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PubMed2001

Neonatal exposure to a novel environment enhances the effects of corticosterone on neuronal excitability and plasticity in adult hippocampus.

Electrophysiological studies have shown that activation of glucocorticoids receptors (GRs) influences neuronal excitability and activity dependent synaptic plasticity. In developmental studies, early life stimulation such as neonatal handling results in an up-regulation of glucocorticoid-receptor (GR) binding in the hippocampus that persists into adulthood. It is, therefore, hypothesized that early environment-induced changes in receptor sensitivity to corticosterone (CORT) might have functional effects on adult neuronal excitability and synaptic plasticity. To test this hypothesis, we exposed rats daily from post-natal days 1-21 to a non-home environment for 3 min. When the animals became adults, we studied the effects of glucocorticoid hormone corticosterone (CORT) on population spike (PS) amplitude and long-term potentiation of population spikes (PS-LTP) in vitro in the hippocampal CA1 region following activation of the Schaffer collateral fibers. Bath application of CORT reduced PS amplitude and subsequent induction of PS-LTP. This inhibitory effect of CORT was significantly greater in the slices from the novelty exposed rats (Novel) than the control rats that remained in their home cage (Home). Inhibition of population spike amplitude during CORT perfusion was 28.0+/-5.3% of baseline in Novel slices, and 9.1+/-4.4% in Home slices. CORT pre-exposure (20 min) also inhibited the subsequent induction of PS-LTP in Novel slices by 57.7+/-17.7% and by 7.5+/-12.1% in Home slices. These results provide electrophysiological evidence that neonatal novelty exposure results in functional increases in receptor sensitivity to CORT that enhances the inhibitory effects of CORT on field CA1 neuronal excitability and plasticity.

Action Potentials↗
PubMed2000

Seasonal plasticity in the adult brain.

Seasonal plasticity of structure and function is a fundamental feature of nervous systems in a wide variety of animals that occupy seasonal environments. Excellent examples of seasonal brain changes are found in the avian song control system, which has become a leading model of morphological and functional plasticity in the adult CNS. The volumes of entire brain regions that control song increase dramatically in anticipation of the breeding season. These volumetric changes are induced primarily by vernal increases in circulating sex steroids and are accompanied by increases in neuronal size, number and spacing. In several species, these structural changes in the song control circuitry are associated with seasonal changes in song production and learning. Songbirds provide important insights into the mechanisms and behavioral consequences of plasticity in the adult brain.

Age Factors↗
PubMed2002

Long-term plasticity at GABAergic and glycinergic synapses: mechanisms and functional significance.

Activity-dependent long-term changes in synaptic efficacy are thought to be important in learning, memory formation, neuronal development and pathological states of neuronal excitability in the CNS. For the past two decades, numerous studies have investigated long-term changes in synaptic efficacy at excitatory glutamatergic synapses. Although inhibitory synapses are essential for proper functioning of the neuronal network, attention has focused only recently on describing and characterizing plasticity at these types of synapse. Not surprisingly, different forms of plasticity at GABAergic, and the closely related glycinergic, synapses have been reported in several regions of the brain. Here we review these different forms of plasticity and focus on their possible roles in developing and adult neuronal networks.

Animals↗
PubMed2003

It could be habit forming: drugs of abuse and striatal synaptic plasticity.

Drug addiction can take control of the brain and behavior, activating behavioral patterns that are directed excessively and compulsively toward drug usage. Such patterns often involve the development of repetitive and nearly automatic behaviors that we call habits. The striatum, a subcortical brain region important for proper motor function as well as for the formation of behavioral habits, is a major target for drugs of abuse. Here, we review recent studies of long-term synaptic plasticity in the striatum, emphasizing that drugs of abuse can exert pronounced influences on these processes, both in the striatum and in the dopaminergic midbrain. Synaptic plasticity in the ventral striatum appears to play a prominent role in early stages of drug use, whereas dopamine- and endocannabinoid-dependent synaptic plasticity in the dorsal striatum could contribute to the formation of persistent drug-related habits when casual drug use progresses towards compulsive drug use and addiction.

Animals↗
PubMed2003

Molecular basis of plasticity in the visual cortex.

