NMDA receptors and plasticity in adult primate somatosensory cortex

Garraghty, Preston E.; Muja, Naser

doi:10.1002/(sici)1096-9861(19960401)367:2<319::aid-cne12>3.0.co;2-l

Cited by 134 publications

(82 citation statements)

References 49 publications

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“…In contrast, no alterations are seen in ligand binding for AMPA or dopamine receptors in the striatum. NMDA receptors in primate somatosensory cortex appear to play an important role in the cortical reorganization that allows recovery of responsiveness over 4 weeks after transection of the median nerve (Garraghty and Muja, 1996). Blockade of NMDA receptor function during that period largely prevents recovery of cortical responsiveness.…”

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confidence: 66%

Altered Glutamate Receptor Function during Recovery of Bladder Detrusor-External Urethral Sphincter Coordination in a Rat Model of Spinal Cord Injury

Pikov¹,

Wrathall²

2002

J Pharmacol Exp Ther

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Coordination of the bladder detrusor and the external urethral sphincter is a supraspinally controlled reflex that is essential for efficient micturition. This coordination is permanently lost after spinal cord transection but can recover chronically after incomplete spinal cord injury (SCI). As glutamatergic transmission plays a key role in all levels of detrusor-external urethral sphincter coordination, we examined the role of potential alterations in glutamatergic control in its recovery after SCI. Rats were subjected to standardized incomplete contusion injury. Detrusorexternal urethral sphincter coordination was evaluated urodynamically at 5 days (subacute) and 8 weeks (chronic) after SCI. Sensitivity of coordinated activation of the external urethral sphincter in response to bladder distension to the ␣ -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid/kainate antagonist 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo(f)quinoxaline-7-sulfonamide disodium (NBQX) and to the N-methyl-Daspartate (NMDA) antagonist R(Ϫ-3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid (CPP) was determined by intrathecal application at the L6 spinal cord level during urodynamic recordings. We found that while detrusor contractions recovered at 5 days after SCI, coordinated activation of the external urethral sphincter was significantly impaired at 5 days and recovered only by 8 weeks. There was no difference in sensitivity of detrusor-external urethral sphincter coordination to NBQX at the subacute or chronic time points. However, external urethral sphincter response to bladder distension was sensitive to a 50% lower dose of CPP at 5 days compared with uninjured rats or chronic recovered SCI rats. Thus, alterations in NMDA receptor function appeared to be involved in recovery of detrusor-external urethral sphincter coordination after incomplete SCI.

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confidence: 66%

Altered Glutamate Receptor Function during Recovery of Bladder Detrusor-External Urethral Sphincter Coordination in a Rat Model of Spinal Cord Injury

Pikov¹,

Wrathall²

2002

J Pharmacol Exp Ther

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“…Modifications in synaptic transmission, yielding increased excitability in sensory and motor cortical representations both contralateral and ipsilateral to the injury, are an important neuroplasticity mechanism underlying cortical reorganization. For example, the extent of the somatosensory cortex reorganization after nerve injury was reduced after systemic administration of NMDA antagonist (50,51) and was tightly correlated to NMDA receptor-mediated plasticity (52). Increases in cortical excitability were also shown to be accompanied by increases in AMPA receptor autoradiographic binding (53) and decreases in GABA staining in the deprived S1 (53,54).…”

