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PubMed2000

Effects of subdural haematoma on sensorimotor functioning and spatial learning in rats.

Twenty per cent of all strokes are haemorrhagic in character and are associated with severe disturbances in sensorimotor behaviour and cognition. Although spontaneous recovery of pre-stroke functioning occurs in some cases, the process is demanding, slow, and often incomplete. A first step in the preclinical testing of new putative, neuroprotective and recovery-supporting therapeutics is to validate animal models of brain injury. In a series of four experiments we evaluated the behavioural impairments and the time course of recovery of functional deficits in rats with an experimentally induced subdural haematoma. We found that unilateral subdural haematoma resulted in dysfunction in both simple reflexive (experiment 1) and skilled sensorimotor behaviour (experiment 2). Reflexive behaviour did not recover, or recovered only marginally, and neither did the deficits in skilled forepaw use. Bilateral subdural haematoma impaired the learning and memory performance of adult (experiment 3) and old rats (experiment 4) in the Morris water escape task. Considering the diversity of the deficits found in our experiments, we conclude that different models are needed to cover the broad range of deficits seen in stroke patients.

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PubMed1982

The integrative sensorimotor function of the LP-pulvinar complex.

An important number of studies have paid attention to the sensorial function of the LP-pulvinar complex and its probable polisensorial integrative role. In the present review, on the basis of some experimental results, we have tried to emphasize the importance of the LP-pulvinar complex in the motor function. In this sense, this thalamic complex appears as a probable sensorimotor integrative structure. Considering the behavior elicited by electrical as well as chemical stimulation of the LP-pulvinar complex, it would seem that this structure is related to the type of behavior that researches and examines the environment, mainly, by internal motivation. Furthermore, the possible role of the LP-pulvinar complex in the sleep and wakefulness mechanism and in the epileptic phenomena, is mentioned.

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PubMedDate not supplied

Properties and plasticity of the primate somatosensory and motor cortex related to orofacial sensorimotor function.

1. The lateral pericentral region of the cerebral cortex has been well documented in primates to be important in sensorimotor integration and control and in the learning of new motor skills. 2. The present article provides, first, an overview of limb sensorimotor cortical mechanisms and, second, outlines recent evidence pointing to an important role for the face sensorimotor cortex in semi-automatic, as well as trained, orofacial motor behaviour and to its propensity for neuroplastic changes in association with orofacial motor skill acquisition or an altered oral environment.

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PubMed1997

Sensorimotor function and neuropathology five to six weeks after hypoxia-ischemia in seven-day-old rats.

Various therapeutic interventions after hypoxia-ischemia (HI) have been shown to reduce brain injury in the short-term perspective, but it remains uncertain whether such findings are accompanied by long-term functional and structural improvements. HI was induced in 7-d-old rats as follows. The left carotid artery was ligated, and the rat was exposed to 100 min of hypoxia (7.70% oxygen in nitrogen). At postnatal d 42 the rats were assessed using four sensorimotor tests. The results were correlated with the extent of brain damage expressed as volume of deficit of the left hemisphere as percent of the right hemisphere. In the grip-traction test, the time to falling was 2.2 times shorter in the HI animals compared with controls (p < 0.01). Asymmetries of limb-placing and foot-faults (p < 0.001) were detected in HI animals, and the motor function was abnormal in the postural reflex test (p < 0.001). We found a moderate correspondence between functional and neuropathologic outcome (r = 0.842, p < 0.001). A set of four easily performed sensorimotor tests is presented for the long-term evaluation of neurologic function in the 7-d-old rat model of HI.

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PubMed1975

Sensorimotor functions and cognitive disturbance in psychiatric patients.

The authors studied 109 consecutive admissions to an acute psychiatric unit in a general hospital to determine the relationship of specific sensorimotor impairments to cognitive disturbance. The results indicated a strong but not exclusive correlation between neurological impairment and thought disorder as well as between neurological impairment and schizophrenia. The theoretical and etiological implications are discussed, as well as the relationship of these findings to other variables.

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PubMed1976

Activation-induced restoration of sensorimotor functions in rats with dopamine-depleting brain lesions.

