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Results for “Cortical plasticity”

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At least 19 recordsLinked to original sources

PubMed2002

Neuromodulatory transmitter systems in the cortex and their role in cortical plasticity.

Cortical neuromodulatory transmitter systems refer to those classical neurotransmitters such as acetylcholine and monoamines, which share a number of common features. For instance, their centers are located in subcortical regions and send long projection axons to innervate the cortex. The same transmitter can either excite or inhibit cortical neurons depending on the composition of postsynaptic transmitter receptor subtypes. The overall functions of these transmitters are believed to serve as chemical bases of arousal, attention and motivation. The anatomy and physiology of neuromodulatory transmitter systems and their innervations in the cerebral cortex have been well characterized. In addition, ample evidence is available indicating that neuromodulatory transmitters also play roles in development and plasticity of the cortex. In this article, the anatomical organization and physiological function of each of the following neuromodulatory transmitters, acetylcholine, noradrenaline, serotonin, dopamine, and histamine, in the cortex will be described. The involvement of these transmitters in cortical plasticity will then be discussed. Available data suggest that neuromodulatory transmitters can modulate the excitability of cortical neurons, enhance the signal-to-noise ratio of cortical responses, and modify the threshold for activity-dependent synaptic modifications. Synaptic transmissions of these neuromodulatory transmitters are mediated via numerous subtype receptors, which are linked to multiple signal transduction mechanisms. Among the neuromodulatory transmitter receptor subtypes, cholinergic M(1), noradrenergic beta(1) and serotonergic 5-HT(2C) receptors appear to be more important than other receptor subtypes for cortical plasticity. In general, the contribution of neuromodulatory transmitter systems to cortical plasticity may be made through a facilitation of NMDA receptor-gated processes.

Acetylcholine↗

PubMed1985

Electrophysiological analysis of motor cortical plasticity after cortical lesions in newborn rats.

Intracortical microstimulation of the motor cortex in normal adult rats evoked low threshold contralateral forelimb movements and high threshold ipsilateral movements. Ablation of the opposite sensorimotor cortex in adult animals did not alter these thresholds. However, stimulation of the unablated hemisphere in adult rats that sustained unilateral sensorimotor cortical lesions as neonates elicited low threshold ipsilateral forelimb movements that were similar to contralateral movements. These low threshold ipsilateral movements may be mediated via aberrant corticofugal pathways which are known to develop following neonatal cortical lesions.

Animals↗

PubMed2002

Cortical plasticity: learning from cortical reorganisation.

Neocortical circuits can undergo dynamic rearrangements, not only in response to injury, but also when new skills are acquired. But although training can lead to functional rewiring of the cortex, we are far from being able to reprogram an animal by manipulating its cortical circuitry directly.

Acoustic Stimulation↗

PubMed2003

Lesions of the Basal forebrain cholinergic system impair task acquisition and abolish cortical plasticity associated with motor skill learning.

The contribution of the basal forebrain cholinergic system in mediating plasticity of cortical sensorimotor representations was examined in the context of normal learning. The effects of specific basal forebrain cholinergic lesions upon cortical reorganization associated with learning a skilled motor task were investigated, addressing, for the first time, the functional consequences of blocking cortical map plasticity. Results demonstrate that disrupting basal forebrain cholinergic function disrupts cortical map reorganization and impairs motor learning. Cholinergic lesions do not impair associative fear learning or overall sensorimotor function. These results support the hypothesis that the basal forebrain cholinergic system may be specifically implicated in forms of learning requiring plasticity of cortical representations.

Acetylcholine↗

PubMed2003

Post-infarct cortical plasticity and behavioral recovery using concurrent cortical stimulation and rehabilitative training: a feasibility study in primates.

Stroke is often characterized by incomplete recovery and chronic motor impairments. A nonhuman primate model of cortical ischemia was used to evaluate the feasibility of using device-assisted cortical stimulation combined with rehabilitative training to enhance behavioral recovery and cortical plasticity. Following pre-infarct training on a unimanual motor task, maps of movement representations in primary motor cortex were derived. Then, an ischemic infarct was produced which destroyed the hand representation. Several weeks later, a second cortical map was derived to guide implantation of a surface electrode over peri-infarct motor cortex. After several months of spontaneous recovery, monkeys underwent subthreshold electrical stimulation combined with rehabilitative training for several weeks. Post-therapy behavioral performance was tracked for several additional months. A third cortical map was derived several weeks post-therapy to examine changes in motor representations. Monkeys showed significant improvements in motor performance (success, speed, and efficiency) following therapy, which persisted for several months. Cortical mapping revealed large-scale emergence of new hand representations in peri-infarct motor cortex, primarily in cortical tissue underlying the electrode. Results support the feasibility of using a therapy approach combining peri-infarct electrical stimulation with rehabilitative training to alleviate chronic motor deficits and promote recovery from cortical ischemic injury.

