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 73 records · Page 4Linked to original sources
PubMed1995

Posttraumatic brain hypothermia provides protection from sensorimotor and cognitive behavioral deficits.

The purpose of this study was to determine the degree of sensorimotor and cognitive protection conferred by posttraumatic brain hypothermia. Baseline measurements were taken on sensorimotor tasks involving forelimb placing and beam-walking, as well as on a spatial navigational task utilizing the water maze. Twenty-four hours after the last baseline measurements, normothermic (37 degrees C) animals were subjected to a fluid percussion pulse (1.9-2.4 atm) over the right parietal sensorimotor cortex. Following trauma, brain temperature was maintained for 3 h at either normothermic (37 degrees C, group TBI-N, n = 12) or hypothermic levels (30 degrees C, group TBI-H, n = 11). Shams (n = 10) underwent all surgical procedures including posttraumatic brain injury (TBI) temperature manipulation, but were not subjected to the fluid percussive pulse. Beam-walking and forelimb placing measures were begun 24 h post-TBI and continued for 2 weeks. Animals were tested on the water maze task for 2 days beginning 24 h post-TBI. TBI produced substantial deficits in contralateral limb placing, which recovered over approximately one week. Hypothermia provided partial protection from these deficits, with TBI-H animals exhibiting intermediate scores that differed from both sham and TBI-N animals (p < 0.03). In the water maze, there was a distinction between groups in the ability to navigate 48 h after TBI. TBI-N animals performed significantly worse than sham and TBI-H animals (both p < 0.01), whereas there was no significant difference between the scores of sham and TBI-H animals. The present data demonstrate that moderate postinjury brain hypothermia can provide protection from sensorimotor and cognitive behavioral deficits as well as neuropathology in a model of traumatic brain injury associated with early neuronal and microvascular injury.

Animals↗
PubMed1996

Neuroprotective effects of riluzole on a model of Parkinson's disease in the rat.

The aim of the present study was to analyse whether riluzole, a compound that interacts with the voltage-dependent sodium channel and impairs glutamatergic transmission, would exhibit a neuroprotective activity in a model of Parkinson's disease in the rat. Impaired skilled forelimb use, circling behavior, and altered dopaminergic metabolism of the mesotelencephalic system were evaluated in unilaterally 6-hydroxydopamine-lesioned rats. Riluzole was administered twice 15 min before, and 24 h after, the lesion. Riluzole reduced both the contralateral rotations induced by apomorphine and the ipsilateral ones elicited by amphetamine. Moreover, the decreased dopaminergic metabolism seen after 6-hydroxydopamine injection was attenuated in the riluzole-treated animals, at both the striatal and nigral levels. These biochemical and behavioral results demonstrate the ability of riluzole partially to protect the degeneration of the nigrostriatal dopaminergic neurons induced by the toxin 6-hydroxydopamine. Perhaps, the most striking evidence for the protective effect of riluzole was that this compound improved the skilled paw use, a complex sensorimotor behavior which is not easily ameliorated by palliative therapies such as dopaminergic grafts. These results extend previous data showing that riluzole counteracts the toxicity induced by 1-methyl-4-1,2,3,6-tetrahydropyridine and 1-methyl-4-phenylpyridinium in rodent dopaminergic neurons. The use of riluzole may be considered of potential interest for the neuroprotective therapy of Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1981

Sensorimotor skills and language comprehension in autistic children.

The objectives of this study were to examine the level of sensorimotor concepts of young autistic children and to relate these concepts to language comprehension. A sample of 16 autistic children with a mean mental age of 24.8 months was administered a standardized scale of sensorimotor intelligence and of receptive language. The autistic children demonstrated surprisingly sophisticated sensorimotor skills, particularly object permanence. While their initial performance was inferior to that of normal controls matched on mental age, particularly in their use of objects in combination, the difference between groups diminished on the second test administration. On the receptive language measure, the autistic children were less able to identify words correctly. The sensorimotor behavior of autistic children who demonstrated language comprehension did not differ from those who showed no language comprehension, except that the former group tended to use an object as an instrument somewhat more frequently. The fact that the autistic children were so impaired in language even with fairly good sensorimotor skills suggests that these skills, particularly object permanence, play a minor role in their language acquisition.

