Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “sensorimotor behavior”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

Context estimation for sensorimotor control.

Human motor behavior is remarkably accurate and appropriate even though the properties of our own bodies as well as the objects we interact with vary over time. To adjust appropriately, the motor system has to estimate the context, that is the properties of objects in the world and the prevailing environmental conditions. Here we show that to determine the current context the CNS uses information from both prior knowledge of how the context might evolve over time and from the comparison of predicted and actual sensory feedback. We show that these two sources of information may be modeled within the CNS and combined to derive an accurate estimate of the context which adjusts motor command selection. This provides a novel probabilistic framework for sensorimotor control.

Adaptation, Physiological↗

Building neural representations of habits.

Memories for habits and skills ("implicit or procedural memory") and memories for facts ("explicit or episodic memory") are built up in different brain systems and are vulnerable to different neurodegenerative disorders in humans. So that the striatum-based mechanisms underlying habit formation could be studied, chronic recordings from ensembles of striatal neurons were made with multiple tetrodes as rats learned a T-maze procedural task. Large and widely distributed changes in the neuronal activity patterns occurred in the sensorimotor striatum during behavioral acquisition, culminating in task-related activity emphasizing the beginning and end of the automatized procedure. The new ensemble patterns remained stable during weeks of subsequent performance of the same task. These results suggest that the encoding of action in the sensorimotor striatum undergoes dynamic reorganization as habit learning proceeds.

Action Potentials↗

Visuomotor learning in immersive 3D virtual reality in Parkinson's disease and in aging.

Successful adaptation to novel sensorimotor contexts critically depends on efficient sensory processing and integration mechanisms, particularly those required to combine visual and proprioceptive inputs. If the basal ganglia are a critical part of specialized circuits that adapt motor behavior to new sensorimotor contexts, then patients who are suffering from basal ganglia dysfunction, as in Parkinson's disease should show sensorimotor learning impairments. However, this issue has been under-explored. We tested the ability of 8 patients with Parkinson's disease (PD), off medication, ten healthy elderly subjects and ten healthy young adults to reach to a remembered 3D location presented in an immersive virtual environment. A multi-phase learning paradigm was used having four conditions: baseline, initial learning, reversal learning and aftereffect. In initial learning, the computer altered the position of a simulated arm endpoint used for movement feedback by shifting its apparent location diagonally, requiring thereby both horizontal and vertical compensations. This visual distortion forced subjects to learn new coordinations between what they saw in the virtual environment and the actual position of their limbs, which they had to derive from proprioceptive information (or efference copy). In reversal learning, the sign of the distortion was reversed. Both elderly subjects and PD patients showed learning phase-dependent difficulties. First, elderly controls were slower than young subjects when learning both dimensions of the initial biaxial discordance. However, their performance improved during reversal learning and as a result elderly and young controls showed similar adaptation rates during reversal learning. Second, in striking contrast to healthy elderly subjects, PD patients were more profoundly impaired during the reversal phase of learning. PD patients were able to learn the initial biaxial discordance but were on average slower than age-matched controls in adapting to the horizontal component of the biaxial discordance. More importantly, when the biaxial discordance was reversed, PD patients were unable to make appropriate movement corrections. Therefore, they showed significantly degraded learning indices relative to age-matched controls for both dimensions of the biaxial discordance. Together, these results suggest that the ability to adapt to a sudden biaxial visuomotor discordance applied in three-dimensional space declines in normal aging and Parkinson disease. Furthermore, the presence of learning rate differences in the PD patients relative to age-matched controls supports an important contribution of basal ganglia-related circuits in learning novel visuomotor coordinations, particularly those in which subjects must learn to adapt to sensorimotor contingencies that were reversed from those just learned.

Adaptation, Physiological↗

Role of preoperative and postoperative sensorimotor training on restoration of the equilibrium behavior in adult mice following cerebellectomy.

