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PubMed2000

Acute blockade of nitric oxide synthesis induces disorganization and amplifies lesion-induced plasticity in the rat retinotectal projection.

In the rat visual system, the uncrossed retinotectal projection undergoes a topographical refinement within the first two postnatal weeks. We have studied the role of nitric oxide (NO), a retrograde messenger which couples pre- and postsynaptic activation, in the development of the uncrossed retinotectal projection and in the plasticity of this pathway as a result of a restricted retinal lesion in the opposite eye. During development, maximal nitric oxide synthase (NOS) activity was observed in homogenates of tectal tissue at postnatal day 5 (PND 5), followed by a two-step decrease at the end of the topographical fine tuning period (PND 21) and the adult stage (PND 42). We also tested the effects of an acute in vivo blockade of NOS during the development of both animals that had not been operated on, and lesioned animals. Animals ranging from PND 4 to PND 42 were treated either with the NOS inhibitor, L-nitro-arginine (Narg 50 mg/kg ip.) or vehicle (NaCl 0.9%) during 4 days (from PND 4-7 or PND 9-12) or 8 days (from PND 20-27 or PND 34-41). Reduction of NOS activity induced sprouting of the ipsilateral pathway up to the second postnatal week in the animals that had not been operated on. Rats that had been operated on, however, showed an amplification of the lesion-induced plasticity up to the fourth postnatal week under NOS blockade. The data suggest that NO plays a role in the stabilization of retinotectal synapses during the critical period of topographic refinement, and indicate that an acute blockade of retrograde signals enables plastic rearrangements in the visual system within this time window.

Animals↗
PubMed2000

Overview on the structure, composition, function, development, and plasticity of hippocampal dendritic spines.

There has been an explosion of new information on the neurobiology of dendritic spines in synaptic signaling, integration, and plasticity. Novel imaging and analytical techniques have provided important new insights into dendritic spine structure and function. Results are accumulating across many disciplines, and a step toward consolidating some of this work has resulted in Dendritic Spines of the Hippocampus. Leaders in the field provide a discussion at the level of advanced under-graduates, with sufficient detail to be a contemporary resource for research scientists. Critical reviews are presented on topics ranging from spine structure, formation, and maintenance, to molecular composition, plasticity, and the role of spines in learning and memory. Dendritic Spines of the Hippocampus provides a timely discussion of our current understanding of form and function at these excitatory synapses. We asked authors to include areas of controversy in their papers so as to distinguish results that are generally agreed upon from those where multiple interpretations are possible. We thank the contributors for their insights and thoughtful discussions. In this paper we provide background on the structure, composition, function, development, plasticity, and pathology of hippocampal dendritic spines. In addition, we highlight where each of these subjects will be elaborated upon in subsequent papers of this special issue of Hippocampus.

Animals↗
PubMed2000

Testosterone decreases CA1 plasticity in vivo in gonadectomized male rats.

Estrogen has been reported to enhance CA1 functional plasticity in adult rats, as measured by the induction of long-term potentiation (LTP). In the present study, the effects of androgens on CA1 LTP were assessed in adult male Sprague-Dawley rats in vivo following peripubertal castration. Castrated rats with cholesterol implants showed significantly greater plasticity, both in degree and duration of potentiation, than castrated rats given testosterone or dihydrotestosterone implants. An LTP paradigm reported to produce decremental LTP in vitro produced nondecremental LTP in androgen-deprived rats, but decremental LTP in androgen-treated rats. These results suggest that androgens, unlike estrogens, act to reduce CA1 plasticity in the adult rat.

Animals↗
PubMed1995

Factors that are critical for plasticity in the visual cortex.

Factors that may be critical for plasticity in the visual cortex are evaluated according to three criteria. (1) Do antagonists to the factor abolish plasticity? (2) Does the concentration or activity of the factor peak with the critical period for plasticity? (3) Does rearing in the dark, which postpones the critical period, affect the factor in a similar fashion? N-methyl-D-aspartate receptors fulfil all three criteria. Metabotropic glutamate receptors fulfil two of them. Most other putative factors do not fulfil more than one.

Animals↗
PubMed2005

Severe lead poisoning in the plastics industry: a report of three cases.