Age Factors↗
PubMed2002

Orienting responses and vocalizations produced by microstimulation in the superior colliculus of the echolocating bat, Eptesicus fuscus.

An echolocating bat actively controls the spatial acoustic information that drives its behavior by directing its head and ears and by modulating the spectro-temporal structure of its outgoing sonar emissions. The superior colliculus may function in the coordination of these orienting components of the bat's echolocation system. To test this hypothesis, chemical and electrical microstimulation experiments were carried out in the superior colliculus of the echolocating bat, Eptesicus fuscus, a species that uses frequency modulated sonar signals. Microstimulation elicited pinna and head movements, similar to those reported in other vertebrate species, and the direction of the evoked behaviors corresponded to the site of stimulation, yielding a map of orienting movements in the superior colliculus. Microstimulation of the bat superior colliculus also elicited sonar vocalizations, a motor behavior specific to the bat's acoustic orientation by echolocation. Electrical stimulation of the adjacent periaqueductal gray, shown to be involved in vocal production in other mammalian species, elicited vocal signals resembling acoustic communication calls of E. fuscus. The control of vocal signals in the bat is an integral part of its acoustic orienting system, and our findings suggest that the superior colliculus supports diverse and species-relevant sensorimotor behaviors, including those used for echolocation.

Acoustics↗
PubMed1983

Posture-independent sensorimotor analysis of inter-hemispheric receptor asymmetries in neostriatum.

Nigrostriatal dopaminergic neurons are thought to be critically important for somato-sensorimotor behavior. Following unilateral irreversible elimination of these neurons, an animal shows an ipsiversive postural bias and permanently fails to orient its head toward tactile stimuli placed on the contralateral side of the body. In response to apomorphine, a dopamine agonist, these rats display contraversive circling. This effect is thought to reflect denervation-induced proliferation of dopamine receptors in the ipsilateral striatum. We have developed a sensitive procedure that measures sensorimotor function independent of postural and circling biases. We record the latencies to remove small pieces of adhesive stimuli placed onto the snout or radial surface of the forelimbs. The stimuli are placed symmetrically and simultaneously, which is analogous to tactile-extinction procedures used clinically. In the first study we found that rats with unilateral 6-hydroxydopamine (6-OHDA)-induced lesions of the nigrostriatal pathway showed a contralateral sensorimotor bias in response to doses of apomorphine below those necessary to produce contraversive circling. In a second study, unilateral striatal microinjections of kainic acid (KA) were used to destroy the neurons on which the postsynaptic dopaminergic receptors of the nigrostriatal system are contained. Compared to 6-OHDA, KA produced unexpected results in standard orientation tests. None of the KA-treated rats showed contralateral neglect, and some even showed ipsilateral deficits. However, the standard orientation tests are confounded by postural asymmetries, which were irregular in the KA-treated group. Using again the posture-independent sensorimotor procedure, we found that all KA-treated rats, like the 6-OHDA-treated rats, uniformly displayed ipsilateral sensorimotor biases. Sensorimotor function relating to inter-striatal asymmetries may be more specifically assessed with the bilateral-adhesive tests.

Animals↗
PubMed2000

Cognitive deficits after focal cerebral ischemia in mice.

