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T Schallert

Publications and source records attributed to T Schallert.

At least 19 recordsLinked to original sources

Transplantation of hNT neurons into the ischemic cortex: cell survival and effect on sensorimotor behavior.

Cell transplantation offers a potential new treatment for stroke. Animal studies using models that produce ischemic damage in both the striatum and the frontal cortex have shown beneficial effects when hNT cells (postmitotic immature neurons) were transplanted into the ischemic striatum. In this study, we investigated the effect of hNT cells in a model of stroke in which the striatum remains intact and damage is restricted to the cortex. hNT cells were transplanted into the ischemic cortex 1 week after stroke induced by distal middle cerebral artery occlusion (dMCAo). The cells exhibited robust survival at 4 weeks posttransplant even at the lesion border. hNT cells did not migrate, but they did extend long neurites into the surrounding parenchyma mainly through the white matter. Neurite extension was predominantly toward the lesion in ischemic animals but was bidirectional in uninjured animals. Extension of neurites through the cortex toward the lesion was also seen when there was some surviving cortical tissue between the graft and the infarct. Prolonged deficits were obtained in four tests of sensory-motor function. hNT-transplanted animals showed a significant improvement in functional recovery on one motor test, but there was no effect on the other three tests relative to control animals. Thus, despite clear evidence of graft survival and neurite extension, the functional benefit of hNT cells after ischemia is not guaranteed. Functional benefit could depend on other variables, such as infarct location, whether the cells mature, the behavioral tests employed, rehabilitation training, or as yet unidentified factors.

Analysis of Variance↗

Behavioral recovery from unilateral photothrombotic infarcts of the forelimb sensorimotor cortex in rats: role of the contralateral cortex.

During sensorimotor recovery following stroke ipsi- and contralesional alterations in brain function have been characterized in patients as well as animal models of focal ischemia, but the contribution of these bilateral processes to the functional improvement is only poorly understood. Here we examined the role of the homotopic contralateral cortex for sensorimotor recovery after focal ischemic infarcts at different time periods after the insult. One group of animals received a unilateral single photothrombotic infarct in the forelimb sensorimotor cortex, while four additional groups received a second lesion in the contralateral homotopic cortex either immediately or 2 days, 7 days, or 10 days after the first infarct. The time course of functional recovery of the impaired forelimbs was assessed using different sensorimotor scores: forelimb-activity during exploratory behavior and frequency of forelimb-sliding in the glass cylinder as well as forelimb misplacement during grid walking. Focal infarcts in the forelimb sensorimotor cortex area significantly impaired the function of the contralateral forelimb in these different behavioral tests. The subsequent damage of the contralateral homotopic forelimb sensorimotor cortex only affected the forelimb opposite to the new lesion but did not reinstate the original deficit. The time course of sensorimotor recovery after bilateral sequential cortical infarcts did not significantly differ from animals with unilateral single lesions. These data indicate that following small ischemic cortical infarcts in the forelimb sensorimotor cortex the contralateral cortex homotopic to the lesion plays only a minor role for functional recovery.

Animals↗

Alterations in intracerebral hemorrhage-induced brain injury in the iron deficient rat.

BACKGROUND: Iron contributes to brain edema and cellular toxicity after intracerebral hemorrhage (ICH). Knowledge regarding ICH in the context of iron deficiency anemia (IDA), a common nutritional disorder, is limited. OBJECTIVE: To determine the effect of IDA on brain and behavioral outcome after ICH in rats. METHODS: Six-week-old male rats (n = 75) were randomized to non-IDA or IDA groups. After 1 month of iron sufficient or deficient diets, 100 microl autologous blood was infused into the right basal ganglia (BG). Brains were assessed for iron concentration, regional water content, BG transferrin, and transferrin receptor concentrations after ICH. Recovery of upper extremity sensorimotor function was assessed. Brain and behavioral variables were compared by diet group. Significance was set at p < 0.05. RESULTS: Whole brain iron was decreased and water content was increased for IDA rats in injured cortex and BG at day 3 (p < 0.05) compared with non-IDA rats. Transferrin and transferrin receptor content were increased in injured BG for IDA compared to non-IDA in the first week after ICH (p < 0.05). IDA rats had greater left vibrissae-stimulated forelimb-placing deficits and forelimb-use asymmetry than non-IDA after ICH (p < 0.05). CONCLUSIONS: Brain iron status may be an important determinant of injury severity and recovery after ICH.