Bilateral electrolytic lesions of the lateral hypothalamus or intraventricular 6-hydroxydopamine injections produced substantial depletions of striatal dopamine in rates. All animals with brain damage showed marked sensorimotor impairments. However, they began to move and respond appropriately to environmental stimuli when placed in a sink of water, in a shallow ice bath, or among a colony of cats or rats. A reversal of the sensorimotor dysfunctions was still apparent shortly after the animals were removed from each activating situation. However, the terapeutic effects dissipated rapidly, and by 4 hr after an exposure the rats responded as poorly as they had prior to activation. These findings are strikingly similar to the "paradoxical kinesia" seen in parkinsonism, a clinical disorder attributed to degeneration of central dopamine-containing neurons. Collectively, they suggest the importance of activation in maintaining responsiveness to senory stimuli in rats following dopamine-depleting brain lesions.

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PubMed1986

Control of sensorimotor function by dopaminergic nigrostriatal neurons: influence on eating and drinking.

The literature on the effects of lesions of the lateral hypothalamic area (LHA) on eating and drinking is reviewed in an effort to understand the function of the neural substrate destroyed. The data suggest that damage to the dopaminergic nigrostriatal neurons that course through the LHA results in a decrease in sensorimotor facilitation; that is, an increase in the threshold for responding to stimuli that elicit orientation, approach and consumption. This increase results in decreased consumption of food and water. Evidence is also reviewed suggesting the possibility that striatal dopaminergic activity may mediate a negative feedback signal related to blood glucose level that influences responsiveness to food, and therefore eating. There is no evidence that the nigrostriatal system mediates a similar signal related to water balance and drinking. A second deficit associated with LHA lesions, caused by damage to the pallidofugal neurons that descend through this area, is a dysfunction of motor control of the head and mouth. This results in an increase in the effort required to consume food and water, also leading to decreased consumption. These two behavioral factors: an increased threshold for responding to the sensory properties of food and water and an increase in the effort required to eat and drink are used to explain the symptoms making up the lateral hypothalamic syndrome without postulating changes in physiological regulatory (set point) mechanisms.

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PubMed1996

Lubeluzole protects sensorimotor function and reduces infarct size in a photochemical stroke model in rats.

Posttreatment with lubeluzole, the S-isomer of a novel 3,4-difluoro benzothiazole, potently rescued tactile/proprioceptive hindlimb placing reactions contralateral to unilateral thrombotic infarcts in the hindlimb area of the parietal sensorimotor neocortex of rats. Administered at 5 min postinfarct, a single i.v. bolus of lubeluzole was three times as potent as the racemate, whereas the R-isomer was inactive. Neurological protection was near-maximal for treatment delays through 1 hr postinfarct, but declined with longer delays. However, when administered at 6 hr, 1.25 mg/kg i.v. still protected 60% of infarcted rats. An i.v. bolus followed by a 1-hr i.v. infusion produced equieffective neurologic protection at both 6- and 3-hr delays. This optimal lubeluzole regimen, started at 5 min postinfarct, reduced infarct volume by 22 to 24% at 4 hr postinfarct and by 28% at 7 days postinfarct. Again, the R-isomer was inactive. Down-regulation of the glutamate-activated nitric oxide synthase pathway leading to neurotoxicity and neuronal death may constitute a neuroprotective mechanism of action for lubeluzole.

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PubMed2002

Sensorimotor functions in transgenic mice expressing the neurofilament/heavy-LacZ fusion protein on two genetic backgrounds.

NFH-LacZ transgenic mice are characterized by expression of a non-endogenous fusion protein between a truncated form of mouse NFH (neurofilament of heavy molecular weight) and the complete Escherichia coli beta-galactosidase protein. These transgenic mice were compared to their respective controls on two background strains (C3H and FVB) in several sensorimotor tests. NFH-LacZ mice were deficient in tests requiring balance and equilibrium in a manner generally independent of genetic background. In particular, NFH-LacZ mice fell more quickly than controls from two stationary beams and had fewer rears in an open-field. The transgenic mice were also impaired during the initial trials of sensorimotor learning on the rotorod. We conclude that despite the absence of overt signs of sensorimotor weakness in their home cage, the disruption of the NFH gene, causing neurofilament accumulations in the cell body and diminished axonal calibers of motoneurons, is sufficient to cause motor deficits that resemble the early stages of amyotrophic lateral sclerosis.