BACKGROUND AND PURPOSE: The interpretation of cognitive data in many experimental stroke studies is problematic because middle cerebral artery occlusion (MCAO) is associated with sensorimotor alterations that may become confounding factors in cognitive testing. The purpose of the current study was to determine if it is possible to measure MCAO-induced cognitive deficits by using short durations of ischemia that do not result in alterations in sensorimotor behavior in mice. METHODS: Male C57/Bl6 mice were subjected to 60 or 90 minutes of intraluminal MCAO or sham surgery. In the first cohort of animals (n=12/group), locomotor activity, balance, and coordination were evaluated 2 weeks after surgery. In a second cohort of animals (n=10/group), the effects of 60 minutes of MCAO on subsequent learning and memory were assessed with a step-down passive avoidance task beginning 1 week after surgery. In a third cohort of animals (n=8 to 10/group), training in a passive avoidance task was completed before 60 minutes of MCAO, then retention of the task was assessed 1 week after surgery. In all animals, infarction size was determined after 14 days of reperfusion with use of cresyl violet staining and quantitative image analysis. RESULTS: There was no significant difference in infarction volume in the cerebral cortex or caudoputamen after 60 versus 90 minutes of MCAO. However, there was a significant increase in latency to move 1 body length in the 90-minute MCAO group compared with the 60-minute MCAO and sham groups. In 2 additional cohorts of animals, 60-minute MCAO was associated with a deficit in the acquisition and retention of a passive avoidance task regardless of whether the task training occurred before or after MCAO. CONCLUSIONS: Long-term cognitive deficits can be induced in mice by using a short duration of MCAO (60 minutes) that does not result in concomitant sensorimotor deficits.

Animals↗
PubMed2006

Cerebellar synaptic defects and abnormal motor behavior in mice lacking alpha- and beta-dystrobrevin.

The dystrobrevins (alphaDB and betaDB) bind directly to dystrophin and are components of a transmembrane dystrophin-glycoprotein complex (DGC) that links the cytoskeleton to extracellular proteins in many tissues. We show here that alphaDB, betaDB, and dystrophin are all concentrated at a discrete subset of inhibitory synapses on the somata and dendrites of cerebellar Purkinje cells. Dystrophin is depleted from these synapses in mice lacking both alphaDB and betaDB, and DBs are depleted from these synapses in mice lacking dystrophin. In dystrophin mutants and alphaDB,betaDB double mutants, the size and number of GABA receptor clusters are decreased at cerebellar inhibitory synapses, and sensorimotor behaviors that reflect cerebellar function are perturbed. Synaptic and behavioral abnormalities are minimal in mice lacking either alphaDB or betaDB. Together, our results show that the DGC is required for proper maturation and function of a subset of inhibitory synapses, that DB is a key component of this DGC, and that interference with this DGC leads to behavioral abnormalities. We suggest that motor deficits in muscular dystrophy patients, which are their cardinal symptoms, may reflect not only peripheral derangements but also CNS defects.

Animals↗
PubMed2004

Spectrum of cutaneous hyperalgesias/allodynias in neuropathic pain patients.

OBJECTIVES: The aim of this study was to discern the pathophysio-logical bases for neuropathic hyperalgesias. METHODS: In this study, neurological and neurophysiological evaluation of 132 consecutive hyperalgesia patients using rigorous clinical and laboratory protocols were carried out. RESULTS: Two discrete semeiologic entities emerged: classic neurological vs atypical, fulfilling taxonomically complex regional pain syndrome (CRPS) II and I, respectively. The classic group (34.9%) exhibited sensorimotor patterns restricted to nerve distribution and documented nerve fiber dysfunction. Among them four (3.03%) had sensitization of C-nociceptors, seven (5.3%) had central release of nociceptive input, and 35 (26.52%) probable ectopic nerve impulse generation. The atypical group (65.1%) displayed weakness with interrupted effort; non-anatomical hypoesthesia and hyperalgesia; hypoesthesia or paresis reversed by placebo, or atypical abnormal movements, and physiological normality of motor and sensory pathways. CONCLUSIONS: Spatiotemporal features of neuropathic hyperalgesia constitute key criteria for differential diagnosis between CRPS II and I and, together with other behavioral sensorimotor features, signal psychogenic pseudoneurological dysfunction vs structural neuropathology. 'Neuropathic' hyperalgesias may reflect neuropathological or psychopathological disorders.

Adolescent↗
PubMed1992

Age-related changes in spontaneous behavior and learning in NMRI mice from middle to old age.

