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Motor Learning (motor + learning)

Distribution by Scientific Domains

Medical Sciences	55%
Life Sciences	33%

Selected Abstracts

Prenatal Development of Interlimb Motor Learning in the Rat Fetus

INFANCY, Issue 3 2008
Scott R. Robinson
The role of sensory feedback in the early ontogeny of motor coordination remains a topic of speculation and debate. On E20 of gestation (the 20th day after conception, 2 days before birth), rat fetuses can alter interlimb coordination after a period of training with an interlimb yoke, which constrains limb movement and promotes synchronized, conjugate movement of the yoked limbs. The aim of this study was to determine how the ability to express this form of motor learning may change during prenatal development. Fetal rats were prepared for in vivo study at 4 ages (E18,21) and tested in a 65-min training-and-testing session examining hind limb motor learning. A significant increase in conjugate hind limb activity was expressed by El9, but not El 8 fetuses, with further increases in conjugate hind limb activity on E20 and E21. These findings suggest substantial development of the ability of fetal rats to modify patterns of interlimb coordination in response to kinesthetic feedback during motor training before birth. [source]

Conjugate limb coordination after experience with an interlimb yoke: Evidence for motor learning in the rat fetus

DEVELOPMENTAL PSYCHOBIOLOGY, Issue 4 2005
Scott R. Robinson
Abstract This study investigated the capacity of the E20 rat fetus to adaptively alter patterns of interlimb coordination in a prenatal model of motor learning. Fetal limb movement was manipulated with an interlimb yoke, consisting of a fine thread attached at the ankles, which created a physical linkage between two limbs. Exposure to the yoke resulted in a gradual increase in conjugate movements of the yoked limbs during a 30-min training period, which persisted after removal of the yoke. Training effects were evident when the yoke was applied to two hindlimbs, two forelimbs, or a homolateral forelimb,hindlimb pair. A savings in the rate of acquisition also was observed when fetuses experienced yoke training in a second session. These data argue that the rat fetus can respond to kinesthetic feedback resulting from variation in motor performance, which suggests that experience contributes to the development of coordinated motor behavior before birth. © 2005 Wiley Periodicals, Inc. Dev Psychobiol 47: 328,344, 2005. [source]

Deficient long-term synaptic depression in the rostral cerebellum correlated with impaired motor learning in phospholipase C ,4 mutant mice

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2001
Mariko Miyata
Abstract Long-term depression (LTD) at parallel fibre,Purkinje cell synapse of the cerebellum is thought to be a cellular substrate for motor learning. LTD requires activation of metabotropic glutamate receptor subtype 1 (mGluR1) and its downstream signalling pathways, which invariably involves phospholipase C,s (PLC,s). PLC,s consist of four isoforms (PLC,1,4) among which PLC,4 is the major isoform in most Purkinje cells in the rostral cerebellum (lobule 1 to the rostral half of lobule 6). We studied mutant mice deficient in PLC,4, and found that LTD was deficient in the rostral but not in the caudal cerebellum of the mutant. Basic properties of parallel fibre,Purkinje cell synapses and voltage-gated Ca2+ channel currents appeared normal. The mGluR1-mediated Ca2+ release induced by repetitive parallel fibre stimulation was absent in the rostral cerebellum of the mutant, suggesting that their LTD lesion was due to the defect in the mGluR1-mediated signalling in Purkinje cells. Importantly, the eyeblink conditioning, a simple form of discrete motor learning, was severely impaired in PLC,4 mutant mice. Wild-type mice developed the conditioned eyeblink response, when pairs of the conditioned stimulus (tone) and the unconditioned stimulus (periorbital shock) were repeatedly applied. In contrast, PLC,4 mutant mice could not learn the association between the conditioned and unconditioned stimuli, although their behavioural responses to the tone or to the periorbital shock appeared normal. These results strongly suggest that PLC,4 is essential for LTD in the rostral cerebellum, which may be required for the acuisition of the conditioned eyeblink response. [source]