Animals↗

PubMed2006

Visual cortical plasticity following unilateral sensorimotor cortical lesions in the neonatal rat.

Previous work has shown that unilateral sensorimotor cortex (SMC) lesions in newborn rats resulted in an apparent shift of the motor cortex map in the spared hemisphere, particularly of the hindlimb cortex. In view of such findings, the present study was initiated to determine if the visual cortex located both ipsilateral and contralateral to neonatal SMC, or contralateral to occipital cortical (OC) lesions, would show similar remodeling. Visual evoked potentials (VEPs) were used to map the visual cortex electrophysiologically. The results show an expansion of the visual cortex, in both the contralateral and ipsilateral hemisphere, into normally motor cortical areas in adult animals that had sustained unilateral neonatal unilateral SMC lesions. In contrast, similar changes were not seen within the spared visual cortex after unilateral occipital cortical lesions, suggesting that the shift in the visual map was specifically in response to the SMC lesion and was not a generalized response to neonatal cortical damage. Histological analysis showed a functional expansion in the rostral boundary of visual cortex with no corresponding cytoarchitectural alterations.

Animals↗

PubMed1979

Restoration of visual cortical plasticity by local microperfusion of norepinephrine.

Using a newly developed technique of continuous microperfusion, we obtained further evidence in support of our hypothesis that the neocortical catecholamines (CAs), particularly norepinephrine (NE), are responsible for a high level of cortical plasticity. We used the visual cortical changes in ocular dominance which follow a brief monocular deprivation as a simple and reliable index of cortical plasticity. Local perfusion of kitten visual cortex with 1 mg/ml (4.0 mM) 6-hydroxydopamine (6-OHDA) prevented the effects of monocular deprivation in kittens, thus replicating the results we had obtained using intraventricular injections (Kasamatsu and Pettigrew, '76b, '79). Locally perfused NE at a concentration of of 10(-2) mg/ml (48.6 micron) restored visual cortical plasticity in animals which were no longer susceptible to brief monocular lid-suture. These numbers refer to the concentration of solutions in the cannula/minipump system. The effective concentrations at the site of recording (about 2 mm away) are probably much lower than these. This effect of NE perfusion was seen both in kittens which had received prior 6-OHDA treatment as well as in older animals which had outgrown the susceptible period. In the kittens we obtained as a nearly complete shift in ocular dominance toward the open eye and in the older animals a decrease in binocularity was obtained. The changes were found only in the local region of visual cortex perfused with either NE or 6-OHDA, while nearby cortical regions in the same animals were unaffected. There were no obvious changes in receptive field properties of individual neurons other than ocularity, and externally perfused NE did not itself reduce binocularity in normal animals: the effects of NE described about only occurred when the animal's visual experience was simultaneously altered. These results support the view that NE plays an important role in cortical plasticity.

Age Factors↗

PubMed2005

Cortical plasticity following surgical extension of lower limbs.

Human cortical plasticity has been studied after peripheral sensory alterations due to amputations or grafts, while sudden 'quasi-physiological' changes in the dimension of body parts have not been investigated yet. We examined the cortical reorganization in achondroplastic dwarfs submitted to progressive elongation (PE) of lower limbs through the Ilizarov technique. This paradigm is ideal for studying cortical plasticity because it avoids the perturbation connected with deafferentation and re-afferentation. Somatosensory evoked-potentials (SEP) and fMRI studies were performed before and after PE during foot and knee stimulation, above and below the surgical fracture. A body schema test was also performed. Following PE, cortical modifications were observed in the primary somatosensory cortex for foot stimulation and in higher order somatosensory cortices for foot and knee. The former modifications tended to decrease 6 months after the elongation ending, whereas the latter tended to persist. Results are interpreted in terms of cortical adaptation mediated by temporary disorganization.

Achondroplasia↗

PubMed2000

Effects of neurotrophins on cortical plasticity: same or different?