Spontaneous behavior, sensorimotor reflexes and learning of 3-, 11-, 17- and 22-month-old virgin female NMRI mice were compared. Sensorimotor abilities decreased significantly from the age of 17 months in proportion to the muscular and equilibrium demand of the test. Open-field activity, hole board exploration as well as activity in the Y maze and plus maze decreased from the age of 11 months. However, in the open-field and Y maze, it was not possible to distinguish between 11-, 17- and 22-month-old mice, whereas in the plus maze, activity was drastically decreased in 17- and 22-month-old mice. In the plus maze, indices of fear-motivated behavior suggest a greater sensitivity to the situation in the age groups of 17 and 22 months. Spontaneous alternation also decreased from the age of 11 months, but at the age of 22 months, a rotational behavior emerged. Spatial learning was markedly impaired from middle age, i.e., 11 months, as indicated by longer latencies and absence of spatial bias in place learning. In cued learning, the 11- and 17-month groups eventually reached the level of the 3-month-old mice, while the 22-month age group remained impaired. Changes in swimming ability or speed did not appear to account for the swimming maze deficits. In contrast, a sensory or perceptual deficit cannot be excluded for the oldest mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed2002

Uranyl acetate-induced sensorimotor deficit and increased nitric oxide generation in the central nervous system in rats.

We investigated the effects of uranyl acetate on sensorimotor behavior, generation of nitric oxide and the central cholinergic system of rats. Male Sprague-Dawley rats were treated with intramuscular injection of 0.1 and 1 mg/kg uranyl acetate in water, daily for 7 days. Control animals received equivalent amount of water. The treatment was stopped after the seventh injection because the animals in the 1-mg/kg group appeared lethargic. The animals were maintained for an additional observation period of 30 days. The study was initiated as a dose-finding study that covered doses of 10 and 100 mg/kg, as well. However, all the animals in the 100-mg/kg treatment group died after the third and fourth injections, and all animals given 10 mg/kg died after the fifth and sixth injections. On Day 30 following the cessation of treatment, the sensorimotor functions of the animals in the 0.1- and 1-mg/kg treatment groups were evaluated using a battery of tests that included measurements of postural reflexes, limb placing, orientation to vibrissae touch, grip time, beam walking and inclined plane performance. The animals were sacrificed the same day and the cerebral cortex, brainstem, cerebellum and midbrain were dissected. The levels of nitric oxide as marker for increased oxidative stress, and the integrity of the cholinergic system as reflected in acetylcholinesterase (AChE) activity and m2 muscarinic acetylcholine receptors ligand binding, were determined. The data from behavioral observations show that there was a dose-related deficit at the 0.1- and 1-mg/kg treatment groups for inclined plane performance. Both doses reduced grip time, but there was no significant difference between the two doses. Similarly, both beam-walk score and beam-walk time were impaired at both doses as compared with the controls. A significant increase in nitric oxide was seen at 0.1 mg/kg dose in cortex and midbrain, whereas brainstem and cerebellum showed an insignificant decrease at both the doses. Similarly, there was no significant change in nitric oxide levels in kidneys and liver of the treated animals as compared with the controls. There was a significant increase in AChE activity in the cortex of the animals treated with 1 mg/kg uranyl acetate, but not in other brain regions. Ligand binding densities for the m2 muscarinic receptor did not show any change. These results show that low-dose, multiple exposure to uranyl acetate caused prolonged neurobehavioral deficits after the initial exposure has ceased.

Acetylcholinesterase↗
PubMed2006

Singing, but not seizure, induces synaptotagmin IV in zebra finch song circuit nuclei.

Synaptotagmins are a family of proteins that function in membrane fusion events, including synaptic vesicle exocytosis. Within this family, synaptotagmin IV (Syt IV) is unique in being a depolarization-induced immediate early gene (IEG). Experimental perturbation of Syt IV modulates neurotransmitter release in mice, flies, and PC12 cells, and modulates learning in mice. Despite these features, induction of Syt IV expression by a natural behavior has not been previously reported. We used the zebra finch, a songbird species, to investigate Syt IV because song is a naturally learned behavior whose neuroanatomical basis is largely identified. We observed that, similar to rodents, Syt IV is inducible in songbirds. This induction was selective and depended on the nature of neuronal depolarization. Generalized seizures caused by the GABA(A) receptor antagonist, metrazole, induced the IEG, ZENK, in zebra finch brain. However, these same seizures failed to induce Syt IV in song control areas. In contrast, when nontreated birds sang, three song control areas showed striking Syt IV induction. Further, this induction appeared sensitive to the social context in which song was sung. Together, these data suggest that neural activity during singing can drive Syt IV expression within song circuitry whereas generalized seizure activity fails to do so even though song control areas are depolarized. Our findings indicate that, within this neural circuit for a procedurally learned sensorimotor behavior, Syt IV is selective and requires precisely patterned neural activity and/or neuromodulation associated with singing.

