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At least 415 records · Page 23Linked to original sources

PubMed2005

Reversal of age-related deficits in object recognition memory in rats with l-deprenyl.

The monoamine-oxidase-B (MAO-B) inhibitor l-deprenyl (selegiline) is effective in treating Parkinson's disease and possibly cognitive deficits associated with aging, Alzheimer's disease and HIV dementia. The aim of the present study was to investigate the effects of l-deprenyl on short- and long-term recognition memory in aged rats. Young adult and aged male Wistar rats were trained in a novel object recognition task. Retention test trials were carried out at 1.5 or 24 h after training. Aged rats showed impaired recognition memory retention 24 h after training when compared to young animals. Treatment with a daily systemic injection of l-deprenyl (1.0 mg/kg) for 21 days reversed the memory impairment. A control experiment indicated that l-deprenyl did not affect sensorimotor functions. The results suggest that l-deprenyl reverses age-related deficits in long-term recognition memory.

Aging↗

PubMed2006

A conditionally immortal clonal stem cell line from human cortical neuroepithelium for the treatment of ischemic stroke.

Transplantation of neural stem cells into the brain is a novel approach to the treatment of chronic stroke disability. For clinical application, safety and efficacy of defined, stable cell lines produced under GMP conditions are required. To this end, a human neural stem cell line, CTX0E03, was derived from human somatic stem cells following genetic modification with a conditional immortalizing gene, c-mycER(TAM). This transgene generates a fusion protein that stimulates cell proliferation in the presence of a synthetic drug 4-hydroxy-tamoxifen (4-OHT). The cell line is clonal, expands rapidly in culture (doubling time 50-60 h) and has a normal human karyotype (46 XY). In the absence of growth factors and 4-OHT, the cells undergo growth arrest and differentiate into neurons and astrocytes. Transplantation of CTX0E03 in a rat model of stroke (MCAo) caused statistically significant improvements in both sensorimotor function and gross motor asymmetry at 6-12 weeks post-grafting. In addition, cell migration and long-term survival in vivo were not associated with significant cell proliferation. These data indicate that CTX0E03 has the appropriate biological and manufacturing characteristics necessary for development as a therapeutic cell line.

Analysis of Variance↗

PubMed2006

Hip-phase-dependent flexion reflex modulation and expression of spasms in patients with spinal cord injury.

The flexion reflex in human spinal cord injury (SCI) is believed to incorporate interneuronal circuits that consist elements of the stepping generator while ample evidence suggest that hip proprioceptive input is a controlling signal of locomotor output. In this study, we examined the expression of the non-nociceptive flexion reflex in response to imposed sinusoidal passive movements of the ipsilateral hip in human SCI. The flexion reflex was elicited by low-intensity stimulation (300 Hz, 30 ms pulse train) of the right sural nerve at the lateral malleolus, and recorded from the tibialis anterior (TA) muscle. Sinusoidal hip movements were imposed to the right hip joint at 0.2 Hz by a Biodex system while subjects were supine. The effects of leg movement on five leg muscles along with hip, knee, and ankle joint torques were established simultaneously with the modulation pattern of the flexion reflex during hip oscillations. Phase-dependent modulation of the flexion reflex was present during hip movement, with the reflex to be significantly facilitated during hip extension and suppressed during hip flexion. The phase-dependent flexion reflex modulation coincided with no changes in TA pre- and post-stimulus background ongoing activity during hip extension and flexion. Reflexive muscle and joint torque responses, induced by the hip movement and substantiated by excitation of flexion reflex afferents, were entrained to specific phases of hip movement. Joint torque responses were consistent with multi-joint spasmodic muscle activity, which was present mostly during the transition phase of the hip from flexion to extension and from mid- to peak extension. Our findings provide further evidence on the interaction of hip proprioceptors with spinal interneuronal circuits engaged in locomotor pathways, and such interaction should be considered in rehabilitation protocols employed to restore sensorimotor function in people with SCI.

Adult↗

PubMed2005

Novel oral drug administration in an animal model of neuroleptic therapy.