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PubMed1988

Recovery of sensorimotor function after frontal cortex damage in rats: evidence that the serial lesion effect is due to serial recovery.

Multiple-staged brain lesions produce fewer and smaller behavioral effects than does damage produced in a single surgery. This is called the serial lesion effect. Two hypotheses were tested, the reduced deficit hypothesis and the serial recovery hypothesis, which attempt to explain the serial lesion effect. The effects of lesions of the medial frontal cortex on sensorimotor behavior were investigated in rats that received bilateral damage in a single surgery (n = 7), in two unilateral stages separated by 3 weeks (n = 16), or unilateral damage followed 3 weeks later by a sham surgery (n = 5). Unilateral damage produced deficits on the contralateral side in responsivity to visual, tactile, and olfactory stimuli and impairments in roll-over and paw withdrawal motor responses. All behavioral impairments except visual placement recovered over the next 3 weeks. A second unilateral lesion on the contralateral side produced the same symptoms but on the opposite side of the body. There was no reinstatement of the previously recovered deficits. Bilateral damage incurred in a single stage produced these same deficits on both sides. Because the effects of the second unilateral lesion in the two-stage group produced comparable contralateral effects to those produced in the single-stage group, but no reinstatement of ipsilateral deficits occurred, the reduced deficit hypothesis was rejected. It was concluded that at least for medial frontal cortex damage, the serial lesion effect occurred as a result of serial recovery of the deficits.

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PubMed2000

Enoxaparin, a low molecular weight heparin decreases infarct size and improves sensorimotor function in a rat model of focal cerebral ischemia.

Possible neuroprotective effects of the low molecular weight heparin (LMWH) enoxaparin sodium (Lovenox) were evaluated in a rat model of focal ischemia. Male Sprague-Dawley rats were subjected to 90 min of occlusion of the right middle cerebral artery using the intraluminal suture method. Enoxaparin at doses of 0, 10 or 15 mg/kg was administered to groups of rats 1, 8, 24 and 32 h after artery occlusion. Motor impairment was evaluated by performance on the traverse beam and accelerating rotarod tests. Animals were sacrificed 48 h after occlusion and brain sections were stained with 2% 2,3,5-triphenyltetrazolium chloride for determination of infarct volume. Forty percent of the rats receiving 15 mg/kg enoxaparin died as a result of intracranial hemorrhage. Untreated rats exhibited large lesions involving the caudate putamen and much of the cortex. In enoxaparin - treated rats the damage was mainly confined to the caudate putamen. The sensorimotor behavior of the 10 mg/kg enoxaparin group was significantly better than that of untreated animals. Motor performance of the survivors in the 15 mg/kg group was poor due to hypoactivity and weakness resulting from excessive bleeding. These results suggest that LMWH may have a neuroprotective function.

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PubMed1994

Recovery of sensorimotor function after distal middle cerebral artery photothrombotic occlusion in rats.

BACKGROUND AND PURPOSE: The purpose of the present study was to delineate the behavioral correlates of focal thrombotic occlusion of the distal middle cerebral artery in rats and to compare the pattern of deficits and subsequent recovery to that following proximal middle cerebral artery occlusion. METHODS: Ten Sprague-Dawley rats underwent photothrombotic occlusion of the distal middle cerebral artery with tandem occlusion of the common carotid arteries (dMCAO group); 10 animals served as operated controls. Beginning on postischemia day 2, animals were given a battery of five tests that assessed sensorimotor integration, attentional mechanisms, and muscle strength; testing continued twice weekly until day 30. Nine days of cognitive testing on the learning set of the water maze task were then given. Infarct volume and hemispheric atrophy were determined for each dMCAO animal. RESULTS: After ischemia, the dMCAO group exhibited significant behavioral deficits in posture reflex, ability to place a forelimb to various stimuli, limb adduction during rearing, and neglect of contralateral space. These deficits showed variable recovery rates. No deficits were observed in muscle strength or cognitive performance. The deficits and patterns of recovery were related to infarct location and to degree of hemisphere atrophy. CONCLUSIONS: The present study suggests that a battery of tests is necessary to fully characterize the pattern of behavioral deficits after focal cerebral ischemia. Location of infarct damage and associated degree of hemispheric atrophy were important variables in determining behavioral outcome. The present results are compared with those of the more traditional model of electrocoagulation of the proximal middle cerebral artery.