Animals↗
PubMed2000

Stimulation of the locus coeruleus suppresses trigeminal sensorimotor function in the rat.

The nucleus locus coeruleus (LC) has been implicated in the modulation of the spinal sensorimotor function. The aim of the present study was to examine the effect of electrical stimulation of the LC on sensorimotor function in the trigeminal system. The following two cases of sensorimotor behaviors mediated by the trigeminal brainstem sensory nuclear complex were examined: (1) the activity of the masseter muscle evoked by pressure on the region of the temporomandibular joint (TMJ); and (2) the activity of the digastric muscle evoked by electrical stimulation of the tooth pulp, resulting in the jaw-opening reflex. In the first case, LC stimulation at 10, 30 and 50 microA resulted in a 70%, 68% and 55% reduction in the magnitude of electromyogram (EMG) activity of the masseter muscle compared with the control (without LC stimulation), respectively. The threshold intensity for the onset of masseter EMG activity increaced to 106%, 111% and 121% of the control with 10, 30 and 50 microA LC stimulation, respectively. In the second case, EMG magnitude in response to the digastric muscle decreased to 42% of the control when 30 microA of LC stimulation was delivered. These results suggest that descending influences from the LC can act in suppression of the trigeminal sensorimotor function.

Animals↗
PubMed1996

Neurobehavioral consequences of induced spreading depression following photothrombotic middle cerebral artery occlusion.

In a model of experimental focal cerebral ischemia, we have recently reported a strong correlation between the magnitude of ischemic depolarizations in the peri-infarct borderzone and the extent of histological injury. In the present study, we assessed the neurobehavioral consequences of spontaneously occurring and induced ischemic depolarizations in rats following middle cerebral artery (MCA) occlusion, as well as the effects of induced spreading depression (SD) in intact animals. Halothane-anesthetized, artificially ventilated Sprague-Dawley rats underwent photothrombotic MCA occlusion coupled with ipsilateral common carotid artery (CCA) occlusion. The electroencephalogram and direct current (DC) potential were recorded in the parietal infarct borderzone-corresponding to the cortical forelimb area-for 3 h following MCA occlusion. Group 1 rats (n = 9) received MCA/CCA occlusion, and the spontaneously occurring negative DC shifts were recorded in the ischemic borderzone. In Group 2 animals (n = 9), the (non-ischemic) frontal pole of the ipsilateral hemisphere was electrically stimulated in order to double the frequency of peri-infarct DC shifts occurring over the initial 3 h postocclusion. Group 3 consisted of intact rats (n = 3) in which SD was repeatedly evoked in the frontal pole. Four animals served as sham-operated controls. A battery of sensorimotor behavioral tests, consisting of beam balance, postural reflex and elicited forelimb placing, was applied in a blinded fashion. Sham controls and animals of Groups 1 and 2 were tested 24 h after surgery, and Group 3 rats were tested 2, 6 and 24 h after generation of SDs. A cumulative neurobehavioral index, ranging from 0 to 144, was calculated by adding the individual test results. Brains were perfusion-fixed 24 h following surgery for calculation of volumes of infarction and scattered neuronal injury. Functional outcome at 24 h was significantly worse in Group 2 animals (spontaneous plus induced ischemic depolarizations) (neurobehavior index 43 +/- 19, mean +/- S.D.) compared to Group 1 rats, in which only spontaneous depolarizations occurred (neurobehavior index 24 +/- 19, P < 0.05). The cumulative neurobehavioral index of Group 1 and 2 animals correlated positively with the volume of total ischemic injury (r = 0.765, P < 0.001) and with the frequency of ischemic depolarizations (r = 0.474, P < 0.05). Correlations between severe forelimb placing deficits and severe degrees of histological injury (necrosis or ischemic cell change) in the corresponding primary sensorimotor cortical region FR1 were significant in these rats. Group 3 rats showed severe neurobehavioral deficits at 2 and 6 h following SD stimulation (index 57 +/- 1 and 39 +/- 1, respectively) but returned to normal at 24 h (4 +/- 0). The findings indicate that cortical spreading depression is accompanied by transient neurobehavioral deterioration and that SD in the ischemic hemisphere of animals subjected to MCA occlusion worsened functional outcome 24 h after surgery.