Sensory experience is known to shape the maturation of cortical circuits during development. A paradigmatic example is the effect of monocular deprivation on ocular dominance of visual cortical neurons. Although visual cortical plasticity has been widely studied since its initial discovery by Hubel and Wiesel >40 years ago, the description of the underlying molecular mechanisms has lagged behind. Several new findings are now beginning to close this gap. Recent data deepen our knowledge of the factors involved in the intercellular communication and intracellular signaling that mediate experience-dependent plasticity in the developing visual cortex. In addition, new findings suggest a role for the extracellular matrix in inhibition of ocular-dominance plasticity in the adult visual cortex.

Animals↗
PubMed1996

Neural cell adhesion molecules in activity-dependent development and synaptic plasticity.

Cell adhesion molecules (CAMs) have a vital role in forming connections between neurons during embryonic development. Increasing evidence suggests that CAMs also participate in activity-dependent plasticity during development and synaptic plasticity in adults. Neural impulses of appropriate patterns can regulate expression of specific CAMs in mouse neurons from dorsal-root ganglia, alter cell-cell adhesion and produce structural reorganization of axon terminals in culture. Synaptic plasticity in Aplysia, learning in chick and long-term potentiation in rat hippocampus are accompanied by changes in CAM expression. Long-term potentiation can be blocked by disrupting CAM function in rat hippocampus, and learning deficits result from antibody blockade of CAMs in chicks and in transgenic mice lacking specific CAMs. Cell adhesion molecules might produce these effects by controlling several cellular processes, including cell adhesion, cytoskeletal structure and intracellular signaling.

Animals↗
PubMed1998

Plasticity of the olivocerebellar pathway.

The adult olivocerebellar axons and their terminal arbours, the climbing fibres, are capable of remarkable structural plasticity, regulated through their interaction with Purkinje cells. When these cells are deleted,terminal climbing fibre branches retract. In contrast,there is a vigorous outgrowth of entire terminal arbours when extra postsynaptic neurones are available. The new connections lead to a functional, highly specific pattern of innervation at the single Purkinje cell level and are topographically organized according to the principles of the original projection map.A reversible climbing fibre retraction occurs following depression of electrical activity of the cerebellar cortex. These remarkable plastic properties, together with the fact that these neurones express several growth-associated genes constitutively, suggest that the climbing fibre synapses might be adjusted dynamically to participate in physiological plasticity.

Animals↗
PubMed1997

Crystallinity in starch plastics: consequences for material properties.

The processing of starches with biodegradable additives has made biodegradable plastics suitable for a number of applications. Starch plastics are partially crystalline as a result of residual crystallinity and the recrystallization of amylose and amylopectin. Such crystallinity is a key determinant of the product's properties. This article describes the influence of processing and storage conditions on starch crystallinity and offers possible explanations for the various properties of starch plastics, in particular for the problems associated with ageing, in terms of the different crystalline structures.

Biodegradation, Environmental↗
PubMed2000

Synaptic microenvironments--structural plasticity, adhesion molecules, proteases and their inhibitors.

Proteolytic regulation might be essential in neural plasticity in mature brain as well as the developing brain. An increasing number of studies support the idea that structural changes in the synapses are closely associated with synaptic plasticity. Proteases and their inhibitors in a synaptic microenvironment are important in the regulation of dynamic changes in the extracellular matrix components associated with synaptic plasticity. In the present article, the possible roles of neuronal proteases, protease inhibitors and extracellular macromolecules are reviewed.

Animals↗
PubMed1998

Primitivism and plasticity of pain--implication of polymodal receptors.

Bio-warning and defense mechanisms play the most fundamental roles in living organisms. From an evolutionary point of view, nociceptive systems are very primitive and are richly provided with humoral signaling mechanisms of aboriginal humoral defense systems, as reflected in the primitive nature of the polymodal receptor, a poorly differentiated sensory receptor signaling nociceptive information. Recent advances in studies on pain have made it possible to explain neural mechanisms of pain systems under physiological conditions and reveal that there is a large gap between physiological and pathological pains. Protracted nociceptive inputs under pathological conditions induce plastic, either functional or structural, alterations in the nociceptive pathways. These plastic changes lead to crosstalk among the neural networks, including circuits related to motor, autonomic, or psychological functions. These plastic changes, once established, persist even after the original pain sources disappear in a memory-like fashion. Thus, it is revealed that chronic pain cannot be treated by blocking pain pathways, which is effective against acute pain, but require treatment from a multidisciplinary perspective.

Animals↗
PubMed1982

Plasticizer migration from polyvinyl chloride film to solvents and foods.