BACKGROUND: Lead stabilizers (e.g., lead sulfate, lead stearate) are common additives in plastics used in electrical devices. In 1997, three plastics compounders at one California company were severely lead-poisoned. METHODS: The poisonings were investigated by interviewing the workers, employer, and treating physician and reviewing medical records and environmental monitoring results. In addition to measuring blood lead levels (BLLs), noninvasive K X-ray fluorescence was used to measure bone lead concentration of the index case. RESULTS: Blood lead concentrations of the three workers at time of diagnosis were 159, 114, and 108 microg/dl. The worker with highest exposure presented with clinical findings of crampy abdominal pain, constipation, normocytic anemia, fatigue, and reversible azotemia. Bone lead concentration in his tibia, calcaneous, and patella were 102, 219, and 182 ppm, respectively. The poisonings resulted from uncontrolled use of powdered lead sulfate stabilizer. CONCLUSION: Clinicians should be aware of potential serious overexposure to lead in compounding of plastics.

Abdominal Pain↗
PubMed1985

Spontaneous abortions among women employed in the plastics industry.

A matched case-control study was done to analyze whether certain occupational exposures in the plastics industry were related to the risk of spontaneous abortions. Information on spontaneous abortions (cases) and births (controls) was obtained from the hospital discharge register; data on occupational exposures were obtained from the occupational health services of the workplaces. No increased risk of spontaneous abortions was observed among workers processing polymerized plastics or heated plastics made of vinyl chloride or of styrene. Owing to the low statistical power of the study, only strong effects can be ruled out. The odds ratio for workers actually processing polyurethane was increased (1.9, not statistically significant), and that for all workers in polyurethane-processing factories was significantly increased (3.0, p = 0.02). The finding needs to be investigated further in future studies.

Abortion, Spontaneous↗
PubMed1990

Respiratory morbidity of pattern and model makers exposed to wood, plastic, and metal products.

Pattern and model makers are skilled tradespersons who may be exposed to hardwoods, softwoods, phenol-formaldehyde resin-impregnated woods, epoxy and polyester/styrene resin systems, and welding and metal-casting fumes. The relationship of respiratory symptoms (wheezing, chronic bronchitis, dyspnea) and pulmonary function (FVC% predicted, FEV1% predicted, FEV1/FVC% predicted) with interview-derived cumulative exposure estimates to specific workplace agents and to all work with wood, plastic, or metal products was investigated in 751 pattern and model makers in southeast Michigan. In stratified analyses and age- and smoking-adjusted linear and logistic regression models, measures of cumulative wood exposures were associated with decrements in pulmonary function and dyspnea, but not with other symptoms. In similar analyses, measures of cumulative plastic exposures were associated with wheezing, chronic bronchitis, and dyspnea, but not with decrements in pulmonary function. Prior studies of exposure levels among pattern and model makers and of respiratory health effects of specific agents among other occupational groups support the plausibility of wood-related effects more strongly than that of plastic-related effects.

Adult↗
PubMed2002

Functional recovery and neuroanatomical plasticity following middle cerebral artery occlusion and IN-1 antibody treatment in the adult rat.

Stroke is a prevalent and devastating disorder, and no treatment is currently available to restore lost neuronal function after stroke occurs. One unique therapy that may improve functional recovery after stroke is blockade of the neurite inhibitory protein Nogo-A with the monoclonal antibody IN-1, through enhancement of neuroanatomical plasticity from uninjured areas of the central nervous system. In the present study, we combined IN-1 treatment with an ischemic lesion (permanent middle cerebral artery occlusion) to determine the effect of Nogo-A neutralization on cortical plasticity and functional recovery. We report here that, following ischemic stroke and treatment with IN-1, adult rats demonstrated functional recovery on a forelimb-reaching task and new cortico-efferent projections from the opposite, unlesioned hemisphere. These results support the efficacy of Nogo-A blockade as a treatment for ischemic stroke and implicate plasticity from the unlesioned hemisphere as a mechanism for recovery.

Age Factors↗
PubMed2005

Cortical influences on sizes and rapid plasticity of tactile receptive fields in the dorsal column nuclei.

