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Results for “Neuronal Plasticity”

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At least 937 records · Page 52Linked to original sources
PubMed2001

AMPA receptors: potential implications in development and disease.

Alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptors are one type of ionotropic glutamate receptor involved in rapid excitatory synaptic transmission. AMPA receptors have been increasingly implicated in long-term potentiation, and recent evidence suggests that they may play a role in disorders affecting the nervous system. The finding that early in postnatal development AMPA receptors are not expressed has lately been the focus of much attention. Resolving the factors involved in AMPA receptor expression suggests that their induction is a developmentally regulated process with the possibility that alterations in receptor expression may be correlated with pathology in neurological disorders. This paper provides an overview of factors involved in AMPA receptor induction as well as of their role in plasticity and neuronal pathologies.

Aging↗
PubMed1989

The role of Ca2+ channels of the L-type in neurotransmitter plasticity of cultured sympathetic neurons.

We have studied the effects of Ca2+ antagonists and agonists on the development of choline acetyltransferase (ChAT), tyrosine hydroxylase (TOH) and acetylcholinesterase (AChE) in cultures of rat sympathetic neurons maintained for 6-9 days in low K+ (5 mM) or high K+ (35 mM) medium. Previous experiments have shown that high K+ medium increases TOH activity and TOH-mRNA level up to 3.5-fold and depresses the development of AChE, in particular of its asymmetric A12 form. Moreover, high K+ medium inhibits ChAT induction by 90% in muscle-conditioned medium (Raynaud et al., Dev. Biol., 119 (1987) 305-312; 121 (1987) 548-558). None of the Ca2+ antagonists tested affected the development of ChAT, TOH or AChE in low K+ medium. In high K+ medium, nitrendipine (3 microM) or fluspirilene (1 microM) fully restored ChAT induction by conditioned medium to the level observed in low K+ medium. Other drugs (1 microM) gave partial reversion: flunarizine greater than (+)-PN 200-110 greater than (-)-D-888 greater than cinnarizine = lidoflazine. On the other hand, ChAT induction was not restored by a calmodulin inhibitor, calmidazolium (1 microM). Fluspirilene, PN 200-110, and nitrendipine also totally abolished TOH induction by high K+ medium; fluspirilene (1 microM) suppressed the inhibitory effect of high K+ medium on AChE development and restored the development of A12 AChE. Conditioned medium also depresses AChE and blocks the development of A12 AChE (Swerts et al., Dev. Biol., 103 (1984) 230-234), but these effects were insensitive to fluspirilene. The Ca2+ agonist Bay K 8644 (1 microM) potentiated the effects of elevated K+ on both ChAT and TOH. The data suggest that the effects of long-term depolarization on ChAT, TOH and AChE are mediated by Ca2+ entry specifically through voltage-sensitive channels of the L-type. Our results on cultured sympathetic neurons raise the possibility that Ca2+ antagonists, which are widely used clinically, may affect the expression of neurotransmitter phenotypic traits in vivo and interfere with trans-synaptic induction of enzymes.

Acetylcholinesterase↗
PubMed2004

Enhancement of synaptic plasticity through chronically reduced Ca2+ flux during uncorrelated activity.

The plasticity of synapses within neural circuits is regulated by activity, but the underlying mechanisms remain elusive. Using the dye FM1-43 to directly image presynaptic function, we found that large numbers of presynaptic terminals in hippocampal cultures have a low release probability. While these terminals were not readily modifiable, a transient but not permanent long-term reduction of network activity or Ca2+ influx could increase their modifiability. This modulation of plasticity was mediated by Ca2+ flux through NMDA and voltage-gated calcium channels and was lost within 48 hr. A more permanent enhancement of synaptic plasticity was achieved by selectively reducing the Ca2+ flux associated with uncorrelated activity via adjustment of the voltage-dependent Mg2+ block of the NMDAR. Upregulation of NR2B-containing NMDARs induced by this treatment is an important but not sole contributor to the enhancement of plasticity. Thus, quantity and quality of activity have differential effects on the intrinsic plasticity of neurons.

Animals↗
PubMed2003

Protein kinase C and ERK involvement in dendritic spine plasticity in cultured rodent hippocampal neurons.

The roles of protein kinase C and the MAP-kinase extracellular receptor kinase in structural changes associated with long-term potentiation of network activity were examined in cultured hippocampal neurons. A brief exposure to a conditioning medium that favours activation of the N-methyl-d-aspartate receptor caused a rapid and specific increase in staining of neurons for the phosphorylated form of extracellular receptor kinase as well as of cyclic AMP response element binding protein. Exposure of the cultures to the conditioning medium was followed by a protein synthesis-dependent formation of novel dendritic spines. An extracellular receptor kinase antagonist PD98059 blocked the phosphorylated form of extracellular receptor kinase response and the formation of novel spines. A selective protein kinase C agonist, phorbol 12-myristate 13-acetate, caused activation of extracellular receptor kinase and formation of novel spines. The protein kinase C antagonist GF109203x blocked the phosphorylated form of extracellular receptor kinase response and the subsequent spine formation by phorbol 12-myristate 13-acetate. Both the conditioning medium and phorbol 12-myristate 13-acetate caused a delayed increase in mean amplitude of miniature excitatory postsynaptic currents recorded in the hippocampal neurons. These results indicate that activation of extracellular receptor kinase mediates the effect of a conditioning protocol on the formation of dendritic spines. The formation of novel spines was associated with long-term increase in network activity and functional synaptic connectivity among the cultured neurons.

Activating Transcription Factor 1↗
PubMed2004

A role for MHC class I molecules in synaptic plasticity and regeneration of neurons after axotomy.