Anemia, Iron-Deficiency↗

The role of thrombin in gliomas.

BACKGROUND: In a previous study we found that intracerebral infusion of argatroban, a specific thrombin inhibitor, reduces brain edema and neurologic deficits in a C6 glioma model. OBJECTIVES: To examine the role of thrombin in gliomas and whether systemic argatroban administration can reduce glioma mass and neurologic deficits and extend survival time in C6 and F98 gliomas. METHODS: The presence of thrombin in human glioblastoma samples and rat C6 glioma cells (in vitro and in vivo) was assessed using immunohistochemistry. The effect of thrombin on C6 cell proliferation in vitro was assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. The role of thrombin in vivo was assessed in rat C6 and F98 glioma cell models using argatroban, a thrombin inhibitor. The effects of argatroban on tumor mass, neurologic deficits and survival time were investigated. RESULTS: Thrombin immunoreactivity was found in cultured rat C6 glioma cells and human glioblastomas. Thrombin induced C6 cell proliferation in vitro. In C6 glioma, argatroban reduced glioma mass (P < 0.05) and neurologic deficits (P < 0.05) at day 9. In F98 glioma, argatroban prolonged survival time (P < 0.05). CONCLUSION: These results suggest that thrombin plays an important role in glioma growth. Thrombin may be a new therapeutic target for gliomas.

Animals↗

Systemic use of argatroban reduces tumor mass, attenuates neurological deficits and prolongs survival time in rat glioma models.

Our previous studies showed that intracerebral infusion of argatroban, a specific thrombin inhibitor, reduces brain edema and neurological deficits in a C6 glioma model. The present study investigated whether systemic argatroban administration can reduce glioma mass and neurological deficits and extend survival time in C6 and F98 gliomas. Rat C6 or F98 glioma cells were infused into the right caudate of adult male Fischer 344 rats. Osmotic minipump loaded with argatroban (0.3 mg/hour) or vehicle was implanted into abdomen immediately after glioma implantation. Tumor mass was determined at day 9. Over the period of the experiment, the animals underwent behavioral testing (forelimb placing and forelimb use asymmetry). In addition, survival time was tested in the F98 glioma model. In C6 glioma, argatroban reduced glioma mass (p < 0.05) and neurological deficits (p < 0.05) at day 9. In F98 glioma, agratroban prolonged the survival time (p < 0.05) and reduced the body weight loss (84 +/- 15 gram vs. 99 +/- 2 gram in the vehicle group, P < 0.05). In conclusion, systemic use of argatroban reduced tumor mass and neurological deficits, and prolonged survival time. These results suggest that thrombin plays a key role in glioma growth and thrombin inhibition with argatroban may be a novel treatment for gliomas.

Animals↗

A thrombin inhibitor reduces brain edema, glioma mass and neurological deficits in a rat glioma model.

Although thrombin is a critical enzyme in the coagulation cascade, it has become apparent that it has many other effects. Thus, it may induce brain edema formation, angiogenesis and cell proliferation. Because of the importance of these three factors in the extremely poor prognosis of glioma patients, the present study examined the role of thrombin in that disease state. We found that thrombin activity is increased in a rat glioma model and thrombin positive cells were present in the tumor. Anti-thrombin treatment with argatroban reduced brain edema, tumor growth, and tumor-related neurological deficits. Our results suggest that thrombin is a new target for glioma treatment.

Animals↗

Early overuse and disuse of the affected forelimb after moderately severe intraluminal suture occlusion of the middle cerebral artery in rats.