The cerebral cortex influences subcortical processing. In the somatosensory system, descending cortical inputs contribute in specific ways to the sizes and plasticity of tactile receptive fields (RFs) in the thalamus, but less is known about cortical influences on these aspects of brainstem RFs. The present studies evaluated how loss of cortical inputs affects sizes and plasticity of RFs in the brainstem dorsal column nuclei (DCN) when peripheral inputs were normal and when peripheral inputs were acutely disrupted. Loss of cortical inputs was produced by acute lesion of somatosensory, motor, and adjacent cortex, whereas disruption of peripheral inputs was produced by cutaneous microinjection of lidocaine (LID). Modest or no changes in sizes of DCN RFs, comparable to changes during control periods of no treatment, were seen in response to cortical lesion. LID caused rapid enlargements in RFs when cortex was intact. LID also caused rapid RF enlargements after cortical lesion, and these enlargements were greater than post-LID enlargements when cortex was intact. These results indicate that normally sized RFs continue to be produced in the DCN after loss of cortical input. Cortex is also not required for RF enlargements after LID; however, cortical inputs have a constraining effect on these enlargements. Considered with findings from previous thalamic studies, these results suggest that cortical influences on RF size and plasticity in the DCN and thalamus differ in some respects.

Anesthetics, Local↗
PubMed1985

Dark rearing prolongs physiological but not anatomical plasticity of the cat visual cortex.

Recent studies (Cynader and Mitchell, '80; Mower et al., '81) have shown that total dark rearing prolongs susceptibility to the physiological effects of monocular deprivation (MD) in visual cortex beyond the normal age limits. The present study addressed whether this delayed physiological plasticity is accompanied by delayed anatomical plasticity in the geniculocortical pathway. Ocular dominance (OD) columns as defined by transsynaptic autoradiography following injection of 3H proline into one eye were studied both qualitatively and quantitatively in 17 cats. Compared to normal rearing (N-3), both binocular eyelid suture (N-2) and total dark rearing (N-3) resulted in incomplete segregation of OD columns in area 17. This apparent immaturity after binocular deprivation, however, did not reflect a delayed capacity for development and plasticity. Visual experience after dark rearing produced no marked changes. In cats who experienced MD after dark rearing, injection of either the nondeprived (N-2) or deprived eye (N-3) resulted in a nearly uniform distribution of label throughout layer IV of area 17. The same result occurred with binocular vision after dark rearing (N-1). MD from birth, however, produced expansion of columns from the nondeprived eye (N-1) and contraction of columns from the deprived eye (N-1). MD imposed after 4 months of normal vision resulted in normal OD columns (N-1). Electrophysiological studies revealed a high proportion of binocular cells within layer IV in cats who experienced monocular or binocular vision after dark rearing. Outside of layer IV there were clear environmental effects on OD of single cells in these cats. Measurements of cell sizes in the clateral geniculate nucleus showed shrinkage of cells innervated by the deprived eye when MD was initiated at birth (N-3). MD after dark rearing (N-4) produced no differences in cell sizes. It is concluded that visual input is necessary for the formation of normal OD columns, the critical period for formation and environmental modification of OD columns is limited to early life, and the physiological effects of visual experience after dark rearing reflect changes occurring beyond the geniculocortical pathway.

Animals↗
PubMed1986

Plasticity in the rat olfactory cortex.

The relationship of age to deafferentation plasticity was studied in the rat olfactory cortex (OC). Ablation of a single olfactory bulb (OB) was performed in each of several rats of selected postnatal (PN) ages: PN2.5, 6, 9, 13, and 21 days and in adults of PN100 days. Following survival times sufficient to remove the resultant degeneration, a cortical lesion was placed in the ipsilateral OC. The patterns of degeneration from the OC lesion were studied and mapped in the adjacent deafferented OC. The results show a spread or sprouting of the usually deep-lying afferents (interrupted by the OC lesion), onto the deafferented superficial dendrites (normally occupied by the OB afferents) in all of the ages. The spread is most striking at PN2.5 to PN9, gradually reduced by PN13 to PN21, and least in the adult (PN100). There is also an apparent increase of afferents to the deeper dendrites nearer the cell bodies in all cases except in the PN 100 group. Shrinkage of layer I is not seen in PN2.5 subjects, is minimal by PN9, but is most marked in the adult PN100 with total OB lesions. Incomplete OB lesions sparing some lateral olfactory tract (LOT) fibers greatly reduce the shrinkage of layer I and the spread of afferents in all ages. Thus, a capacity for reorganization of afferents occurs at least through PN9, with PN13-21 a possible "critical period" after which plasticity is limited and transneuronal effects are more permanent. The association, centrifugal, and olfactory-entorhinal pathways are possible origins for this plasticity. Factors contributing to limitations in this reorganization are discussed.