The equilibrium behavior of cerebellectomized C57/BL6 adult mice was studied on a rota rod rotating at 20 revolutions per minute and the influence of preoperative or/and postoperative training on restoration of equilibrium capabilities investigated. The duration of the preoperative training was either short (1 day) or long (7 days). The postoperative training began either the day after cerebellectomy or was delayed by 7 days. The results demonstrate that postoperative training was efficient in restoring the equilibrium behavior in all cases, except for the animals which were trained for a long period (7 days) before the lesion. Preoperative training was also efficient providing it was long enough (7 days), except for the animals which postoperative training began the day after cerebellectomy. It can be stated that both preoperative and postoperative trainings influence the restoration of the equilibrium following a cerebellectomy and that, in some instances, preoperative training can be as efficient as postoperative.

Animals↗

Age-dependent neurobehavioral plasticity following forebrain dopamine depletions.

The differential neurobehavioral effects of forebrain dopamine (DA) depletions in neonatal and adult rats are reviewed. In contrast to the severe and long-lasting parkinsonian sensorimotor deficits seen in rats sustaining large DA depletions as adults, rats comparably depleted as neonates are spared from these gross behavioral deficits. While DA released from residual striatal DA terminals remains necessary for the gradual recovery of sensorimotor function in rats lesioned as adults and the sparing from deficits in rats lesioned as neonates, the specific roles of D1- and D2-like receptors differ between the two age groups. Coactivation of striatal D1 and D2 receptors by residual DA is necessary for the expression of sensorimotor behavior in rats depleted of DA as adults (and in intact rats) whereas activation of either D1 or D2 receptors is sufficient for these behaviors in rats depleted of DA as neonates. We discuss the D1/D2 modulation of several important markers for striatal transmission (acetylcholine release from interneurons, induction of c-fos, and the expression of GAD65 mRNA in striatal efferents) as potential mechanisms underlying this striking age-dependent plasticity following forebrain DA depletions.

Aging↗

Functional reactivation of the deafferented neostriatum by nigral transplants.

Functional deficits following brain lesions can be due not only to the disruption of conduction in specific input and output pathways passing through the site of injury, but also to the loss of important regulatory systems controlling the functional state of neuronal circuitries in areas distant from the lesion. For example, the behavioural disturbances that result from lesions of the nigrostriatal dopamine (DA) pathways can be reversed by administration of dopamine receptor-activating drugs, such as L-dopa or apomorphine. This suggests that the lesioned dopaminergic system, rather than conveying specific input and output signals, is normally acting on neuronal machineries whose activity levels are set by the activity at the dopaminergic synapses. Thus the neurological deficits resulting from these lesions are due to functional inactivation of otherwise intact neostriatal circuitries. Previous studies have shown that intracerebral transplants of embryonic substantia nigra can compensate for drug-induced as well as spontaneous asymmetric motor behaviour (expressed as a tendency to move in circles towards the lesioned side), whereas the sensorimotor asymmetry, which is pronounced in rats with a unilateral lesion of the nigrostriatal DA pathway, was unaffected by the transplant. We report here that restoration of striatal dopaminergic neurotransmission by nigral transplants in animals with bilateral, complete lesions of the nigral transplants in animals with bilateral, complete lesions of the nigrostriatal DA pathways can reinstate not only certain aspects of spontaneous motor behavior, but also sensorimotor orientation and sensory attention on the side of the body contralateral to the graft.

Animals↗

Mapping behavioral traits by use of genome-tagged mice.