Recently, MHC class I molecules have been shown to be important for the retraction of synaptic connections that normally occurs during development [Huh, G.S., Boulanger, L. M., Du, H., Riquelme, P. A., Brotz, T. M. & Shatz, C. J. (2000) Science 290, 2155-2158]. In the adult CNS, a classical response of neurons to axon lesion is the detachment of synapses from the cell body and dendrites. We have investigated whether MHC I molecules are involved also in this type of synaptic detachment by studying the synaptic input to sciatic motoneurons at 1 week after peripheral nerve transection in beta2-microglobulin or transporter associated with antigen processing 1-null mutant mice, in which cell surface MHC I expression is impaired. Surprisingly, lesioned motoneurons in mutant mice showed more extensive synaptic detachments than those in wild-type animals. This surplus removal of synapses was entirely directed toward inhibitory synapses assembled in clusters. In parallel, a significantly smaller population of motoneurons reinnervated the distal stump of the transected sciatic nerve in mutants. MHC I molecules, which traditionally have been linked with immunological mechanisms, are thus crucial for a selective maintenance of synapses during the synaptic removal process in neurons after lesion, and the lack of MHC I expression may impede the ability of neurons to regenerate axons.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

Specific coupling of NMDA receptor activation to nitric oxide neurotoxicity by PSD-95 protein.

The efficiency with which N-methyl-D-aspartate receptors (NMDARs) trigger intracellular signaling pathways governs neuronal plasticity, development, senescence, and disease. In cultured cortical neurons, suppressing the expression of the NMDAR scaffolding protein PSD-95 (postsynaptic density-95) selectively attenuated excitotoxicity triggered via NMDARs, but not by other glutamate or calcium ion (Ca2+) channels. NMDAR function was unaffected, because receptor expression, NMDA currents, and 45Ca2+ loading were unchanged. Suppressing PSD-95 blocked Ca2+-activated nitric oxide production by NMDARs selectively, without affecting neuronal nitric oxide synthase expression or function. Thus, PSD-95 is required for efficient coupling of NMDAR activity to nitric oxide toxicity, and imparts specificity to excitotoxic Ca2+ signaling.

Animals↗
PubMed2001

Distribution of map2 in hippocampus and cerebellum of young and old rats by quantitative immunohistochemistry.

The microtubule-associated protein MAP2 is a cytoskeletal protein that plays a regulatory role in neuronal plasticity and in maintaining the morphology of differentiated neurons. MAP2 distribution was assessed in hippocampus and cerebellum of young and old rats by quantitative immunohistochemistry. In old vs young rats, densitometric analysis showed a significant decrease of MAP2 immunoreactivity in the hippocampus CA1 field (-93%), whereas no difference was found in cerebellar MAP2 distribution. These preliminary data suggest that in areas of the brain involved in memory acquisition and consolidation, MAP2-dependent neuroplasticity and structural integrity are significantly decreased in aging.

Aging↗
PubMedDate not supplied

[The morphochemical characteristics and plastic restructurings of the hippocampal neurons after rhythmic stimulation of an extremity in old rabbits].

The rhythmic activity of CA1 hippocampal neurons was studied after the rhythmic (1-2 Hz) electrocutaneous forelimb stimulation (10-20 min) of 6-84-months-old rabbits. The spectral analysis of neuronal activity revealed the age-dependent decrease in ability to reproduce the rhythm of stimulation. The cytochemical data showed that the protein synthesis in the neurons under study also declined with age.

Aging↗
PubMed1988

Distribution and phosphorylation of the growth-associated protein GAP-43 in regenerating sympathetic neurons in culture.

Sympathetic neurons regenerating in culture were studied in order to gain further insight into the intracellular distribution and phosphorylation of GAP-43, a protein that has been suggested to have a role in axonal outgrowth and neuronal plasticity (Willard et al., 1987). Superior cervical ganglion neurons from embryonic rats were highly reactive with a polyclonal antibody against the growth-associated protein GAP-43 soon after they were placed in culture on a laminin substrate. As these neurons extended neurites, the distribution of GAP-43 reactivity changed. The cell body became progressively less reactive, whereas the growth cone at the tip of the growing neurite reacted strongly. The pattern of immunofluorescence was punctate both in the growth cone and the adjacent neurite, but appeared more diffusely distributed in the cell body. The antibody reacted only with cells that had been subjected to treatment that permeabilized the plasma membrane. When antibody was supplied in the medium of growing neurons, it neither bound to the cells nor altered normal neurite initiation or elongation. Of the different types of cells in these cultures, the antibody reacted only with neurons; it did not react with Schwann cells or fibroblasts. The stimulation of protein kinase C in these cultures resulted in a 7-fold stimulation of the phosphorylation of a protein of similar electrophoretic mobility to GAP-43. These observations demonstrate that GAP-43 is neuron-specific, is present throughout the neuron but at higher levels in the growth cone, and is a major substrate of protein kinase C. The high concentration of GAP-43 in the growth cones may necessitate its increased synthesis in neurons with elongating axons. Its location and phosphorylation by kinase C suggest that it could perform a function in the growth cone that is modulated by extracellular signals, such as those used in pathfinding or in the control of axonal elongation.

Animals↗
PubMed1992

Neuronal specificity and plasticity in the autonomic nervous system.

The autonomic nervous system is divided into the sympathetic, parasympathetic and enteric subdivisions. The present review is focussed upon the highly specialized reflex organization and neurochemistry of sympathetic parasympathetic neurons. The currently available informations allow to conclude that autonomic control of each peripheral target tissue is specifically regulated under normal conditions but nevertheless able to respond to altered conditions by changes in neural activity and mediator expression.

Animals↗