Animals↗
PubMed1997

Afferent and efferent connections of the ventrolateral tegmental area in the rat.

The present study examined the organization of afferent and efferent connections of the rat ventrolateral tegmental area (VLTg) by employing the retrograde and anterograde axonal transport of Fluorogold and Phaseolus vulgaris-leucoagglutinin, respectively. Our interest was focused on whether the anatomical connections of the VLTg would provide evidence as to the involvement of this reticular area in audiomotor behavior. Our retrograde experiments revealed that minor inputs to the VLTg arise in various telencephalic structures, including the cerebral cortex. Stronger projections originate in the lateral preoptic area, the zona incerta, the nucleus of the posterior commissure and some other thalamic areas, the lateral substantia nigra, the deep layers of the superior colliculus, the dorsal and lateral central gray, the deep mesencephalic nucleus, the paralemniscal zone, the intercollicular nucleus, the external cortex of the inferior colliculus, the oral and caudal pontine reticular nucleus, the deep cerebellar nuclei, the gigantocellular and lateral paragigantocellular reticular nuclei, the prepositus hypoglossal nucleus, the spinal trigeminal nuclei, and the intermediate layers of the spinal cord. Most importantly, we disclosed strong auditory afferents arising in the dorsal and ventral cochlear nuclei and in the cochlear root nucleus. The efferent projections of the VLTg were found to be less widespread. Telencephalic structures do not receive any input from the VLTg. Moderate projections were seen to diencephalic reticular areas, the zona incerta, the nucleus of the posterior commissure, and to various other thalamic areas. The major VLTg projections terminate in the deep layers of the superior colliculus, the deep mesencephalic nucleus, the intercollicular nucleus and external cortex of the inferior colliculus, the oral and caudal pontine reticular nucleus, the gigantocellular and lateral paragigantocellular reticular nuclei, and in the medial column of the facial nucleus. From our data, we conclude that the VLTg might play a role in sensorimotor behavior.

Afferent Pathways↗
PubMed1996

Effects of preweaning sensorimotor stimulation on behavioral and neuronal development in motor and visual cortex of the rat.

The present study investigates the effects of early sensorimotor stimulation on behavioral and neuronal cytodifferentiation in motor and visual cortex of lactating rats. Seventy-two male and female Sprague-Dawley albino rats were systematically submitted to environmental stimulation during the early postnatal period (postnatal days 5-21). On postnatal day 22, four behavioral tests were performed (open field, narrow path crossing, hind limb support and ascending on a rope). In order to evaluate dynamic neuronal changes induced by sensorimotor enrichment, brains were stained through the Golgi-Cox-Sholl method. Morphometric studies were carried out in pyramidal neurons located in motor and visual cortical layers II and III, by measuring their basal dendritic length and branching. Further, wide cortical field studies were performed with the aim of evaluating the degree of development reached by clusters of pyramidal cells. The results indicate that sensorimotor stimulation carried out during the suckling period produced a significant increase in neuronal cytodifferentiation as observed in single cell studies. However, collective neuronal evaluations yielded less significant results. Consistently, rats exposed to enriched environments showed a better performance in behavioral adaptive responses.

Animals↗
PubMed2001

Rapid recovery from spinal cord injury after subcutaneously administered polyethylene glycol.