OBJECTIVE: Complex trait mapping has been widely used to analyze the genetics of behavior. However, the approach has some disadvantages, including poor gene localization and low replicability. Genome-tagged mice (GTMs) are sets of congenic mouse strains that span the entire mouse genome and are a promising reagent for localization of genes contributing to behavior. METHODS: In order to map behavioral loci of interest, a GTM was investigated in which the middle region of Chromosome 1 from DBA/2J was introgressed onto a C57BL/6J background. The GTM was analyzed for behaviors related to sensorimotor gating, anxiety, depression, pain sensitivity, and learning and memory. RESULTS: The GTM was found to harbor a locus contributing to learning and memory, replicating results from complex trait analysis. CONCLUSIONS: The GTMs should be a valuable resource for mapping and confirmation of loci contributing to complex behavioral traits in the mouse, with ultimate implications for human genomic-based research, as well.

Animals↗

Behavioral characterization of the Tg2576 transgenic model of Alzheimer's disease through 19 months.

Behavioral characterization of Alzheimer's disease (AD) transgenic models over multiple time points during aging has been largely inadequate, usually being limited to one or two cognitive-based tasks. In this context, the present study utilized a comprehensive 6-week behavioral battery to characterize sensorimotor and cognitive performance of Tg2576 AD transgenic (Tg+) mice and nontransgenic (Tg-) controls aged 3, 9, 14, and 19 months. Compared collectively to Tg- mice over all four time points, Tg+ mice were impaired in Y-maze spontaneous alternation, visible platform recognition, and several sensorimotor tasks; Tg+ mice also showed an overall increase in activity measures. The deficits in visible platform became evident by 9 months of age, while those in sensorimotor tasks became clearly manifest by 14 months. Although the behavioral impairments exhibited by Tg+ mice were usually progressive through 19 months, Tg- animals also showed similar progressive decline in the same behavioral measures; thus, no task revealed a progressive behavioral decline exclusive to Tg+ mice. Moreover, although the 6-week behavioral battery included six cognitively based tasks (i.e., Y-maze, visible platform, Morris water maze, circular platform, passive avoidance, and active avoidance), behavioral analysis through 19 months revealed Tg+ mice to be impaired in only the Y-maze and visible platform tasks. Consequently, Tg2576 mice do not exhibit widespread, profound cognitive impairment, even into old age. This may reflect their predominant C57BL/6 background and an apparent inability of the mutant transgene to profoundly alter performance therein.

Age Factors↗

Neonatal perturbation of neurotrophic signaling results in abnormal sensorimotor gating and social interaction in adults: implication for epidermal growth factor in cognitive development.

Epidermal growth factor (EGF) and its structurally related proteins are implicated in the developmental regulation of various brain neurons, including midbrain dopaminergic neurons. There are EGF and EGF receptor abnormalities in both brain tissues and blood from schizophrenic patients. We administered EGF to neonatal rats to transiently perturb endogenous EGF receptor signaling and evaluated the neurobehavioral consequences. EGF-treatment-induced transient impairment in tyrosine hydroxylase expression. The animals grew normally, exhibited normal weight increase, glial growth, and gross brain structures, and later lost the tyrosine hydroxylase abnormality. During and after development, however, the rats began to display various behavioral abnormalities. Abnormal sensorimotor gating was apparent, as measured by deficits in prepulse inhibition of acoustic startle. Motor activity and social interaction scores of the EGF-treated animals were also impaired in adult rats, though not in earlier developmental stages. In parallel, there was a significant abnormality in dopamine metabolism in the brain stem of the adult animals. Gross learning ability appeared to be normal as measured by active avoidance. These behavioral alterations, which are often present in schizophrenic models, were ameliorated by subchronic treatment with clozapine. Although the molecular and/or physiologic background(s) of these behavioral abnormalities await further investigation, the results of the present experiment indicate that abnormal EGF receptor stimulation given during limited neonatal stages can result in severe and persistent cognitive/behavioral dysfunctions, which appear only in adulthood.

Animals↗

Amelioration of sensory attention and sensorimotor deficits by chromaffin cell grafts to the cerebral cortex of nucleus basalis magnocellularis lesioned rats.