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PubMed2004

Characterization of hemizygous SOD1/wild-type transgenic mice with the SHIRPA primary screen and tests of sensorimotor function and anxiety.

SOD1 is one of several overexpressed genes in Down's syndrome. In order to dissect genetic causes of the syndrome, hemizygous human wild-type SOD1 transgenic mice were compared to FVB/N non-transgenic controls at 3 months of age in the SHIRPA primary screen of neurologic function as well as in tests of motor activity and coordination. The responsiveness of SOD1/wt transgenic mice to visual and somatosensory stimuli was reduced in placing, pinna, corneal, and toe-pinch tests. In addition, SOD1/wt transgenic mice crossed fewer segments on a stationary beam. On the contrary, there was no intergroup difference for motor activity and anxiety in open-field and emergence tests and for latencies before falling on the stationary beam, coat-hanger, and rotorod. These results indicate mild deficits in sensorimotor responsiveness in a mouse model expressing human SOD1 and that the overexpressed gene may be responsible for some Down symptoms.

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PubMed1996

Effect of chronic vitamin E deficiency on sympathetic and sensorimotor function in rat mesenteric arteries.

1. Mesenteric arterial beds from male rats deprived of vitamin E for 12 months postweaning were isolated and perfused at 5 ml min-1. 2. The basal perfusion pressure of vitamin E-deficient preparations was significantly higher (34.0 +/- 1.9 mmHg, n = 15) than in age-matched controls (26.1 +/- 2 mmHg, n = 14; P < 0.01). 3. At basal tone, vasoconstrictor responses to electrical field stimulation (EFS) were not attenuated by vitamin E deficiency; at high stimulation frequencies, responses were enhanced. According to dose-response curves, exogenous noradrenaline was significantly more efficacious in preparations from vitamin E-deficient rats (P < 0.05). 4. In preparations with tone raised by methoxamine (6-20 microM) and in the presence of guanethidine (5 microM), EFS of perivascular sensorimotor nerves elicited frequency-dependent vasodilatation which was significantly attenuated by vitamin E deficiency. There was no difference in relaxation to calcitonin gene-related peptide (CGRP; 1.5 x 10(-11) mol), or to the sensory neurotoxin capsaicin (5 x 10(-11) mol). 5. Immunohistochemical analysis of CGRP-containing nerves in the superior mesenteric artery showed no differences in density of innervation. 6. In conclusion, chronic vitamin E deficiency impairs sensorimotor vasodilatation in rat mesenteric arteries; this does not appear to be due to changes in postjunctional receptors, or to a depletion of transmitter (CGRP) content of the superior mesenteric artery. Sensorimotor nerves appear to be more vulnerable than sympathetic nerves to chronic vitamin E deficiency.

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PubMed2006

Influence of sympathetic nervous system on sensorimotor function: whiplash associated disorders (WAD) as a model.

There is increasing interest about the possible involvement of the sympathetic nervous system (SNS) in initiation and maintenance of chronic muscle pain syndromes of different aetiology. Epidemiological data show that stresses of different nature, e.g. work-related, psychosocial, etc., typically characterised by SNS activation, may be a co-factor in the development of the pain syndrome and/or negatively affect its time course. In spite of their clear traumatic origin, whiplash associated disorders (WAD) appear to share many common features with other chronic pain syndromes affecting the musculo-skeletal system. These features do not only include symptoms, like type of pain or sensory and motor dysfunctions, but possibly also some of the pathophysiological mechanisms that may concur to establish the chronic pain syndrome. This review focuses on WAD, particular emphasis being devoted to sensorimotor symptoms, and on the actions exerted by the sympathetic system at muscle level. Besides its well-known action on muscle blood flow, the SNS is able to affect the contractility of muscle fibres, to modulate the proprioceptive information arising from the muscle spindle receptors and, under certain conditions, to modulate nociceptive information. Furthermore, the activity of the SNS itself is in turn affected by muscle conditions, such as its current state of activity, fatigue and pain signals originating in the muscle. The possible involvement of the SNS in the development of WAD is discussed in light of the several positive feedback loops in which it is implicated.