Section: Discussionmentioning

confidence: 99%

Optogenetic-guided cortical plasticity after nerve injury

Downey

Bar‐Shir

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Peripheral nerve injury causes sensory dysfunctions that are thought to be attributable to changes in neuronal activity occurring in somatosensory cortices both contralateral and ipsilateral to the injury. Recent studies suggest that distorted functional response observed in deprived primary somatosensory cortex (S1) may be the result of an increase in inhibitory interneuron activity and is mediated by the transcallosal pathway. The goal of this study was to develop a strategy to manipulate and control the transcallosal activity to facilitate appropriate plasticity by guiding the cortical reorganization in a rat model of sensory deprivation. Since transcallosal fibers originate mainly from excitatory pyramidal neurons somata situated in laminae III and V, the excitatory neurons in rat S1 were engineered to express halorhodopsin, a light-sensitive chloride pump that triggers neuronal hyperpolarization. Results from electrophysiology, optical imaging, and functional MRI measurements are concordant with that within the deprived S1, activity in response to intact forepaw electrical stimulation was significantly increased by concurrent illumination of halorhodopsin over the healthy S1. Optogenetic manipulations effectively decreased the adverse inhibition of deprived cortex and revealed the major contribution of the transcallosal projections, showing interhemispheric neuroplasticity and thus, setting a foundation to develop improved rehabilitation strategies to restore cortical functions.recovery | amputation A lthough 20 million Americans suffer from peripheral nerve injury caused by trauma, metabolic, endocrine, and autoimmune disorders, there are few strategies to promote recovery. Surgical nerve repair and training of the injured limb are the classical rehabilitation approaches. Nevertheless, the clinical outcome in adults is generally poor, with persisting sensory dysfunction and pain (1).Recent evidence suggests that sensory dysfunctions caused by nerve injury should be attributable not only to the functional, cellular, and biochemical events occurring in peripheral nerve but also functional and anatomical changes occurring in cerebral cortical representations. It is well-documented in humans (2), non-human primates (3), cats (4), and rodents (5-7) that peripheral nerve injury can lead to expansion of neighboring cortical representation of peripheral regions within the affected (deprived) hemisphere (intrahemispheric neuroplasticity). Peripheral nerve injury and direct cortical lesions have been shown to also modify functional communication between cortical hemispheres (interhemispheric neuroplasticity) (8-19). Specifically, peripheral inputs normally evoking neuronal responses in the contralateral hemisphere cause inappropriate functional responses in the ipsilateral hemisphere. Previously, using singleunit electrophysiology recordings and juxtacellular labeling, it was shown that the inappropriate ipsilateral functional magnetic resonance imaging (fMRI) responses observed in deprived primary somatosensory cor...

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“…We hypothesize that ␣-CaMKII activation induces an LTP-like process that involves NMDAR NR2A subunit, a direct or indirect target of the kinase in the postsynaptic density (Gardoni et al, 1998(Gardoni et al, , 1999(Gardoni et al, , 2003. Blockade of NMDAR in the adult SI cortex disrupts the expansion of intact representational zones within the deprived area but does not affect an already expanded map (Kano and Iino, 1991;Jablonska et al, 1995;Garraghty and Muja, 1996). Our study shows that the NMDAR NR2A subunit is mainly involved in the protraction of map expansion.…”

Section: Involvement Of Glutamatergic Excitation In Somatosensory Mapmentioning

confidence: 94%

Nursing-Induced Somatosensory Cortex Plasticity: Temporally Decoupled Changes in Neuronal Receptive Field Properties Are Accompanied by Modifications in Activity-Dependent Protein Expression

Rosselet¹,

Zennou-Azogui²,

Xerri³

2006

J. Neurosci.

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This study is an attempt to gain insight into the malleability of representational maps in the primary somatosensory cortex in relation to the expression of proteins involved in inhibitory and excitatory neurotransmitter systems that contribute to maintain these maps in a dynamic state. Malleability of somatosensory maps is characterized by changes in the sizes of neuron receptive fields (RFs) affecting the representational grain and in the locations and submodalities of these RFs modifying the map extent. The concomitance of these alterations remains so far hypothetical. We used nursing as an evolving source of ethologically significant cutaneous stimulation. This cyclic behavior is particularly suited to investigating the time course of experience-dependent cortical changes. Electrophysiological maps of the ventrum skin were recorded twice in the same lactating rats between nursing initiation and several weeks after nursing. We found that reduction in RF size occurred earlier than map expansion. As nursing time declined, the map expansion was maintained longer than the RF sharpening. Based on this difference in time course, we compared the expression patterns of several activity-dependent proteins in relation to the RF plasticity. Western blot analysis showed an increase in glutamic acid decarboxylase expression that was concomitant with RF contraction. In contrast, NR2A subunit of NMDA and ␣ calcium/calmodulin kinase type II were upregulated at times when map expansion was observed. We propose that inhibitory and excitatory plasticity mechanisms operating with different time courses may contribute to the temporal dissociation of nursing-induced RF reshaping and map expansion.

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NMDA receptors and plasticity in adult primate somatosensory cortex

Cited by 134 publications

References 49 publications

Altered Glutamate Receptor Function during Recovery of Bladder Detrusor-External Urethral Sphincter Coordination in a Rat Model of Spinal Cord Injury

Altered Glutamate Receptor Function during Recovery of Bladder Detrusor-External Urethral Sphincter Coordination in a Rat Model of Spinal Cord Injury

Optogenetic-guided cortical plasticity after nerve injury

Nursing-Induced Somatosensory Cortex Plasticity: Temporally Decoupled Changes in Neuronal Receptive Field Properties Are Accompanied by Modifications in Activity-Dependent Protein Expression

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