Rats that have received lesions to the nucleus basalis magnocellularis display with a variety of behavioral deficits; among these are decreases in performance of maze tests as well as deficiencies on measures of general health, sensory attention and sensorimotor abilities. We have previously shown that grafts of chromaffin cells placed in the cerebral cortex of nucleus basalis magnocellularis lesioned rats can ameliorate the lesion-induced deficits in performance of a task involving spatial memory. In the present study, we find that lesion-induced deficits in the sensory attention measure of exploration of the environment (head scanning) as well as the sensorimotor behavior involving a rat righting itself when placed nose down on an inclined grid are evident at 8 weeks post-lesion in lesioned-alone rats; these deficits are significantly ameliorated by chromaffin cell grafts in the cerebral cortex placed two weeks following the lesion procedure. These findings may have relevance to the use of chromaffin cells for grafting in neurodegenerative disorders in which sensorimotor or attention deficit components are involved.

Acetylcholinesterase↗

Segregation of behavior-specific synaptic inputs to a vertebrate neuronal oscillator.

Although essential for understanding the mechanisms underlying sensorimotor integration and motor control of behaviors, very little is known about the degree to which different behaviors share neural elements of the sensorimotor command chain by which they are controlled. Here, we provide, to our knowledge, the first direct physiological evidence that various modulatory premotor inputs to a vertebrate central pattern generator, the pacemaker nucleus in gymnotiform electric fish, carrying distinctly different behavioral information, can remain segregated from their various sites of origin in the diencephalon to the synaptic termination sites on different target neurons in the medullary pacemaker nucleus. During pharmacological activation of each of the premotor inputs originating from the three prepacemaker nuclei so far identified, we determined in vivo the changes in input resistance in the neuronal elements of the pacemaker nucleus, i.e., relay cells and pacemaker cells. We found that each input yields significantly different effects on these cells; the inputs from the two diencephalic prepacemaker nuclei, PPnC and PPnG, which resulted in increased oscillator activity, caused significantly lower input resistances in relay and pacemaker cells, respectively, exhibiting drastically different time courses. The input from the sublemniscal prepacemaker nucleus, which resulted in reduced oscillator activity, however, caused a significant increase in input resistance only in relay cells. Considering that the sensory pathways processing stimuli yielding these behaviors are separated as well, this study indicates that sensorimotor control of different behaviors can occur in strictly segregated channels from the sensory input of the brain all through to the synaptic input level of the final premotor command nucleus.

Animals↗

Prepulse inhibition of the acoustic startle response is disrupted by N-ethyl-3,4-methylenedioxyamphetamine (MDEA) in the rat.

N-Ethyl-3,4-methylenedioxyamphetamine (MDEA) is a derivative of methylenedioxyamphetamine (MDA), a substituted amphetamine with demonstrated abuse liability. MDA, MDEA and a third substituted amphetamine, methylenedioxymethamphetamine (MDMA), all produce a destructive action on central serotonin neurons and appear to induce some similar behavioral effects. The present study investigated the effects of racemic MDEA and its stereoisomers on prepulse inhibition of the acoustic startle response, a behavioral model of sensorimotor gating that is sensitive to psychostimulant drugs. Rats were subjected to 122 dB[A] acoustic noises, some of which were preceded by a weak 80 dB[A] prepulse noise. In vehicle-injected control rats, the prepulse induced a significant decrease in startle amplitude when compared to trials in which startle stimuli were not preceded by prepulses. Administration of racemic MDEA (0.3-10.0 mg/kg) and (+) MDEA (0.1-3.0 mg/kg) induced a significant attenuation in prepulse inhibition, while (-) MDEA (0.3-10.0 mg/kg) did not. Racemic MDMA (0.3-10.0 mg/kg) produced similar though not significant effects. These results confirm a stimulant-like behavioral effect of MDEA despite its relatively modest effects on dopamine markers, and support findings that the (+) stereoisomers of substituted amphetamines are more potent than tha (-) stereoisomers in producing psychostimulant-like biochemical and behavioral effects.

