GSK189254, a histamine H 3 receptor antagonist, we determined its influence on the modulation of hippocampal neural cell adhesion molecule (NCAM) polysialylation (PSA) state, a necessary neuroplastic mechanism for learning and memory consolidation. A 4-day treatment with GSK189254 significantly increased basal expression of dentate polysialylated cells in rats with the maximal effect being observed at 0.03-0.3 mg/kg. At the optimal dose (0.3 mg/kg), GSK189254 enhanced water maze learning and the associated transient increase in NCAM-polysialylated cells. The increase in dentate polysialylated cell frequency induced by GSK189254 was not attributable to enhanced neurogenesis, although it did induce a small, but significant, increase in the survival of these newborn cells. GSK189254 (0.3 mg/kg) was without effect on polysialylated cell frequency in the entorhinal and perirhinal cortex, but significantly increased the diffuse PSA staining observed in the anterior, ventromedial, and dorsomedial aspects of the hypothalamus. Consistent with its ability to enhance the learning-associated, post-training increases in NCAM PSA state, GSK189254 (0.3 mg/kg) reversed the amnesia induced by scopolamine given in the 6-h post-training period after training in an odor discrimination paradigm. Moreover, GSK189254 significantly improved the performance accuracy of a delayed match-to-position paradigm, a task dependent on the prefrontal cortex and degree of cortical arousal, the latter may be related to enhanced NCAM PSA-associated plasticity in the hypothalamus. The procognitive actions of H3 antagonism combined with increased NCAM PSA expression may exert a disease-modifying action in conditions harboring fundamental deficits in NCAM-mediated neuroplasticity, such as schizophrenia and Alzheimer's disease.

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Excitation and Inhibition Jointly Regulate Cortical Reorganization in Adult Rats

Cited by 55 publications

References 77 publications

Progressive Motor Cortex Functional Reorganization Following 6-Hydroxydopamine Lesioning in Rats

Progressive Motor Cortex Functional Reorganization Following 6-Hydroxydopamine Lesioning in Rats

Chondroitinase Enhances Cortical Map Plasticity and Increases Functionally Active Sprouting Axons after Brain Injury

H3 Receptor Antagonism Enhances NCAM PSA-Mediated Plasticity and Improves Memory Consolidation in Odor Discrimination and Delayed Match-to-Position Paradigms

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