We have previously shown that early forced overuse of the affected forelimb worsens outcome following moderately severe transient focal cortical ischemic stroke in rats using a distal middle cerebral artery occlusion (MCAo) model. This effect may be site-dependent, because we have also found that early forced use of the affected limb after unilateral 6-OHDA induced degeneration of ascending nigrostriatal dopamine neurons markedly enhanced functional outcome and is neuroprotective. The present study examines the effects of early overuse and disuse following a moderately severe proximal MCAo model, by means of intraluminal suture occlusion. Ischemia was produced in male Long-Evans rats with 60 min of occlusion, or sham surgery was performed. Early overuse or disuse of the affected forelimb was forced by immobilizing either the ipsilateral or contralateral forelimb, respectively, in a plaster cast or the animal was left uncasted. Casts were removed on day 10 and sensorimotor testing was performed weekly during days 17-38. Animals were sacrificed on day 45 and brains were fixed for later cresyl violet staining. The MCAo+contralateral cast group performed worse than all other groups on tests of forelimb sensorimotor function. All MCAo groups regardless of cast condition had significant atrophy of the ischemic striatum, but there was no significant atrophy of the ischemic cortex in any group. Forced disuse, but not overuse, of the affected forelimb immediately following proximal ischemia using the intraluminal suture model has detrimental effects on functional outcome, without exaggerating anatomical damage. The effects of disuse and overuse during the first 10 days after stroke differ depending on cortical or subcortical involvement.

Animals↗

Forced limb-use effects on the behavioral and neurochemical effects of 6-hydroxydopamine.

Rats with unilateral depletion of striatal dopamine (DA) show marked preferential use of the ipsilateral forelimb. Previous studies have shown that implementation of motor therapy after stroke improves functional outcome (Taub et al., 1999). Thus, we have examined the impact of forced use of the impaired forelimb during or soon after unilateral exposure to the DA neurotoxin 6-hydroxydopamine (6-OHDA). In one group of animals, the nonimpaired forelimb was immobilized using a cast, which forced exclusive use of the impaired limb for the first 7 d after infusion. The animals that received a cast displayed no detectable impairment or asymmetry of limb use, could use the contralateral (impaired) forelimb independently for vertical and lateral weight shifting, and showed no contralateral turning to apomorphine. The behavioral effects were maintained throughout the 60 d of observation. In addition to the behavioral sparing, these animals showed remarkable sparing of striatal DA, its metabolites, and the expression of the vesicular monoamine transporter, suggesting a decrease in the extent of DA neuron degeneration. Behavioral and neurochemical sparing appeared to be complete when the 7 d period of immobilization was initiated immediately after 6-OHDA infusion, only partial sparing was evident when immobilization was initiated 3 d postoperatively, and no sparing was detected when immobilization was initiated 7 d after 6-OHDA treatment. These results suggest that physical therapy may be beneficial in Parkinson's disease.

3,4-Dihydroxyphenylacetic Acid↗

Glial cell line-derived neurotrophic factor (GDNF) gene delivery protects dopaminergic terminals from degeneration.

Previously, we observed that injection of an adenoviral (Ad) vector expressing glial cell line-derived neurotrophic factor (GDNF) into the striatum, but not the substantia nigra (SN), prior to a partial 6-OHDA lesion protects dopaminergic (DA) neuronal function and prevents the development of behavioral impairment in the aged rat. This suggests that striatal injection of AdGDNF maintains nigrostriatal function either by protecting DA terminals or by stimulating axonal sprouting to the denervated striatum. To distinguish between these possible mechanisms, the present study examines the effect of GDNF gene delivery on molecular markers of DA terminals and neuronal sprouting in the aged (20 month) rat brain. AdGDNF or a control vector coding for beta-galactosidase (AdLacZ) was injected unilaterally into either the striatum or the SN. One week later, rats received a unilateral intrastriatal injection of 6-OHDA on the side of vector injection. Two weeks postlesion, rats injected with AdGDNF into either the striatum or the SN exhibited a reduction in the area of striatal denervation and increased binding of the DA transporter ligand [(125)I]IPCIT in the lesioned striatum compared to control animals. Furthermore, injections of AdGDNF into the striatum, but not the SN, increased levels of tyrosine hydroxylase mRNA in lesioned DA neurons in the SN and prevented the development of amphetamine-induced rotational asymmetry. In contrast, the level of T1 alpha-tubulin mRNA, a marker of neuronal sprouting, was not increased in lesioned DA neurons in the SN following injection of AdGDNF either into the striatum or into the SN. These results suggest that GDNF gene delivery prior to a partial lesion ameliorates damage caused by 6-OHDA in aged rats by inhibiting the degeneration of DA terminals rather than by inducing sprouting of nigrostriatal axons.