3,4-Methylenedioxyamphetamine↗

Transient cerebral dysfunction secondary to high-dose methotrexate.

A transient acute neurologic syndrome occurred in 22 patients receiving high-dose methotrexate (HDMTX) (8 to 9 g/m2) for a variety of malignancies. The neurologic signs were similar in all cases. The syndrome occurred an average of six days after the second or third weekly treatment. Common findings included behavioral abnormalities, focal sensorimotor signs, and abnormal reflexes. Signs often alternated from one side to the other. Evaluations including computed tomography (CT) scan, lumbar puncture, hemogram, and blood chemistry were normal. The EEG revealed some slowing in all cases. The cause of this syndrome is unknown. It is transient and usually does not recur. Its appearance does not preclude further treatment with HDMTX.

Adolescent↗

Citicoline for treatment of experimental focal ischemia: histologic and behavioral outcome.

We evaluated the effect of chronic administration of CDP-choline, an intermediate of phospholipid synthesis, on outcome from middle cerebral artery occlusion, ranging from 30 to 120 min in duration in spontaneously hypertensive rats. Rats were randomly assigned to either CDP-choline 500 mg kg-1 or saline. CDP-choline treatment was initiated by intraperitoneal injection 15 min after the onset of ischemia and continued once a day for 14 days. Morphologic damage and behavioral dysfunction (motor and sensorimotor performance) were evaluated, and the maximal morphologic damage (Volmax), maximal behavioral dysfunction (BDmax) as well as the duration of ischemia producing half-maximal morphologic damage (T50) or behavioral dysfunction (BD50) were calculated using a curve-fitting program (ALLFIT). Ischemia in control animals produced a Volmax of 103.3 +/- 13.6 mm3. CDP-choline did not affect this value (Volmax of 101.6 +/- 11.4 mm3). However, CDP-choline significantly extended the T50 from 38.3 +/- 5.9 to 60.5 +/- 4.3 min (p < 0.05). Similar to the morphologic outcome, CDP-choline had no effect on BDmax but significantly extended BD50 from 41.9 +/- 4.6 to 72.9 +/- 24.5 min (p < 0.05). Our results suggest that the effectiveness of CDP-choline is greater in animals demonstrating submaximal ischemic injury which in this model is produced by 30-75 min of ischemia (effect on T50 and BD50), than in animals suffering maximal ischemic injury produced by ischemia longer than 75 min (no effect on Volmax and BDmax). These results may reflect a threshold of biological membrane damage within which CDP-choline is able to restore phospholipid content/arrangement and retain membrane integrity.

Animals↗

Basal forebrain cholinergic modulation of auditory activity in the zebra finch song system.

The cholinergic basis of auditory "gating" in the sensorimotor nucleus HVc and its efferent target robustus archistriatalis (RA) was investigated in anesthetized zebra finches. Injections of cholinergic agonists carbachol or muscarine into HVc strongly affected discharge rates and diminished auditory responsiveness in both HVc and its target RA, changes toward an awake-like condition. HVc nicotine injections produced similar strong effects in HVc, but weaker and inconsistent effects in RA. Stimulation of basal forebrain (BF) produced an initial transient network shutdown followed by diminished auditory responsiveness in HVc and RA. All stimulation effects were blocked when preceded by HVc injections of nicotinic or muscarinic antagonists. Thus, BF cholinergic modulation of song system auditory activity acting via functionally distinct HVc circuits can contribute to auditory gating. We hypothesize that wakeful BF activity levels block sensory input to motor systems and adaptively change during behavior to allow sensorimotor feedback such as auditory feedback during singing.

Acoustic Stimulation↗

Expanding cyst of the septum pellucidum. Case report.