Arguably a seminal event in most trauma and disease is the breakdown of the cell membrane. In most cells, this is first observed as a collapse of the axolemmas barrier properties allowing a derangement of ions to occur, leading to a progressive dissolution of the cell or its process. We have shown that an artificial sealing of mechanically damaged membranes by topical application of hydrophilic polymers such as polyethylene glycol (PEG) immediately restores variable levels of nerve impulse conduction through the lesion. This was documented by a rapid recovery of somatosensory evoked potential (SSEP) conduction, and by recovery of the cutaneous trunchi muscle (CTM) reflex in PEG-treated animals. The CTM reflex is a sensorimotor behavior dependent on an intact (and identified) white matter tract within the ventrolateral funiculus of the spinal cord, and is thus an excellent index of white matter integrity. We show that PEG can be safely introduced into the bloodstream by several routes of administration. Using a fluorescein decorated PEG, we demonstrate that the polymer specifically targets the hemorrhagic contusion of the adult guinea pig spinal cord when administered through the vasculature, but not intact regions of the spinal cord. A single subcutaneous injection (30% weight by weight in sterile saline) made 6 hr after a standardized spinal cord contusion in adult guinea pigs was sufficient to produce a rapid recovery of SSEP propagation through the lesion in only PEG-treated animals, accompanied by a statistically significant recovery of the CTM reflex. These data suggest that parenterally administered PEG may be a novel treatment for not only spinal injury, but head injury and stroke as well.

Animals↗
PubMed2005

Comparing the function of the corticospinal system in different species: organizational differences for motor specialization?

An appreciation of the comparative functions of the corticospinal tract is of direct relevance to the understanding of how results from animal models can advance knowledge of the human motor system and its disorders. Two critical functions of the corticospinal tract are discussed: first, the role of descending projections to the dorsal horn in the control of sensory afferent input, and second, the capacity of direct cortico-motoneuronal projections to support voluntary execution of skilled hand and finger movements. We stress that there are some important differences in corticospinal projections from different cortical regions within a particular species and that these projections support different functions. Therefore, any differences in the organization of corticospinal projections across species may well reflect differences in their functional roles. Such differences most likely reflect features of the sensorimotor behavior that are characteristic of that species. Insights into corticospinal function in different animal models are of direct relevance to understanding the human motor system, providing they are interpreted in relation to the functions they underpin in a given model. Studies in non-human primates will continue to be needed for understanding special features of the human motor system, including feed-forward control of skilled hand movements. These movements are often particularly vulnerable to neurological disease, including stroke, cerebral palsy, movement disorders, spinal injury, and motor neuron disease.

Afferent Pathways↗
PubMed2001

Space coding in primate posterior parietal cortex.

Neuropsychological studies of patients with lesions of right frontal (premotor) or posterior parietal cortex often show severe impairments of attentive sensorimotor behavior. Such patients frequently manifest symptoms like hemispatial neglect or extinction. Interestingly, these behavioral deficits occur across different sensory modalities and are often organized in head- or body-centered coordinates. These neuropsychological data provide evidence for the existence of a network of polymodal areas in (primate) premotor and inferior parietal cortex representing visual spatial information in a nonretinocentric frame of reference. In the monkey, a highly modular structural and functional specialization has been demonstrated especially within posterior parietal cortex. One such functionally specialized area is the ventral intraparietal area (VIP). This area is located in the fundus of the intraparietal sulcus and contains many neurons that show polymodal directionally selective discharges, i.e., these neurons respond to moving visual, tactile, vestibular, or auditory stimuli. Many of these neurons also encode sensory information from different modalities in a common, probably head-centered, frame of reference. Functional imaging data on humans reveal a network of cortical areas that respond to polymodal stimuli conveying motion information. One of these regions of activation is located in the depth of human intraparietal sulcus. Accordingly, it is suggested that this area constitutes the human equivalent of monkey area VIP. The functional role of area VIP for polymodal spatial perception in normals as well as the functional implications of lesions of area VIP in parietal patients needs to be established in further experiments.

Animals↗