A novel method of oral drug administration was used in a neuroleptic animal study. Seventy male Sprague-Dawley rats were randomly subdivided into four groups, which were treated with clozapine, haloperidol, diazepam or a vehicle solution (5% sucrose solution). Oral drug treatment was achieved by training the rats to drink the drug of choice mixed with five percent sucrose or vehicle solution from a syringe. Within 3-4 weeks the haloperidol group developed vacuous chewing movement, which did not disappear with discontinuation of the drug. Significant weight gain was observed for all drug groups in relation to the control group, whereas only the diazepam group showed a significant increase in response latency on the disengage test of sensorimotor function, which disappeared with drug withdrawal. A novel means of testing the motivational status showed that all drug-treated groups engaged in eating chocolate before grooming (t=11.69, p<0.001), whereas the control group showed no specific tendency towards either task. Furthermore, there was a significant delay in grooming for the haloperidol group compared to the other drug groups and controls. In conclusion, a novel method of oral drug administration with minimum stress was introduced that was sufficient to cause the described changes in behavioural parameters. Additionally, the combination of tests used provided an efficient discrimination between the behavioural effects of clozapine, haloperidol and diazepam in rodents.

Administration, Oral↗

PubMed2004

Behavioral testing strategies in a localized animal model of multiple sclerosis.

To assess neurological impairments quantitatively in an animal model of multiple sclerosis (MS), we have used a targeted model of experimental autoimmune encephalomyelitis (EAE), which leads to the formation of anatomically defined lesions in the spinal cord. Deficits in the hindlimb locomotion are therefore well defined and highly reproducible, in contrast to the situation in generalized EAE with disseminated lesions. Behavioral tests for hindlimb sensorimotor functions, originally established for traumatic spinal cord injury, revealed temporary or persistent deficits in open field locomotion, the grid walk, the narrow beam and the measurement of the foot exorotation angle. Such refined behavioral testing in EAE will be crucial for the analysis of new therapeutic approaches for MS that seek to improve or prevent neurological impairment.

Animals↗

PubMed2005

[Results of 46 digital replantations. With a minimal follow-up of one year].

Forty six digital replantations were analysed with a minimum follow-up of one year. The mechanism of the injury and the level of the amputation were systematically analysed to asses the objective (mobility, sensitivity, prehension), and the subjective results (pain, vasomotor dysfunction, satisfaction). The replantations were typically in the long fingers in young men (index and middle fingers at the level of the middle phalanx) by work or industrial accident (complete section or digital crushing). Seventeen replantations (37%) were secondarily amputated. Arterial thrombosis was the main cause of amputation in 94% of the cases and had occurred in 50% of the cases by the forty eight postoperative hour. An early revascularization procedure was attempted in ten cases (21%). Among these ten revascularizations procedures, we noted eight failures (80%). During the first six postoperative weeks, the complications of the replantations were skeletal displacements, tendon ruptures and joint subluxations. After six weeks, the complications were joint stiffness (26%), sensory deficits (19.5%), severe cold intolerance (13%), vasomotor dysfunction (10%) with stiffness of the proximal interphalangeal joints in 60% of the cases. We noted other complications such as neuroma of distal stump, cutaneous retraction and deformation of the fingers. Finally, only nine digital replantations (19.5%) evolved favourably with complete restoration of sensorimotor function without any complication. The best results were obtained from amputations of the middle finger with the mechanism of section being a circular saw (40%).

Accidents, Occupational↗

PubMed2004

Axonal responses to cellularly delivered NT-4/5 after spinal cord injury.

Neurotrophic factors delivered to the injured spinal cord have been shown to enhance axonal growth, prevent neuronal degeneration and partially improve sensorimotor function. The present study examined the effects of NT-4/5 on growth of spinal and supraspinal axons, glia, and functional outcome after spinal cord injury. Adult Fischer 344 rats received spinal cord dorsal hemisections or complete transections at the midthoracic level. Fibroblasts modified to secrete NT-4/5 or green fluorescent protein as controls were immediately grafted to the lesion site. Axonal growth responses were determined between 3 and 6 months postinjury by retrograde and anterograde tracing and immunohistochemistry. Motor axons, coerulospinal, reticulospinal, and propriospinal axons responded to NT-4/5 delivery after thoracic spinal cord injury with significantly increased axonal penetration into NT-4/5 secreting grafts compared to GFP-expressing control grafts. Axonal growth beyond NT-4/5-producing grafts and functional recovery were not observed. Numerous Schwann cells, but not oligodendrocytes, were present within NT-4/5-secreting grafts and remyelinated axons inside the graft. Thus, NT-4/5 and BDNF appear to be interchangeable to elicit substantial axonal growth in the injured spinal cord.