Expanding cysts of the septum pellucidum, although rare, may be a cause of significant neurological dysfunction. Most become symptomatic as a result of obstruction of the interventricular foramina and produce headaches, papilledema, emesis, and loss of consciousness. Behavioral, autonomic, and sensorimotor symptoms occur when an expanding cyst impinges on the structures of the hypothalamoseptal triangle or impairs the deep cerebral venous drainage. Neuroophthalmological symptoms may develop as a consequence of hydrocephalus or direct compression of visual structures. The authors describe the case of a young boy with an expanding septum pellucidum cyst who presented with a sudden, severe headache and loss of consciousness. In addition, he had a history of hyperactivity and progressively declining school performance. All symptoms resolved following decompression of the cyst. Seventeen cases from the literature are reviewed. The pathophysiological mechanisms underlying the development of symptoms secondary to expanding septum pellucidum cysts are outlined, and the related clinical neuroanatomy is described. A model is proposed for the natural history of expanding septum pellucidum cysts that provides a rational basis for understanding their clinical behavior and response to intervention. In most cases, fenestration or shunting will relieve the obstructive hydrocephalus and mass effect caused by the cyst and will produce rapid symptomatic improvement.

Brain Diseases↗

Neuroanatomical distribution of cannabinoid receptor gene expression in the brain of the rough-skinned newt, Taricha granulosa.

Type I cannabinoid receptor (CB1) is a G-protein coupled receptor with a widespread distribution in the central nervous system in mammals. In a urodele amphibian, the rough-skinned newt (Taricha granulosa), recent evidence indicates that endogenous cannabinoids (endocannabinoids) mediate behavioral responses to acute stress and electrophysiological responses to corticosterone. To identify possible sites of action for endocannabinoids, in situ hybridization using a gene and species specific cRNA probe was used to label CB1 mRNA in brains of male T. granulosa. Labeling of CB1 mRNA in the telencephalon was observed in the olfactory bulb and all areas of the pallium, as well as the bed nucleus of the stria terminalis and nucleus amygdalae dorsolateralis. The labeling of CB1 mRNA was also found in regions of the preoptic area, thalamus, midbrain tegmentum and tectum, cerebellum, and the stratum griseum of the hindbrain. A notable difference in CB1 labeling between this amphibian and mammals is the abundance of labeling in areas associated with olfaction (anterior olfactory nuclei, nucleus amygdalae dorsolateralis, and lateral pallium), which hints that endocannabinoids might modulate responses to odors as well as pheromones. This widespread distribution of CB1 labeling, particularly in sensory and motor control centers, fits with prior results showing that endocannabinoids modulate sensorimotor processing and behavioral output in this species. The distribution of CB1 in the brain of T. granulosa was in many of the same sites previously observed in the brain of the anuran amphibian, Xenopus laevis, as well as those of different species of mammals, suggesting that endocannabinoid signaling pathways are conserved.

Animals↗

Developmental modulation of the temporal relationship between brain and behavior.

Humans and songbirds shape learned vocalizations during a sensorimotor sensitive period or "babbling" phase. The brain mechanisms that underlie the shaping of vocalizations by sensory feedback are not known. We examined song behavior and brain activity in zebra finches during singing as they actively shaped their song toward a tutor model. We now show that the temporal relationship of behavior and activity in the premotor area HVC changes with the development of song behavior. During sensorimotor learning, HVC bursting activity both preceded and followed learned vocalizations by hundreds of milliseconds. Correspondingly, the duration of bursts that occurred during ongoing song motif behavior was prolonged in juveniles, as compared with adults, and was inversely correlated with song maturation. Multielectrode single-unit recording in juveniles revealed that single fast-spiking neurons were active both before and after vocalization. These same neurons responded to auditory stimuli. Collectively, these data indicate that a key aspect of sensory critical periods--prolonged bursting--also applies to sensorimotor development. In addition, prolonged motor discharge and sensory input coincide in single neurons of the developing song system, providing the necessary cellular elements for sensorimotor shaping through activity-dependent mechanisms.

Action Potentials↗