Aging↗

Transplantation of genetically modified fibroblasts expressing BDNF in adult rats with a subtotal hemisection improves specific motor and sensory functions.

OBJECTIVE: We have previously reported that grafting fibroblasts genetically modified to express brain-derived neurotrophic factor (BDNF) into a subtotal cervical hemisection site that destroys the entire lateral funiculus will promote regeneration of rubrospinal axons and growth of other axons, prevent atrophy and death of axotomized red nucleus neurons, and improve forelimb use during spontaneous vertical exploration. We have now extended these studies by using additional sensorimotor tests to examine recovery. METHODS: The range of tests used included those in which the intervention did not improve recovery, those in which the intervention was associated with recovery, and those that showed little deficit. The selected tasks tested both sensory and motor functions and both forelimb and forelimb function. We used the open-field locomotor rating scale (BBB), locomotion on a narrow beam, forelimb use during swimming, horizontal rope walking, and a somatosensory asymmetry (patch-removal) test. After testing during an 8-week recovery period, a second lesion was made just rostral to the initial lesion/transplant site to test the role of the transplant in recovery. The rats were then retested for a further 5 weeks after the repeated lesion. RESULTS: The horizontal rope, swim, and patch-removal tests were reliably sensitive to the subtotal hemisection injury. Fb/BDNF-transplanted animals recovered motor functions on the horizontal rope-crossing test, and this recovery was abolished by a second lesion just rostral to the first lesion/transplant. In the patch-removal test, the latency to contact the affected limb was shorter in Fb/BDNF-treated rats than in the control group, and this effect was completely abolished by a second lesion. CONCLUSIONS: The rope-crossing and patch-removal tests are particularly useful tasks for assessing the beneficial effects of BDNF-expressing grafts in this injury model.

Animals↗

CNS plasticity and assessment of forelimb sensorimotor outcome in unilateral rat models of stroke, cortical ablation, parkinsonism and spinal cord injury.

We have reviewed a battery of useful tests for evaluating sensorimotor function and plasticity acutely and chronically in unilateral rat models of central nervous system injury. These tests include forelimb use for weight shifting during vertical exploration in a cylindrical enclosure, an adhesive removal test of sensory function, and forelimb placing. These tests monitor recovery of sensorimotor function independent of the extent of test experience. Data are presented for four models, including permanent focal ischemia, focal injury to the forelimb area of sensorimotor cortex, dopaminergic neurodegeneration of the nigrostriatal system, and cervical spinal cord injury. The effect of the dendrite growth promoting factor, Osteogenic Protein-1 (OP-1) on outcome following permanent middle cerebral artery (MCA) occlusion was used as an example to illustrate how the tests can be applied preclinically. OP-1 showed a beneficial effect on limb use asymmetry in the cylinder test.

Animals↗

Delivery of a GDNF gene into the substantia nigra after a progressive 6-OHDA lesion maintains functional nigrostriatal connections.

The effects of delivering GDNF via an adenoviral vector (AdGDNF) 1 week after lesioning dopaminergic neurons in the rat substantia nigra (SN) with 6-hydroxydopamine (6-OHDA) were examined. Rats were unilaterally lesioned by injection of 6-OHDA into the striatum, resulting in progressive degeneration of dopaminergic neurons in the SN. One week later, when substantial damage had already occurred, AdGDNF or a control vector harboring beta-galactosidase (AdLacZ) was injected into either the striatum or SN (3.2 x 10(7) PFU/microl in 2 microl). Rats were examined behaviorally with the amphetamine-induced rotation test and for forelimb use for weight-bearing movements. On day 30 postlesion, the extent of nigrostriatal tract degeneration was determined by injecting a retrograde tracer (FluoroGold) bilaterally into the lesioned striatum. Five days later, rats were sacrificed within 2 h of amphetamine injection to examine amphetamine-induced Fos expression in the striatum, a measure of dopaminergic-dependent function in target neurons. AdGDNF injection in the SN rescued dopaminergic neurons in the SN and increased the number of dopaminergic neurons that maintained a connection to the striatum, compared to rats injected with AdLacZ. Further support that these spared SN cells maintained functional connections to the striatum was evidenced by increased Fos expression in striatal target neurons and a decrease in amphetamine-induced rotation. In contrast to the effects observed in rats injected with AdGDNF in the SN, rats injected with AdGDNF in the striatum did not exhibit significant ameliorative effects. This study demonstrates that experimentally increasing levels of GDNF biosynthesis near the dopaminergic neuronal soma is effective in protecting the survival of these neurons and their function even when therapy is begun after 6-OHDA-induced degeneration has commenced. Thus, GDNF gene therapy may ameliorate the consequences of Parkinson's disease through rescuing compromised dopaminergic neurons.