Animals↗

PubMed2004

Behavioral and neuroplastic effects of focal endothelin-1 induced sensorimotor cortex lesions.

Previous studies have established the usefulness of endothelin-1 (ET-1) for the production of focal cerebral ischemia. The present study assessed the behavioral effects of focal ET-1-induced lesions of the sensorimotor cortex (SMC) in adult rats as well as cellular and structural changes in the contralateral homotopic motor cortex at early (2 days) and later (14 days) post-lesion time points. ET-1 lesions resulted in somatosensory and postural-motor impairments in the contralateral (to the lesion) forelimb as assessed on a battery of sensitive measures of sensorimotor function. The lesions also resulted in the development of a hyper-reliance on the ipsilateral forelimb for postural-support behaviors. In comparison to sham-operated rats, in layer V of the motor cortex opposite the lesions, there were time- and laminar-dependent increases in the surface density of dendritic processes immunoreactive for microtubule-associated protein 2, in the optical density of N-methyl-D-asparate receptor (NMDA) subunit 1 immunoreactivity, and in the numerical density of cells immunolabeled for Fos, the protein product of the immediate early gene c-fos. These findings corroborate and extend previous findings of the effects of electrolytic lesions of the SMC. It is likely that compensatory forelimb behavioral changes and transcallosal degeneration play important roles in these changes in the cortex opposite the lesion, similar to previously reported effects of electrolytic SMC lesions.

Animals↗

PubMed2005

Thalamic regulation of striatal acetylcholine efflux is both direct and indirect and qualitatively altered in the dopamine-depleted striatum.

Striatal cholinergic interneurons play a pivotal role in the integrative sensorimotor functions of the basal ganglia. The major excitatory input to these interneurons arises from glutamatergic neurons of the parafascicular nucleus of the thalamus (Pf). Thalamic regulation of cholinergic interneurons, however, may also include an indirect inhibitory component mediated by the axon collaterals of GABAergic medium spiny neurons that are also innervated by Pf. The present study examined thalamic regulation of striatal cholinergic interneurons by employing dual probe in vivo microdialysis in freely moving animals to determine the effect of pharmacological manipulation of Pf on acetylcholine (ACh) efflux in intact and dopamine-lesioned striata. In intact animals, reverse dialysis application of the GABA(A) antagonist bicuculline (50 microM) into Pf, likely disinhibiting Pf neurons, significantly decreased striatal ACh efflux. When striatal GABA(A) receptors were blocked by simultaneous reverse dialysis application of bicuculline (10 microM), however, the same manipulation significantly increased ACh efflux. Qualitatively similar results were obtained in experiments employing a higher concentration of bicuculline (200 microM). Application of the GABA agonist muscimol (500 microM) into Pf, likely inhibiting Pf neurons, decreased ACh efflux only when the experiment was conducted under blockade of striatal GABA(A) receptors. These data are consistent with the existence of an indirect, inhibitory, GABA(A) receptor-mediated component of ACh regulation that is most clearly manifested when Pf is disinhibited and with the existence of a direct excitatory component of ACh regulation, evident when Pf is inhibited. Manipulation of Pf using very high concentrations of drug (500 microM bicuculline, 2 mM muscimol), however, yielded data consistent only with direct excitatory thalamic regulation. In contrast to results obtained in intact animals, in animals with prior (3 weeks) unilateral lesion of the dopaminergic nigrostriatal pathway, bicuculline application (50 muM) in Pf significantly increased striatal ACh efflux, irrespective of simultaneous blockade of striatal GABA(A) receptors. The results of experiments in which muscimol (500 microM) was applied in Pf were similar to those obtained in intact animals, however. Baseline ACh efflux was not significantly elevated in dopamine-lesioned animals. These results indicate a qualitative alteration in the effectiveness of an inhibitory component of the thalamic regulation of ACh efflux in the dopamine depleted striatum, evident during increased thalamostriatal input. Such altered regulation of striatal ACh output is likely to have profound consequences for integrative function in the parkinsonian basal ganglia.

Acetylcholine↗

PubMed2006

Gender differences in long-term beneficial effects of erythropoietin given after neonatal stroke in postnatal day-7 rats.