Abnormal social behaviors in mice lacking Fgf17

GENES, BRAIN AND BEHAVIOR, Issue 3 2008
K. Scearce-Levie
The fibroblast growth factor family of secreted signaling molecules is essential for patterning in the central nervous system. Fibroblast growth factor 17 (Fgf17) has been shown to contribute to regionalization of the rodent frontal cortex. To determine how Fgf17 signaling modulates behavior, both during development and in adulthood, we studied mice lacking one or two copies of the Fgf17 gene. Fgf17-deficient mice showed no abnormalities in overall physical growth, activity level, exploration, anxiety-like behaviors, motor co-ordination, motor learning, acoustic startle, prepulse inhibition, feeding, fear conditioning, aggression and olfactory exploration. However, they displayed striking deficits in several behaviors involving specific social interactions. Fgf17-deficient pups vocalized less than wild-type controls when separated from their mother and siblings. Elimination of Fgf17 also decreased the interaction of adult males with a novel ovariectomized female in a social recognition test and reduced the amount of time opposite-sex pairs spent engaged in prolonged, affiliative interactions during exploration of a novel environment. After social exploration of a novel environment, Fgf17-deficient mice showed less activation of the immediate-early gene Fos in the frontal cortex than wild-type controls. Our findings show that Fgf17 is required for several complex social behaviors and suggest that disturbances in Fgf17 signaling may contribute to neuropsychiatric diseases that affect such behaviors. [source]

Prenatal Development of Interlimb Motor Learning in the Rat Fetus

Mechanisms of oral somatosensory and motor functions and their clinical correlates,

JOURNAL OF ORAL REHABILITATION, Issue 4 2006
B. J. SESSLE
summary, This article provides a review of somatosensory and motor pathways and processes involved in oral sensorimotor function and dysfunction. It reviews somatosensory processes in peripheral tissues, brainstem and higher brain centres such as thalamus and cerebral cortex, with a particular emphasis on nociceptive mechanisms. It also outlines some of the circuits and processes involved in reflexes and motor control. In addition, it emphasizes the concept of neuroplasticity and its applicability to oro-facial pain, to motor control and motor learning, and to adaptation to changes in the oral sensory environment such as may occur with the placement of dental implants. [source]

Dopamine agonists restore cortical plasticity in patients with idiopathic restless legs syndrome,

MOVEMENT DISORDERS, Issue 5 2009
Vincenzo Rizzo MD
Abstract In the present work, we aimed at assessing whether patients with idiopathic restless legs syndrome (RLS) showed alterations of sensory-motor plasticity, an indirect probe for motor learning, within the motor cortex (M1). Previous findings suggest that learning in human M1 occurs through LTP-like mechanisms. To test our hypothesis, we employed the paired associative stimulation (PAS) protocol by transcranial magnetic stimulation (TMS), which is able to induce LTP-like effects in the motor cortex of normal subjects. Twelve patients with idiopathic RLS and 10 age- and sex-matched control subjects were recruited. PAS protocol consisted of 0.05 Hz electrical median nerve stimulation (90 stimuli), paired with 0.05 Hz TMS (90 stimuli) over the hot spot for stimulating the abductor pollicis brevis (APB) muscle given 25 milliseconds after the onset of the electrical stimulus. Corticospinal excitability recorded in APB muscle, as indexed by MEP obtained after single stimulus, was tested before and up to 30 minutes after PAS protocol. Eight of 12 patients were studied before and after 4 weeks of dopaminergic treatment. PAS protocol increased significantly corticospinal excitability as long as 30 minutes in healthy subjects. On the contrary, PAS protocol did not change the amplitude of MEPs in patients with idiopathic RLS without treatment. PAS associative plasticity was restored after 4 weeks of dopaminergic treatment. Our data demonstrated that associative sensory-motor plasticity, an indirect probe for motor learning, is impaired in idiopathic RLS patients but may be reverted to normal after dopaminergic treatment. © 2008 Movement Disorder Society [source]

Striatal synaptic plasticity: Implications for motor learning and Parkinson's disease