Animals↗

Focal brain injury, FGF-2 and the adverse effects of excessive motor demand on cortical and nigral degeneration: marked protection by delayed intermittent exposure to halothane.

The neuroprotective potential of halothane anesthesia was investigated following unilateral electrolytic lesions to the forelimb representation area of the sensorimotor cortex (FL-SMC). Previously, it was found that the FL-SMC lesion increases substantially in size when the intact forelimb is immobilized with a plaster of paris cast for the first 7 days postlesion, which forces extreme overuse of the impaired forelimb during a time when nonlethally damaged tissue is vulnerable to behavioral demand. Initially, the purpose of this study was to investigate whether intracisternal infusion of basic fibroblast growth factor (bFGF or FGF-2), a potent neurotrophic factor that has been shown to have neuroprotective and plasticity promoting properties in focal stroke and other injury models, could prevent this use-dependent exaggeration of injury. Although intracisternal bFGF (starting 24 h after surgery, twice per week) was not found to produce significant neuroprotective or behavioral effects, the brief exposure to halothane anesthesia (15-20 min) during bFGF or vehicle administration was found to prevent expansion of the lesion size, and to reduce delayed loss of neurons in the substantia nigra pars reticulata (SNr). The data have implications for investigations of the effects of neurotrophic factor in vivo, and other investigations requiring brief, intermittent halothane anesthesia.

Animals↗

Experience-associated structural events, subependymal cellular proliferative activity, and functional recovery after injury to the central nervous system.

Considerable structural plasticity is possible in the damaged neocortex and connected brain areas, and the potential for significant functional recovery remains even during the chronic phases of the recovery process. In this article, the authors review the literature on use-dependent morphologic events, focusing on the direct interaction of behavioral experience and structural changes associated with plasticity and degeneration. Experience-associated neural changes have the potential to either hinder or enhance functional recovery; therefore, issues concerning the nature, timing, and intensity of behavior-based intervention strategies are addressed.

Animals↗

Early exclusive use of the affected forelimb after moderate transient focal ischemia in rats : functional and anatomic outcome.

BACKGROUND AND PURPOSE: Previous work by researchers in our laboratory has shown that in the rat, the exclusive use of the affected forelimb during an early critical period exaggerates lesion volume and retards functional recovery after electrolytic lesions of the forelimb sensorimotor cortex. In the present study, we examined the effects of exclusive use of the affected forelimb after middle cerebral artery occlusion (MCAO). METHODS: Ischemia of moderate severity was produced in male Long-Evans rats through 45 minutes of occlusion of the left middle cerebral and both common carotid arteries. Exclusive use of either the affected or unaffected forelimb was forced through immobilization of either the ipsilateral (MCAO+ipsi) or contralateral (MCAO+contra) forelimb, respectively, for 10 days in a plaster cast, or the animal was left uncasted (MCAO+nocast). Sham surgeries were performed, and animals were also casted for 10 days or left uncasted. Sensorimotor testing was performed during days 17 to 38. At the end of sensorimotor testing, cognitive performance was tested with use of the Morris water maze. In a separate experiment, temperatures and corticosterone levels were measured during the 10-day period after 45-minute ischemia and casting. RESULTS: The MCAO+ipsi group performed worse on sensorimotor tasks than the MCAO+contra, MCAO+nocast, and sham groups. Infarct volume was significantly larger in the MCAO+ipsi group than in the sham and MCAO+contra groups but not in the MCAO+nocast group. No group differences were found with the Morris water maze, and no group differences were found in either temperature or plasma corticosterone level. CONCLUSIONS: The exclusive use of the affected forelimb immediately after focal ischemia has detrimental effects on sensorimotor function that cannot be attributed to hyperthermia or stress.