Polyvinyl chloride (PVC) films used for food wraps contain significant concentrations of plasticizers, along with other additives. The rate of migration of these plasticizers to foods and food-simulating solvents is the principal concern of this paper, which reviews prior experimental studies and presents new data for radiolabelled dioctyl adipate. Analytical models are described to correlate many of the data, criteria are presented for identifying the controlling step in the mechanism of transfer of plasticizer from PVC films into foods and food-simulating solvents, and tentative recommendations are offered for the selection of food simulants and for the type of experiment necessary to allow an unambiguous interpretation of the data.

Diffusion↗
PubMed1998

In vivo percutaneous absorption of [14C]DEHP from [14C]DEHP-plasticized polyvinyl chloride film in male Fischer 344 rats.

These studies investigated the migration of di(2-ethylhexyl) phthalate (DEHP) contained as a plasticizer in polyvinyl chloride (PVC) from plastic film and its absorption through rat skin in iivo. Sheets of PVC film (15 cm2) plasticized with [14C]DEHP were applied to the shaved backs of eight male rats in two separate experiments. For Study I, the PVC film was removed after 24 hr, the animals were rewrapped to prevent them from ingesting any residual DEHP at the exposure site, and urine and faeces were collected at regular intervals for 7 days. For Study II, the PVC film was removed after 24 hr, and the animals were immediately killed by CO2 inhalation. Urine and faeces were collected at 24 hr, and the exposure site was washed and rinsed to remove residual [14C]DEHP. In both studies, the amounts of radioactivity transferred from the film were extremely small, amounting to 0.0643% (Study I) and 0.126% (Study II) of that applied. The transferred radioactivity was found to be in three separate fractions. Radioactivity readily removed from the skin (mean 75% of the transferred radioactivity), radioactivity remaining at the application site at sacrifice. and absorbed radioactivity, that is, that distributed systemically or eliminated. The mean absorption rates for DEHP, calculated from the sum of the quantities absorbed plus that present in the exposure site, were: Study I, 0.239, and Study II, 0.242 microg/cm2/hr.

Animals↗
PubMed1998

Assessment of vinyl chloride-induced DNA damage in lymphocytes of plastic industry workers using a single-cell gel electrophoresis technique.

DNA damage and the formation of stable carcinogen-DNA adducts are considered critical events in the initiation of the carcinogenic process. This study was carried out to assess whether exposure of plastics industry workers to the vinyl chloride monomer (VCM) for different periods of time would cause DNA damage, using the single-cell gel electrophoresis (SCGE) technique. Levels of DNA damage was assessed by both extent of DNA migration and numbers of DNA damaged spots in the peripheral blood lymphocytes from 32 plastics workers with different periods of exposure to VCM; they were evaluated by comparison with a group of non-exposed individuals. It was found that plastics workers who were exposed to VCM for different periods of time showed significantly increased levels of DNA damage compared with the non-exposed subjects. There was a significant correlation between the severity of DNA damage and duration of exposure. However, no significant correlation was found between the age of all subjects and DNA damage. Concentrations of VCM in the air inside the factory were found to be significantly higher than values in non-exposed areas, despite being lower than the threshold limit value (TLV). Our results encourage the application of SCGE as a sensitive, simple, fast and useful technique in the regular health screening of workers occupationally exposed to VCM (even at concentrations below the TLV) to assess the possibility of any DNA damage.

Adult↗
PubMed2003

Impact of aging on hippocampal function: plasticity, network dynamics, and cognition.

Aging is associated with specific impairments of learning and memory, some of which are similar to those caused by hippocampal damage. Studies of the effects of aging on hippocampal anatomy, physiology, plasticity, and network dynamics may lead to a better understanding of age-related cognitive deficits. Anatomical and electrophysiological studies indicate that the hippocampus of the aged rat sustains a loss of synapses in the dentate gyrus, a loss of functional synapses in area CA1, a decrease in the NMDA-receptor-mediated response at perforant path synapses onto dentate gyrus granule cells, and an alteration of Ca(2+) regulation in area CA1. These changes may contribute to the observed age-related impairments of synaptic plasticity, which include deficits in the induction and maintenance of long-term potentiation (LTP) and lower thresholds for depotentiation and long-term depression (LTD). This shift in the balance of LTP and LTD could, in turn, impair the encoding of memories and enhance the erasure of memories, and therefore contribute to cognitive deficits experienced by many aged mammals. Altered synaptic plasticity may also change the dynamic interactions among cells in hippocampal networks, causing deficits in the storage and retrieval of information about the spatial organization of the environment. Further studies of the aged hippocampus will not only lead to treatments for age-related cognitive impairments, but may also clarify the mechanisms of learning in adult mammals.