MOVEMENT DISORDERS, Issue 4 2005
Antonio Pisani MD
Abstract Changing the strength of synaptic connections between neurons is widely assumed to be the mechanism by which memory traces are encoded and stored in the central nervous system. Plastic changes appear to follow a regional specialization and underlie the specific type of memory mediated by the brain area in which plasticity occurs. Thus, long-term changes occurring at excitatory corticostriatal synapses should be critically involved in motor learning. Indeed, repetitive stimulation of the corticostriatal pathway can cause either a long-lasting increase or an enduring decrease in synaptic strength, respectively referred to as long-term potentiation (LTP), and long-term depression, both requiring a complex sequence of biochemical events. Once established, LTP can be reversed to control levels by a low-frequency stimulation protocol, an active phenomenon defined "synaptic depotentiation," required to erase redundant information. In the 6-hydroxydopamine rat model of Parkinson's disease (PD), striatal synaptic plasticity has been shown to be impaired, although chronic treatment with levodopa was able to restore it. Of interest, a consistent number of L -dopa,treated animals developed involuntary movements, resembling human dyskinesias. Strikingly, electrophysiological recordings from the dyskinetic group of rats demonstrated a selective impairment of synaptic depotentiation. This survey will provide an overview of plastic changes occurring at striatal synapses. The potential relevance of these findings in the control of motor function and in the pathogenesis both of PD and L -dopa,induced motor complications will be discussed. © 2005 Movement Disorder Society [source]

On the nature and evolution of the neural bases of human language

AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY, Issue S35 2002
Philip Lieberman
Abstract The traditional theory equating the brain bases of language with Broca's and Wernicke's neocortical areas is wrong. Neural circuits linking activity in anatomically segregated populations of neurons in subcortical structures and the neocortex throughout the human brain regulate complex behaviors such as walking, talking, and comprehending the meaning of sentences. When we hear or read a word, neural structures involved in the perception or real-world associations of the word are activated as well as posterior cortical regions adjacent to Wernicke's area. Many areas of the neocortex and subcortical structures support the cortical-striatal-cortical circuits that confer complex syntactic ability, speech production, and a large vocabulary. However, many of these structures also form part of the neural circuits regulating other aspects of behavior. For example, the basal ganglia, which regulate motor control, are also crucial elements in the circuits that confer human linguistic ability andreasoning. The cerebellum, traditionally associated with motor control, is active in motor learning. The basal ganglia are also key elements in reward-based learning. Data from studies of Broca's aphasia, Parkinson's disease, hypoxia, focal brain damage, and a genetically transmitted brain anomaly (the putative "language gene," family KE), and from comparative studies of the brains and behavior of other species, demonstrate that the basal ganglia sequence the discrete elements that constitute a complete motor act, syntactic process, or thought process. Imaging studies of intact human subjects and electrophysiologic and tracer studies of the brains and behavior of other species confirm these findings. As Dobzansky put it, "Nothing in biology makes sense except in the light of evolution" (cited in Mayr, 1982). That applies with as much force to the human brain and the neural bases of language as it does to the human foot or jaw. The converse follows: the mark of evolution on the brains of human beings and other species provides insight into the evolution of the brain bases of human language. The neural substrate that regulated motor control in the common ancestor of apes and humans most likely was modified to enhance cognitive and linguistic ability. Speech communication played a central role in this process. However, the process that ultimately resulted in the human brain may have started when our earliest hominid ancestors began to walk. Yrbk Phys Anthropol 45:36,62, 2002. © 2002 Wiley-Liss, Inc. [source]

Central projections of the saccular and utricular nerves in macaques

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2003
Shawn D. Newlands
Abstract The central projections of the utricular and saccular nerve in macaques were examined using transganglionic labeling of vestibular afferent neurons. In these experiments, biotinylated dextran amine was injected directly into the saccular or utricular neuroepithelium of fascicularis (Macaca fascicularis) or rhesus (Macaca mulatta) monkeys. Two to 5 weeks later, the animals were killed and the peripheral vestibular sensory organs, brainstem, and cerebellum were collected for analysis. The principal brainstem areas of saccular nerve termination were lateral, particularly the spinal vestibular nucleus, the lateral portion of the superior vestibular nucleus, ventral nucleus y, the external cuneate nucleus, and cell group l. The principal cerebellar projection was to the uvula with a less dense projection to the nodulus. Principle brainstem areas of termination of the utricular nerve were the lateral/dorsal medial vestibular nucleus, ventral and lateral portions of the superior vestibular nucleus, and rostral portion of the spinal vestibular nucleus. In the cerebellum, a strong projection was observed to the nodulus and weak projections were present in the flocculus, ventral paraflocculus, bilateral fastigial nuclei, and uvula. Although there is extensive overlap of saccular and utricular projections, saccular inputs to the lateral portions of the vestibular nuclear complex suggest that saccular afferents contribute to the vestibulospinal system. In contrast, the utricular nerve projects more rostrally into areas of known concentration of vestibulo-ocular related cells. Although sparse, the projections of the utricle to the flocculus/ventral paraflocculus suggest a potential convergence with floccular projection inputs from the vestibular brainstem that have been implicated in vestibulo-ocular motor learning. J. Comp. Neurol. 466:31,47, 2003. © 2003 Wiley-Liss, Inc. [source]