Age Factors↗
PubMed1989

Extension of the critical period for developmental plasticity of the corticospinal pathway.

The corticospinal tract (CST) of the rat undergoes a prolonged period of postnatal development. Lesions of the presumptive CST pathway at birth are followed by the aberrant rerouting of the developing corticospinal axons around the lesion site through adjacent undamaged CNS tissue. This developmental plasticity becomes severely restricted by 5-6 days of age, so the axons are no longer capable of growth around the site of injury. The aim of the current study was to determine whether altering the environment at the site of injury by filling the lesion with transplanted fetal spinal cord tissue could prolong the critical period for developmental plasticity of the corticospinal pathway. The spinal cord was damaged (overhemisection) at three stages in the development of the corticospinal (CS) pathway: 1) prior to the arrival of CS axons, 2) after the axons elongated through the cord but prior to synaptogenesis, and 3) after both axonal elongation and synaptogenesis were completed. One to 9 months later, anterograde neuronal tracing with horseradish peroxidase was used to assess the growth of the corticospinal pathway with or without a fetal transplant at the site of injury, and the pattern of labeling was compared with that observed in adult nonlesioned control animals. Our results indicate that the presence of a transplant prolongs the critical period for developmental plasticity of the CST. Transplants elicited growth of CST axons throughout the postnatal period examined. CST axons damaged prior to synaptogenesis exhibited more robust growth than those lesioned after synaptogenesis had been completed. These results suggest that both environmental and neuronal factors interact to regulate the response of immature CS neurons to injury.

Animals↗
PubMed1994

Inverse patterns of myelination and GAP-43 expression in the adult CNS: neurite growth inhibitors as regulators of neuronal plasticity?

In the central nervous system (CNS) myelin is present not only in white matter, but also in varying amounts in many gray matter areas. In addition to the function of electrical insulation of axons, myelin and oligodendrocytes contain molecules that are powerful inhibitors of neurite growth. Nevertheless plastic changes involving sprouting of nerve terminals occur in several brain regions of adult animals after partial lesions. In this study we have tried to correlate the plastic potential of CNS regions with the degree of their myelination. The expression of the growth-associated protein GAP-43 was used as an indicator of the potential for plastic changes, and a histological myelin stain was used to assess myelination. We have found that myelination and GAP-43 expression have strikingly inverse expression patterns in the majority of CNS gray matter areas. Densely myelinated regions, that is, most brainstem nuclei, the tegmentum, and the inferior colliculus, are low in GAP-43. In contrast, unmyelinated or lightly myelinated areas, such as the substantia gelatinosa of the spinal cord, the nucleus of the solitary tract, or the septum, express high levels of GAP-43. Areas known to show lesion-induced sprouting are typically high in GAP-43 and only lightly myelinated. During postnatal development the myelination pattern precedes the GAP-43 pattern, a sequence that is consistent with a role of myelin and the associated neurite growth inhibitors in modifying GAP-43 expression. Our results support the hypothesis that myelin-associated neurite growth inhibitors are involved in regulating the stability of neural connections.

Animals↗
PubMed2003

Morphological plasticity of olfactory ensheathing cells is regulated by cAMP and endothelin-1.