Aged↗
PubMed2001

A functional role for adenosine A3 receptors: modulation of synaptic plasticity in the rat hippocampus.

Adenosine modulates hippocampal synaptic plasticity, namely long-term potentiation (LTP) and long-term depression (LTD), through activation of A1 and A2A receptors. We now report a novel role for the recently described adenosine A3 receptor in the regulation of synaptic plasticity in the CA1 area of hippocampal slices. Activation of adenosine A3 receptors by (1-[2-chloro-6-[[(3-iodophenyl)methyl]amino]-9H-purin-p-yl]-1-deoxy-N-methyl-beta-D-ribofuranuronamide (Cl-IBMECA) (100 nM) increased the magnitude of theta-burst induced LTP (from 1.2+/-0.6% in the control solution to 25.5+/-0.8% in the presence of Cl-IBMECA) and attenuated LTD (from 30.0+/-5.5% decrease in the control solution to 13.6+/-6.6% decrease in the presence of Cl-IBMECA). The selective adenosine A3 receptor antagonist, MRS 1191 (5-10 microM), prevented the effects of Cl-IBMECA. These findings indicate a functional role for adenosine A3 receptors in the modulation of synaptic plasticity.

Adenosine↗
PubMed2001

Aluminum promotes neuronal plasticity events in a mouse neuroblastoma cell line.

The effects of aluminum(III) on microtubular meshwork have been investigated using cultured murine neuroblastoma cells grown in a medium containing aluminum lactate at defined metal concentrations (10-20 microM). A role of aluminum(III) in promoting neuronal plasticity events is suggested. These events including sprouting and neurite outgrowth are associated with an increased tyrosine-tubulin (Tyr-Tub) expression, which can be due to the enhanced needs of recently formed, highly dynamic microtubules typical of neuronal plasticity. After 48 and 72 h aluminum exposure, an upregulation of Tyr-Tub expression is detected and this is concentration-dependent. A high amount of Tyr-Tub is observed also in non-treated cells, although later than in aluminum-exposed cells. Thus, it is possible that aluminum(III) accelerates neuronal plasticity events, for which Tyr-Tub is confirmed to be a useful marker.

Aluminum↗
PubMed2002

Suppression of temporary deafferentation-induced plasticity in the primary somatosensory cortex of rats by GABA antagonist.

Single neurons were simultaneously recorded in the primary somatosensory (SI) cortex of rats to characterize the effects of applied bicuculline on the temporary deafferentation (TD)-induced plasticity. In the absence of TD, bicuculline application caused TD-like plasticity such as the expansion of receptive field (RF) and facilitation of sensory transmission in RF boundary cell. It also induced the originally unresponsive neurons to be responsive to the peripheral stimulation. In RF center neurons, TD-induced suppression of sensory transmission was not changed by bicuculline. However, TD-induced facilitation of sensory transmission to the RF boundary neuron was not observed in the presence of bicuculline. These results provide clear evidence that TD-induced plasticity in the SI cortex is mediated by the reversible suppression of lateral inhibition by GABAergic neurons.

Animals↗
PubMed1998

Plasticity of tyrosine hydroxylase gene expression within BALB/C and C57Black/6 mouse locus coeruleus.

The plasticity of tyrosine hydroxylase (TH) phenotype in the locus coeruleus (LC) of two pure inbred strains of mice, Balb/C (C) and C57Black/6 (B6), was investigated at the molecular level by radioactive in situ hybridization. The results demonstrated that in basal conditions, C mouse LC contains less TH-mRNA-expressing cells than B6. After RU 24722-treatment, which induces long lasting TH gene expression in the LC, we previously reported an increase in TH-expressing cell number in C mouse LC only, equalizing TH phenotype between the two strains. Here, we demonstrate that strain specific plasticity of TH phenotype detected in spatially organized cells is associated with the regulation of TH-mRNA expression above a detectable level. These results suggest that interstrain differences and pharmacologically-induced phenotypic plasticity in TH phenotype may occur at the transcriptional level.

Animals↗

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