Recently, we reported that erythropoietin attenuates neonatal brain injury caused by focal cerebral ischemia. The long-term effects of erythropoietin on focal cerebral ischemia-induced injury to the developing brain and the potential gender differences in these long-term effects have not been studied in detail. The current study demonstrated a similarity in the mean infarct volume in both the vehicle-treated male and female rats at 6 and 12 weeks after focal cerebral ischemia. On the other hand, erythropoietin treatment (1000 U/kg x three doses after focal cerebral ischemia) caused a significant reduction in the mean infarct volume in both males and females at 6 weeks after focal cerebral ischemia when compared with the corresponding vehicle-treated animals (males: 141.4+/-48.2 mm3 vs. 194.0+/-59.2 mm3, P<0.05; females: 85.4+/-31.6 mm3 vs. 183.4+/-46.3 mm3, P<0.05). Interestingly, the reduction in the mean infarct volume in the erythropoietin-treated males was significantly less than that in the erythropoietin-treated females at 6 weeks after focal cerebral ischemia (141.4+/-48.2 mm3 vs. 85.4+/-31.6 mm3, P<0.05). At 12 weeks after focal cerebral ischemia, the mean infarct volume in the erythropoietin-treated males significantly increased to 181.0+/-50.4 mm3 (P<0.05). In contrast, the mean infarct volume in the erythropoietin-treated females remained stable (87.0+/-41.7 mm3). Additionally, erythropoietin treatment significantly improved sensorimotor function recovery with a misstep number similar to the sham-operation group at 6 and 12 weeks after focal cerebral ischemia. Moreover, the mean number of missteps in the erythropoietin-treated females was less than that in males at 6 (13.5+/-2.0 vs. 24.5+/-2.5, P<0.05) and 12 (12.5+/-2.0 vs. 20.0+/-2.0, P<0.05) weeks after focal cerebral ischemia. These results indicate that erythropoietin administration after focal cerebral ischemia produces a significant long-term neuroprotective benefit on the developing brain, and that this effect is more beneficial in the female rats.

Animals↗

PubMed2006

How we interact with objects: learning from brain lesions.

Motor deficits are the most common outcome of brain damage. Although a large part of such disturbances arises from loss of elementary sensorimotor functions, several syndromes cannot be explained purely on these bases. In this article, we briefly describe higher-order motor impairments, with specific attention to the characteristic ability of the human hand to interact with objects and tools. Disruption of this motor skill at several independent levels is used to outline a comprehensive model, in which various current proposals for a modular organization of hand-object interactions can be integrated. In this model, cortical mechanisms related to object interaction are independent from representations of the semantic features of objects.

Brain Injuries↗

PubMed1998

Diagnosis and rehabilitation strategies for patients with hysterical hemiparesis: a report of four cases.

Conversion disorder is a psychological disturbance that produces subconscious alterations in sensorimotor function. Hysterical hemiparesis is a relatively rare, and difficult to diagnose, form of conversion disorder presenting as unilateral motor weakness with or without sensory deficits. We report four patients who required inpatient rehabilitation for hysterical hemiparesis, a diagnosis for which there is little information regarding rehabilitation management. In all cases, an extensive acute care evaluation including multiple imaging studies failed to identify a new neurologic lesion. All patients had rapid functional improvement using functional and behavioral therapies and extensive psychosocial support (mean length of stay of 11 days; mean Functional Independence Measure [FIM] gain of 22; mean discharge FIM of 112), consistent with other published reports of rehabilitation of conversion disorder. Evaluation of these cases reveals consistencies regarding presentation, psychosocial history, and rehabilitation course that can aid clinicians in making the diagnosis. Rehabilitation strategies for hysterical hemiparesis are reviewed.

Activities of Daily Living↗

PubMed1998

Impaired spatial navigation learning in transgenic mice over-expressing heme oxygenase-1.

Transgenic mice expressing heme oxygenase-1 (HO-1) using the neuron-specific enolase promoter were impaired in learning the Morris water maze compared to nontransgenic littermates. The memory of the HO-1 mice for the location of the platform was similarly impaired when tested using a probe trial after 7 training blocks, but performance on visible platform trials was similar for both groups of mice. Importantly, both HO-1 and nontransgenic mice had normal sensorimotor function, and performed the same on a Y-maze alternation task, highlighting the specificity of memory deficit in the spatial navigation task. These results suggest that carbon monoxide, one product of HO-1 activity, interferes in the development of spatial navigation memory, and may play a role in normal memory function.