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PubMed2001

Removing zinc from synaptic vesicles does not impair spatial learning, memory, or sensorimotor functions in the mouse.

Zinc-enriched (ZEN) neurons are distributed widely throughout the brain and spinal cord. Synaptic vesicle zinc in these neurons is thought to function as a neuromodulator upon its release into the synaptic cleft. Consistent with this possibility, zinc or zinc chelators can alter spatial learning, working memory, and nociception in rodents. Here we use zinc transporter-3 (ZnT3) knockout mice, which are depleted of synaptic vesicle zinc, to assess the consequences of removing this potential neuromodulator on the behavior of adult mice. ZnT3 knockout mice performed equally as well as wild-type mice in the rotarod, pole, and cagetop tests of motor coordination. They exhibited normal thermal nociception in the hot-plate and tail-flick tests, and had similar olfactory, auditory and sensorimotor gating capabilities as wild-type mice. ZnT3 knockout mice behaved similarly as wild-type mice in the open field test and in the elevated plus maze test of anxiety. They exhibited normal learning and memory in the passive avoidance, Morris water maze, and fear conditioning tasks, and normal working and reference memory in a water version of the radial arm maze. We conclude that synaptic vesicle zinc is not essential for mice to be able to perform these tasks, despite the abundance of ZEN neurons in the relevant regions of the CNS. Either the neuromodulatory effects of zinc are not relevant for the tasks tested here, or mice are able to compensate easily for the absence of synaptic vesicle zinc.

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PubMed1986

Changes in sensorimotor function associated with the degree of bradykinesia of Parkinson's disease.

Changes in coordinated eye and hand movements associated with the progress of bradykinesia were studied in 31 parkinsonian patients and 8 age-matched healthy subjects. Among the parameters expressing the changes in motor behaviour, the interval between the onset of eye and hand movements was most sensitive. This parameter reflected the difference in the progress of the symptom in the two motor systems. An increase in the reaction time of the hand response appeared in patients of grade II bradykinesia; this was observed for eye movements only in patients with grade III (severe) bradykinesia. While the changes in ocular reaction time remained within the physiological range, a lengthening of the reaction time, a reduction in peak velocity, a decrease in the open-loop gain, a prolongation of movement duration, and a slow build-up in EMG activity, appeared from an early stage in hand movement. These signs of motor disturbance may appear eventually in every motor system at an advanced stage, but their development is not synchronous in different motor systems. An analysis of the responses recorded simultaneously from the two motor systems examined made it possible to evaluate the changes in the sensorimotor processes with different grades of bradykinesia. A comparison between reaction times for eye and hand movements may be useful for assessing the degree of bradykinesia in parkinsonian patients.

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PubMed1992

Complex motor and sensorimotor functions of striatal and accumbens dopamine: involvement in instrumental behavior processes.

The suggestions that dopamine (DA) systems are involved in "motor control" and "reward" represent the classic working hypotheses on the behavioral functions of these systems. The research generated by these hypotheses has yielded results that are far more complicated than the simplest form of either hypothesis would indicate. Pharmacological or lesion-induced interference with DA function does not suppress all aspects of movement control, nor all aspects of reward, nor all aspects of motivation. The deficits produced by interference with DA systems are selective and dissociative in nature, affecting some aspects of motor or motivational function, but leaving others basically intact. In some sense the hypotheses that DA is involved in "motor" or "reward" or "motivational" processes are partly correct, but the processes to which these terms refer are too broad to offer an accurate and detailed description of the behavioral functions of brain DA. A review of the literature on the behavioral pharmacology of DA suggests that the behaviors most easily disrupted by DA antagonists are highly activated and complex learned instrumental responses that are elicited or supported by mild conditioned stimuli, and maintained for considerable periods of time. It is proposed that DA in accumbens and striatum modulates the ability of neocortical and limbic areas involved in sensory, associative, and affective processes to influence complex aspects of motor function, and also modulates the execution of complex motor acts organized by the neocortex. Thus, interference with DA systems produces a "subcortical apraxia", which dissociates complex stimulus processes from complex motor processes, but leaves aspects of those processes intact.

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