Olfactory ensheathing cells (ECs) are a promising tool for the repair of injury in the adult central nervous system. However, important aspects of the cell biology of ECs remain unclear, such as whether ECs exist as a single population or as two subpopulations with Schwann cell-like and astrocyte-like characteristics. The morphologies of these subpopulations are used as defining characteristics, yet ECs are known to be morphologically plastic. To elucidate this apparent inconsistency, we investigated the morphological plasticity of ECs in culture. We defined purified ECs as immunopositive for both p75 neurotrophin receptor and glial fibrillary acidic protein. In MEM (D)-valine modification + 10% dialyzed fetal calf serum, 87%-90% of ECs displayed a flat morphology. In three different serum-free media (N2 medium, neurobasal medium + B27 supplement, and DMEM/F-12 medium + G5 supplement), 78%-84% of ECs displayed process-bearing morphology. Ensheathing cells switched reversibly between these morphologies within a day of the serum conditions being changed. Exposure to 1 nM endothelin-1 in serum-free medium prevented the switch from flat to process-bearing morphology, while 1 mM dibutyryl cAMP accelerated this change. The effects of both agents were completely reversible and similar to that reported for astrocytes. Both flat and process-bearing ECs were immunopositive for brain-derived neurotrophic factor, nerve growth factor, neurotrophin-4, and TrkB but not TrkA. Together, these results suggest that ECs exist as a single morphologically plastic population.

Animals↗
PubMed2005

Macrophage-induced inflammation affects hippocampal plasticity and neuronal development in a murine model of HIV-1 encephalitis.

Cognitive, behavioral, and motor impairments, during progressive human immunodeficiency virus type 1 (HIV-1) infection, are linked to activation of brain mononuclear phagocytes (MP; perivascular macrophages and microglia). Activated MPs effect a giant cell encephalitis and neuroinflammatory responses that are mirrored in severe combined immunodeficient (SCID) mice injected with human monocyte-derived macrophages (MDM). Whether activated human MDMs positioned in the basal ganglia affect hippocampal neuronal plasticity, the brain subregion involved in learning and memory, is unknown. Thus, immunohistochemical techniques were used for detection of newborn neurons (polysialylated neuronal cell adhesion molecule [PSA-NCAM]) and cell proliferation (Ki-67) to assay MDM effects on neuronal development in mouse models of HIV-1 encephalitis. Immunodeficient (C.B.-17/SCID and nonobese diabetic/SCID, NOD/SCID) and immune competent (C.B.-17) mice were injected with uninfected or HIV-1-infected MDM. Sham-operated or unmanipulated mice served as controls. Neuronal plasticity was evaluated in the hippocampal dentate gyrus (DG) at days 7 and 28. By day 7, increased numbers of Ki-67+ cells, PSA-NCAM+ cells and dendrites in DG were observed in sham-operated animals. In contrast, significant reductions in neuronal precursors and altered neuronal morphology paralleled increased microglial activation in both HIV-1-infected and uninfected MDM-injected animals. DG cellular composition was restored at day 28. We posit that activated MDM induce inflammation and diminish DG neuronal plasticity. These data provide novel explanations for the cognitive impairments manifested during advanced HIV-1 infection.

AIDS Dementia Complex↗
PubMed1990

Developmental transition in plasticity properties of differentiating astrocytes: age-related biochemical profile of plasminogen activators in astroglial cultures.

Plasminogen activator (PA) is a key enzyme in control of the cascade of extracellular proteolytic activities, proteases that degrade the extracellular components. Mammalian cells produce two molecular forms of PA, the urokinase type (u-PA) and the tissue type (t-PA); the u-PA type enzyme regulates cell migration/invasion and related tissue plasticity events. Thus, these plasticity properties of cells are defined by their PAs' biochemical profiles. The capacity of the differentiating glial cells of the central nervous system (CNS) to express and regulate the two types of PA activities has been examined as a function of cell age in culture. Results of the study suggest that only the immature astrocyte is endowed with these plasticity properties. Differentiating heterogeneous rat glial cells in culture express PA activity. Astroglia were identified as the primary source for the glial PA activity, as no PA activity was detected in the purified oligodendroglia. Cellular PA activity levels of differentiating rat and mouse astroglia are developmentally regulated. The specific activity of PA reached its highest level in rat astroglia at a cell age corresponding to 20-32 postnatal days (P20-P32) and in mouse astroglia at P8-P14; thereafter, this declined (three- to fourfold decrease) within 2 weeks to a low value. At comparable ages (P0-P35), the magnitudes of the PA specific activities of the differentiating rat astroglia and of the developing cerebrum, the tissue from which these cells were purified, were similar. Differentiating rat astroglia produce u-PA and t-PA, the cellular content of both is developmentally regulated, and the u-PA form is only found in the immature cells. u-PA is the predominant form in the immature astrocyte until age P13. Both forms are found in cells at ages P14-P30, and at later stages u-PA disappears while the t-PA type persists as the sole form. After 3 more weeks neither of the PA types was detected. Astroglia express also PA inhibitory activity; the rat astroglial PA inhibitor (PAI) seemed to be identical to PAI-1, one of the known types of PAIs. Stimulation of astroglial proliferation by their subculturing in contrast to Schwann cells did not lead to an increase; rather, beyond a certain cell age (P13) it resulted in a threefold irreversible decline in the PA specific activity of the daughter cells. It has been established that various biochemical properties of CNS mature glia appear on schedule with cell age in culture, thus defining "mature"glia in vitro.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2007