Climbing fibre-dependent changes in Golgi cell responses to peripheral stimulation

THE JOURNAL OF PHYSIOLOGY, Issue 20 2008
W. Xu
Golgi cells are important elements of the cerebellar cortex, controlling the flow of mossy fibre information to other cells via granule cells. Several anatomical reports suggest that climbing fibre afferents contact Golgi cells, and electrophysiological studies suggest that they depress Golgi cell firing. We reinvestigated this issue and, given that climbing fibres mediate synaptic plasticity in the cerebellar cortex, we have examined the effects of conjunctive stimulation of peripheral afferents and climbing fibres on Golgi cell responses. The results confirm that climbing fibre stimulation depresses Golgi cell firing at short latency. Golgi cells responded to stimulation of peripheral afferents with longer latency depressions of firing and after conjunctive stimulation with climbing fibres these were significantly reduced. The reductions developed progressively over 20 min of conjunctive stimulation and were persistent (up to 84 min). Temporal conjunction of the inputs was important because non-synchronous stimulation of climbing fibres and peripheral afferents failed to alter the peripheral afferent-evoked response in Golgi cells. In control experiments using either the same climbing fibre stimulation alone, or peripheral afferent stimulation paired with brainstem stimulation that did not activate climbing fibres, responses were not depressed. The results thus show that conjunctive stimulation of climbing fibres with other inputs to Golgi cells can induce long-term changes in Golgi cell responses in vivo. This raises the possibility that changes in Golgi cell peripheral responses mediated by climbing fibres can potentially contribute to cerebellar motor learning. [source]

Dopamine-dependent motor learning: Insight into levodopa's long-duration response

ANNALS OF NEUROLOGY, Issue 5 2010
Jeff A. Beeler PhD
Objective Dopamine (DA) is critical for motor performance, motor learning, and corticostriatal plasticity. The relationship between motor performance and learning, and the role of DA in the mediation of them, however, remain unclear. Methods To examine this question, we took advantage of PITx3-deficient mice (aphakia mice), in which DA in the dorsal striatum is reduced by 90%. PITx3-deficient mice do not display obvious motor deficits in their home cage, but are impaired in motor tasks that require new motor skills. We used the accelerating rotarod as a motor learning task. Results We show that the deficiency in motor skill learning in PITx3(,/,) is dramatic and can be rescued with levodopa treatment. In addition, cessation of levodopa treatment after acquisition of the motor skill does not result in an immediate drop in performance. Instead, there is a gradual decline of performance that lasts for a few days, which is not related to levodopa pharmacokinetics. We show that this gradual decline is dependent on the retesting experience. Interpretation This observation resembles the long-duration response to levodopa therapy in its slow buildup of improvement after the initiation of therapy and gradual degradation. We hypothesize that motor learning may play a significant, underappreciated role in the symptomatology of Parkinson disease as well as in the therapeutic effects of levodopa. We suggest that the important, yet enigmatic long-duration response to chronic levodopa treatment is a manifestation of rescued motor learning. ANN NEUROL 2010;67:639,647 [source]

The effects of ageing and cognitive impairment on on-line and off-line motor learning

APPLIED COGNITIVE PSYCHOLOGY, Issue 2 2010
Jin H. Yan
Skilled performance is a collective function of practice-related experiences (online learning) and post-practice memory consolidation during sleep (offline learning). This study examines the effects of ageing and cognitive impairment on the on- and offline learning of a point-to-point arm movement. In a 3-day experiment, older adults (cognitively normal or impaired) and young adults (YAs) were randomly assigned to practice or no-practice conditions. Changes in the dependent measures of movement time and timing error were analysed within and between conditions across days. The findings suggest that both age and cognitive function affect skill learning. YAs improved performance via both on- and offline learning whereas older adults with normal cognitive capacities appeared to learn the movement skill primarily in an online mode. Cognitive impairments were found to hinder both types of skill learning. Implications for motor skill acquisition and rehabilitation are briefly discussed. Copyright © 2009 John Wiley & Sons, Ltd. [source]