Neurotrophins are important regulators of visual cortical plasticity. It is still unclear, however, whether they play similar or different roles and which are their effects on the electrical activity of cortical neurons in vivo. We therefore compared the effects of all neurotrophins, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-4 (NT-4), and neurotrophin-3 (NT-3) on visual cortical plasticity and on cell spontaneous and visually evoked activity. Rats were monocularly deprived for 1 week at the peak of the critical period, and neurotrophins were infused intracortically. The main finding is that, with the exception of NT-3, all neurotrophins affect the outcome of monocular deprivation, but there are clear differences in their mechanisms of action. In particular, NT-4 and NGF counteract monocular deprivation effects without causing detectable alterations either in spontaneous or visually evoked neuronal activity. BDNF is less effective on ocular dominance plasticity and, in addition, strongly affects spontaneous and visually evoked activity in cortical neurons.

Animals↗

PubMed2005

Exploring motor cortical plasticity using transcranial magnetic stimulation in humans.

It is generally accepted that functional properties of the motor cortex in adult humans can be altered through behavioral or pharmacological manipulations, as well as in some pathological conditions. The ability and capacity of adult human cortex to undergo any adaptive or reorganizational changes is referred to as plasticity. Much of the evidence concerning motor cortical plasticity have been derived from studies using the non-invasive technique of transcranial magnetic stimulation (TMS). TMS has proven to be a suitable tool to explore representational plasticity and to interact with neuronal activity in settings of induction protocols either alone or coupled with altered sensory inputs. Furthermore, plastic changes induced by motor learning protocols have attracted particular interest because of their relevance in functional recovery. Recent studies support the view that learning in human motor cortex occurs through long-term potentiation (LTP)-like mechanisms. Purposeful modulation of motor cortical plastic changes by manipulative TMS protocols may offer useful rehabilitative strategies in patients with chronic motor deficits.

Adult↗

PubMed2004

Impaired learning-dependent cortical plasticity in Huntington's disease transgenic mice.

Huntington's disease (HD) is a genetically transmitted neurodegenerative disorder. The neuropathology in HD is a selective neuronal cell death in several brain regions including cortex. Although changes in synaptic plasticity were shown within the hippocampus and striatum of HD transgenic mice, there are no studies considering neocortical synaptic plasticity abnormalities in HD. We examined the impact of the HD transgene upon learning-dependent plasticity of cortical representational maps. The effect of associative learning, in which stimulation of a row of vibrissae was paired with appetitive stimulus, upon functional representations of vibrissae in the barrel cortex, was investigated with 2-deoxyglucose brain mapping in presymptomatic R6/1 HD mice. In wild-type mice, cortical representation of the row of vibrissae involved in the training was expanded, while in HD mice the representation of this row was not expanded. The results suggest that presymptomatic R6/1 HD transgenic mice show deficits in plasticity of primary somatosensory cortex.

Animals↗

PubMedDate not supplied

Sex differences in cortical plasticity and behavior following anterior cortical kindling in rats.

This experiment examined the effect of electrical kindling on the morphology of frontal (Fr1) neocortical layer III pyramidal cell dendrites in both male and female rats. Repeated elicitation of afterdischarge resulted in an increase in the severity of the behavioural seizures and an increase in afterdischarge duration, frequency and amplitude in all rats. The late component of the transcallosal evoked responses also increased following both 7 and 25 kindling sessions in male rats and following 25 kindling sessions in female rats. Analysis of the Golgi-Cox impregnated pyramidal cell dendrites indicated a significant decrease in the amount of apical and basilar dendritic spine density, length and branching in female rats following 7 days, but not 25 days, of kindling. Male rats had significantly lower apical and basilar dendritic spine density and branching measures following 25 days, but not 7 days, of kindling, as well as significantly lower apical and basilar dendritic length following 7 days of kindling. The differential gender effect suggests that males and females recruit similar plastic mechanisms although at different times in response to electrical kindling.

Animals↗

PubMed2005

Cortical plasticity following upper extremity injury and reconstruction.

Today's view of the adult central nervous system is that of an adaptive and responsive system. Plastic surgeons, because of the motor and sensory reconstructions they perform, need to have an understanding of brain plasticity following upper extremity injury, reconstruction, and rehabilitation. Functional MRI and transcranial magnetic stimulation can identify cortical plasticity in humans. For instance, these techniques have identified changes in excitability and body site representation in the motor cortex in patients following motor reconstruction and motor relearning. Therefore, cortical plasticity and its manipulation may be an important contributor to functional outcome following reconstruction. In the future, cortical plasticity may have implications for reconstruction and rehabilitation.

Amputation, Traumatic↗

PubMed1997

Human cortical plasticity: functional recovery with mirror movements.