Animals↗

PubMed1999

Lubeluzole shows neuroprotective effects in an "in-vitro"-model for neuronal lesions in the chicken retina.

In this study, the isolated chicken retina was used as an "in-vitro"-model for investigation of neuronal lesions to show the neuroprotective effects of lubeluzole. Lubeluzole is a neuroprotective compound that has been shown to stereoselectively rescue sensorimotor function and reduce infarct size in photochemical stroke models in rats. In the retina, the typical cell swelling of a developing lesion is accompanied by a very strong intrinsic optical signal (IOS), occurring simultaneous with the electrical signal which is based on changes in light scattering. In the presented model, lesions were elicited electrically with a tungsten microelectrode (0.1 MOmega). The degree of damage was evaluated with optical methods by measuring area and brightness of the affected tissue. Lubeluzole was much more effective in reducing the growth of the lesions than its R-isomer. However, both compounds enhanced the possibility of the neuronal tissue to recover after excitotoxic stimuli.

Animals↗

PubMed2003

Multi-unit activity suppression and sensorimotor deficits after endothelin-1-induced middle cerebral artery occlusion in conscious rats.

Conscious Wistar rats with stereotaxically and unilaterally implanted cannula just above the middle cerebral artery (MCA) were injected with the powerful vasoconstrictor peptide endothelin-1 (ET1, 60 pmol in 3 microl). The purpose was to examine the long-term (from the 1st to the 14th day) changes in neuronal bioelectrical activity together with sensorimotor deficits after ET1-induced MCA occlusion (MCAO). Extracellular multi-unit activity (MUA) recorded from the ipsilateral fronto-parietal cortical area (supplied by MCA) and sensorimotor behavior (one postural reflex test and six limb placing tests) were examined. A significant suppression of the multi-unit activity was observed until the 14th day post-ET1. The rats exhibited significant unilateral sensorimotor deficits with a maximum at the 3-7 days after ET1 and a spontaneous partial recovery by days 11-14. A significant correlation was found between the suppression of the multi-unit activity and the sensorimotor deficits between the 3rd and the 10th day post-ET1. The results suggest that studying the bioelectrical activity in combination with the behavioral sensorimotor functions may be of use to assess the functional disturbances associated with focal cerebral ischemia and would help to examine the therapeutic benefits of various cerebroprotective treatments before initiating human clinical trials.

Action Potentials↗

PubMedDate not supplied

Developmental stress disrupts habituation but spares prepulse inhibition in young rats.

Stress has long been recognized as a factor that contributes to the induction of schizophrenia and results in abnormal sensorimotor functioning and information processing. Patients with schizophrenia show disrupted habituation and prepulse inhibition of the acoustic startle response. This study examined the effects of maternal isolation in rats on the habituation of startle and PPI to assess the potential impact of developmental stress on schizophrenic symptomatology. Evaluation of performance in young adulthood (3-4 months) revealed a disruption of habituation in the isolated group; response amplitude increased over time. PPI was not altered. These results suggest that the disruption of habituation may involve acute effects of elevated stress hormones on neuronal functions. In contrast, disturbance of PPI may require an accrual of neuronal insult and damage to ultimately undermine neurologic function, possibly through impact on N-methyl-D-aspartate-mediated transmission. An analysis of effects at middle age is planned to address this possibility.

Acoustic Stimulation↗

PubMed1989

Afferents and efferents of the vestibular nuclei: the necessity of context-specific interpretation.

A synopsis of physiological and anatomical results is presented that leads to the conclusion that experimental data have to be interpreted in a context meaningful for the system investigated. For example, since there is an obvious spatial relationship between semicircular canals and extraocular muscles, the interdependence between the three-neurone-arc circuitry, and vestibular and visual signals follows quite naturally from a common geometry inherent in the sensory and motor periphery. It is emphasized that signals related to compensatory eye movements have to be interpreted within a vestibular/eye muscle frame of reference. By the same argument, when dealing with the head-neck movement system, the appropriate reference frame will have to be applied to arrive at a meaningful interpretation of related sensorimotor functions. Thus, in general terms, each system has to be interpreted within its own meaningful biological context.

Animals↗

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↗