Animals↗

Movement-related glutamate levels in rat hippocampus, striatum, and sensorimotor cortex.

Changes in brain extracellular glutamate during movement stress were studied using in vivo microdialysis. Male Long-Evans rats were placed in a clear cylinder designed to elicit behavioral activation while undergoing microdialysis sampling from either the hippocampus, striatum or sensorimotor cortex. Glutamate levels were determined by high performance liquid chromatography with fluorescence detection in the dialysates taken before, during, and after exposure to the cylinder. Animals were in a behaviorally quiescent state before exposure to the cylinder, but they demonstrated increases in rearing, locomotion, and turning while in the cylinder. Dialysate glutamate levels were significantly enhanced in the samples taken while the rat was in the cylinder compared with samples taken before or after exposure to the cylinder. In a second study, rats were implanted with bilateral probes in the forelimb sensorimotor cortex, and one forelimb was immobilized by means of a plaster of paris cast. Glutamate, aspartate, serine, and taurine levels were quantified in casted animals. In casted animals, dialysate glutamate levels were lower on the side contralateral to the immobilized limb during both quiescence and movement stress. Aspartate and taurine, but not serine levels increased during movement stress in both the side contralateral and the side ipsilateral to the immobilized limb. These results suggest that there is extracellular overflow of glutamate and other neuroactive amino acids during spontaneous movement, and chronic disuse can suppress extracellular glutamate levels.

Amino Acids↗

Metabolic activation of the subependymal zone after cortical injury.

The subependymal zone (SEZ) of the adult mammalian forebrain contains a population of progenitor cells that proliferate in response to brain injury. This study examined the effect of cortical injury on metabolic activity in the SEZ using quantitative histochemistry of cytochrome oxidase. The SEZ showed significantly enhanced cytochrome oxidase activity in rats with electrolytic cortical injuries relative to sham-operated controls, while other brain regions showed no such changes. The results indicate that the SEZ had increased oxidative energy demands, and thus provide metabolic evidence that SEZ cells are activated in response to brain injury.

Animals↗

Transplants of fibroblasts genetically modified to express BDNF promote regeneration of adult rat rubrospinal axons and recovery of forelimb function.

Adult mammalian CNS neurons do not normally regenerate their severed axons. This failure has been attributed to scar tissue and inhibitory molecules at the injury site that block the regenerating axons, a lack of trophic support for the axotomized neurons, and intrinsic neuronal changes that follow axotomy, including cell atrophy and death. We studied whether transplants of fibroblasts genetically engineered to produce brain-derived neurotrophic factor (BDNF) would promote rubrospinal tract (RST) regeneration in adult rats. Primary fibroblasts were modified by retroviral-mediated transfer of a DNA construct encoding the human BDNF gene, an internal ribosomal entry site, and a fusion gene of lacZ and neomycin resistance genes. The modified fibroblasts produce biologically active BDNF in vitro. These cells were grafted into a partial cervical hemisection cavity that completely interrupted one RST. One and two months after lesion and transplantation, RST regeneration was demonstrated with retrograde and anterograde tracing techniques. Retrograde tracing with fluorogold showed that approximately 7% of RST neurons regenerated axons at least three to four segments caudal to the transplants. Anterograde tracing with biotinylated dextran amine revealed that the RST axons regenerated through and around the transplants, grew for long distances within white matter caudal to the transplant, and terminated in spinal cord gray matter regions that are the normal targets of RST axons. Transplants of unmodified primary fibroblasts or Gelfoam alone did not elicit regeneration. Behavioral tests demonstrated that recipients of BDNF-producing fibroblasts showed significant recovery of forelimb usage, which was abolished by a second lesion that transected the regenerated axons.

Animals↗