Somatosensory cortical plasticity in carpal tunnel syndrome treated by acupuncture.

Carpal tunnel syndrome (CTS) is a common entrapment neuropathy of the median nerve characterized by paresthesias and pain in the first through fourth digits. We hypothesize that aberrant afferent input from CTS will lead to maladaptive cortical plasticity, which may be corrected by appropriate therapy. Functional MRI (fMRI) scanning and clinical testing was performed on CTS patients at baseline and after 5 weeks of acupuncture treatment. As a control, healthy adults were also tested 5 weeks apart. During fMRI, sensory stimulation was performed for median nerve innervated digit 2 (D2) and digit 3 (D3), and ulnar nerve innervated digit 5 (D5). Surface-based and region of interest (ROI)-based analyses demonstrated that while the extent of fMRI activity in contralateral Brodmann Area 1 (BA 1) and BA 4 was increased in CTS compared to healthy adults, after acupuncture there was a significant decrease in contralateral BA 1 (P < 0.005) and BA 4 (P < 0.05) activity during D3 sensory stimulation. Healthy adults demonstrated no significant test-retest differences for any digit tested. While D3/D2 separation was contracted or blurred in CTS patients compared to healthy adults, the D2 SI representation shifted laterally after acupuncture treatment, leading to increased D3/D2 separation. Increasing D3/D2 separation correlated with decreasing paresthesias in CTS patients (P < 0.05). As CTS-induced paresthesias constitute diffuse, synchronized, multidigit symptomatology, our results for maladaptive change and correction are consistent with Hebbian plasticity mechanisms. Acupuncture, a somatosensory conditioning stimulus, shows promise in inducing beneficial cortical plasticity manifested by more focused digital representations.

Acupuncture Therapy↗
PubMed2002

Age-dependent differential regulation of genes encoding APP and alpha-synuclein in hippocampal synaptic plasticity.

We investigated the modulation of the messenger RNA encoding the amyloid precursor protein (APP) and alpha-synuclein following induction of long-term potentiation (LTP) in the dentate gyrus of young and aged rats. Three hours after tetanic stimulation, LTP induced in the young rats was maintained; the aged rats, however, fell into two subgroups: those in which LTP was maintained, and those in which LTP had declined to basal levels. In young rats, the global expression of mRNAs of all isoforms of APP and in particular that of the isoform lacking the KPI domain were significantly upregulated. In aged rats, the global expression of mRNAs of all isoforms of APP was not modified, regardless of whether LTP was maintained or not. The level of mRNA encoding the Kunitz protease-inhibitory (KPI)-minus isoform of APP, however, was increased in aged rats in which LTP was maintained, suggesting that the gene of this isoform may be more specifically regulated by synaptic plasticity. In contrast, we found that the gene encoding alpha-synuclein showed a trend towards being downregulated at the mRNA level in young rats following LTP, and significantly so in aged rats in which LTP was maintained, whereas it was not downregulated in aged rats with decremental LTP. These data suggest that the regulated expression of APP isoforms is part of the tanscriptional response associated with the enduring forms of synaptic plasticity and is altered with age. Whereas the level of alpha-synuclein mRNA is not apparently modified in normal LTP, it may reflect a mechanism of apoptotic cell death in aging that is in part responsible for decremental synaptic plasticity.

Aging↗