Cortical plasticity of the human brain permits functional recovery after brain injury even in the absence of neuronal recovery. We report the combined evaluation, including electrophysiology and functional magnetic resonance imaging, of the pattern of cortical and cerebellar reorganization, in a patient with mirror movements as a sequel of perinatal unilateral brain injury. Recovery resulted in motor control by the healthy hemisphere using direct ipsilateral corticospinal projections and the contralateral cerebellum.

Adolescent↗

PubMed1999

Auditory cortical plasticity: a comparison with other sensory systems.

The auditory cortex has a crucial role in higher cognitive functions, including the perception of speech, music and auditory space. Cortical plasticity, as in other sensory systems, is used in the fine tuning of the auditory system for these higher functions. Auditory cortical plasticity can also be demonstrated after lesions of the cochlea and it appears to participate in generating tinnitus. Early musical training leads to an expansion in the representation of complex harmonic sounds in the auditory cortex. Similarly, the early phonetic environment has a strong influence on speech development and, presumably, on the cortical organization of speech. In auditory spatial perception, the spectral cues generated by the head and outer ears vary between individuals and have to be calibrated by learning, which most probably takes place at the cortical level. The neural mechanisms of plasticity are likely to be the same across all cortical regions. It should be useful, therefore, to relate some of the findings and hypotheses about auditory cortical plasticity to previous studies of other sensory systems.

Animals↗

PubMed2004

Modulation of motor function and cortical plasticity in health and disease.

Basic science studies demonstrated mechanisms of plasticity and metaplasticity. More recent human studies identified some of these mechanisms as operating in multiple areas of human cognition, such as learning and memory, and in functional recovery from lesions in the CNS, as in stroke. One of the goals of neurorehabilitation is the translation of these principles into rational strategies to promote recovery of function. Understanding the mechanisms and functional role of human plasticity could lead to the development of therapeutic options in situations in which there is virtually no treatment alternative, as in chronic stroke. We review some of the work performed to better understand the substrates and mechanisms underlying cortical plasticity and discuss some experimental approaches to enhance cortical plasticity and recovery of function, like cortical stimulation.

Health↗

PubMed1988

6-Hydroxydopamine treatment and beta adrenergic receptor binding in kittens. Relation to visual cortical plasticity.

Under some circumstances intraventricular administration of 6-OHDA decreases visual cortical plasticity of kittens; the mechanism for this change is not known, but depletion of norepinephrine (NE) is not the entire explanation. We have examined the effects of 6-OHDA treatment on beta adrenergic receptor binding in kitten visual cortex. Subjects were given vehicle solution alone, a low dose of 6-OHDA which depleted cortical NE without affecting visuocortical plasticity, or a higher dose of 6-OHDA which depleted cortical NE and decreased visuocortical plasticity. Drugs were administered in single daily injections via intraventricular cannulas. Saturation assays were performed on homogenates of visual cortical tissue using 125I-pindolol (30-400 pM) along w/ isoproterenol (237 microM) as a cold competitor. We measured radioactivity bound to tissue and retained on filters and analyzed the data using the EBDA computer program (McPherson 1983, 1985); we determined the affinity constant (Kd) and receptor density (Bmax) in multiple assays for each animal. Despite 75-90% NE depletion in both experimental groups, only the group receiving the lower dose of 6-OHDA showed any evidence of supersensitivity. The Kds did not differ among the groups. The data suggest that the effects of 6-OHDA on visuocortical plasticity are not secondary to beta adrenergic supersensitivity.

Animals↗

PubMed2001

Long-term effects of neonatal MK-801 treatment on spatial learning and cortical plasticity in adult rats.

RATIONALE AND OBJECTIVES: The long-term effects of neonatal treatment with MK-801 on spatial learning and cortical plasticity were investigated in adult rats. METHODS: Rat pups were injected twice daily with MK-801 (0.1 mg/kg) on postnatal days 7-19, participated in water maze testing between postnatal days 90 and 102, and were then studied electrophysiologically. RESULTS: Treatment with MK-801 in such a low dose resulted in a very slight impairment of performance in the water maze task, but not in the visual cue response. Besides the slight learning impairment, the electrophysiological study revealed a reduction in the capacity for plasticity in the primary motor cortex of the treated animals, which was pronounced in the controls. CONCLUSION: The study demonstrates that even a slight impairment in learning and memory function may be accompanied by a cortical plasticity deficiency that is detectable electrophysiologically.

Animals↗