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Results for “synaptic plasticity”

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At least 1,315 records · Page 73Linked to original sources
PubMed1979

A study of synaptic plasticity in hippocampal slices.

Long-lasting potentiation in the hippocampal pathways is used at present as a model for long-term plasticity in the nervous system. In this study post-tetanic potentiation was investigated in the dentate gyrus-area CA3 pathway by extra- and intracellular recordings from transverse slices of the mouse hippocampus. Tetanization of the dentate gyrus led to a reduction in the latency of action potentials (APs) and EPSPs recorded from area CA3, to an increase in the amplitude of EPSPs and in the steepness of their ascending slope, and to an augmented probability of APs. These changes persisted for a period of several seconds to 30 min after tetanization. Of special interest were records from cells responding with EPSPs: of a short latency (2-3 ms) which was not changed by an increase in the frequency and strength of stimulation. We assume that such EPSPs are monosynaptic. Our results suggest that monosynaptic EPSPs can undergo long-lasting (up to 30 min) post-tetanic potentiation.

Action Potentials↗
PubMed1980

Electron microscopic and morphometric studies on synaptic plasticity in the hippocampus of the rat following conditioning.

1. In 40 three months old Wistar rats (16 trained animals, 14 active controls, 10 passive controls) the influence of learning (brightness discrimination) on the number of electronmicroscopically detectable synapses per area neuropil was studied in the stratum radiatum (CA 1) of the hippocampus. 2. 70 minutes after completion of training, the mean number of synapses has significantly increased as compared to active controls (trained animals 14.26 +/- 2.95 synapses/25 micrometer2; active controls 10.23 +/- 2.80 synapses/25 micrometer2; p less than 0.001). 3. 24 hours after training this increase in trained animals still persisted (trained animals 14.15 +/- 2.60, active controls 11.39 +/- 2.87 synapses/25 micrometer2; p less tha 0.001). 4. 14 days after training, the number of synapses has decreased considerably, but was nevertheless significantly higher than in the active controls (trained animals 12.49 +/- 2.76, active controls 11.45 +/- 3.10; p less than 0.001). 5. The results are discussed with regard to their significance to the different stages of memory formation in the CNS.

Animals↗
PubMed1995

Enduring effects of chronic corticosterone treatment on spatial learning, synaptic plasticity, and hippocampal neuropathology in young and mid-aged rats.

Prolonged treatment with stress levels of corticosterone has been reported to produce changes in the hippocampus. In the experiments reported here, we examined for functional and morphological consequences of this treatment. First, young adult or mid-aged male Long-Evans rats were treated for either 1 or 3 months with corticosterone, at a dose sufficient to mimic the elevated hormone levels observed following exposure to mild stress. Two weeks following the termination of treatment, the animals were tested in the Morris water maze to assess spatial learning. No behavioral deficits were observed after 1 month of treatment. A 3 month treatment period also had no effect in young rats, but produced a learning impairment in the mid-aged rats. We then examined whether the effect of elevated corticosterone in mid-aged animals could be produced by a physiological stressor. Mid-aged rats were maintained for 6 months under conditions of low or high social stress. Six months of exposure to high social stress produced significant spatial learning impairments in the Morris water maze. These effects were absent in high social stress animals that had been previously adrenalectomized (with low-level corticosterone replacement), suggesting that elevated glucocorticoid levels mediate the effects of stress on spatial memory in older animals. In a final experiment, mid-aged rats were treated with corticosterone at levels that mimicked those naturally occurring at the diurnal peak (medium-B: 12-17 micrograms/dl) or in response to stress (high-B: 25-32 micrograms/dl). Only rats exposed to high levels of corticosterone demonstrated impaired performance in the Morris water maze.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1996

Presynaptic phosphoprotein B-50/GAP-43 in neuronal and synaptic plasticity.

B-50/GAP-43 is a growth-associated phosphoprotein enriched in growth cones and in the presynaptic terminal. The expression of the protein is restricted to the nervous system and is highest in the first week after birth. In adult brain, B-50 is enriched in areas with high plasticity. The regulation of expression of the B-50 gene occurs both at the transcriptional and post-transcriptional level by unknown mechanisms. The gene contains 2 regions displaying promoter activity, the most 3' of which (P2) is the active on in vivo. Expression of B-50 in non-neuronal cells results in filopodial extensions whereas antibodies or antisense oligo's to B-50 prevent neurite outgrowth. The protein is important for neuronal pathfinding. Several post-translational modifications have been described, ADP-ribosylation and palmitoylation in the membrane binding domain, phosphorylation by PKC, casein kinase II and phosphorylase kinase, and dephosphorylation by several phosphatases, among which is calcineurin. Interactions of B-50 have been described with calmodulin, PIP kinase, F-actin, and phospholipids. Recent studies indicate that the phosphorylation state and amount of calmodulin bound to B-50 regulate the rate of transmitter release. Induction of long-term potentiation by high frequency stimulation of hippocampal slices results in an increased state of B-50 phosphorylation. This will increase the amount of free calmodulin in the presynaptic terminal and increase the amount of transmitter released. Although B-50 is involved in seemingly unrelated forms of neuronal plasticity, neurite outgrowth and transmitter release, our unifying hypothesis is that the protein plays an (unknown) essential, modulatory role in membrane expansion.

Animals↗
PubMedDate not supplied

[The connection between ultrastructural synaptic plasticity and the number of ribosomes in the dendritic terminals studied in a cell model of conditioning in the rat neocortex].

The dependence was studied of the ultrastructural changes in postsynaptic densities of axodendritic synapses on the size of postsynaptic ribosomal aggregates. A positive correlation was established between the thickness of postsynaptic densities and the number of ribosomes. The role of dendritic mRNA is discussed and the possible mechanisms underlying rapid local protein synthesis in a modification of postsynaptic components which have been observed in case of combined application of two neurotransmitters to the neocortex of rats.

Animals↗
PubMedDate not supplied

Trophic factor-induced plasticity of synaptic connections between identified Lymnaea neurons.

Neurotrophic factors participate in both developmental and adult synaptic plasticity; however, the underlying mechanisms remain unknown. Using soma-soma synapses between the identified Lymnaea neurons, we demonstrate that the brain conditioned medium (CM)-derived trophic factors are required for the formation of excitatory but not the inhibitory synapse. Specifically, identified presynaptic [right pedal dorsal 1 (RPeD1) and visceral dorsal 4 (VD4)] and postsynaptic [visceral dorsal 2/3 (VD2/3) and left pedal dorsal 1 (LPeD1)] neurons were soma-soma paired either in the absence or presence of CM. We show that in defined medium (DM-does not contain extrinsic trophic factors), appropriate excitatory synapses failed to develop between RPeD1 and VD2/3. Instead, inappropriate inhibitory synapses formed between VD2/3 and RPeD1. Similarly, mutual inhibitory synapses developed between VD4 and LPeD1 in DM. These inhibitory synapses were termed novel because they do not exist in the intact brain. To test whether DM-induced, inappropriate inhibitory synapses could be corrected by the addition of CM, cells were first paired in DM for an initial period of 12 hr. DM was then replaced with CM, and simultaneous intracellular recordings were made from paired cells after 6-12 hr of CM substitution. Not only did CM induce the formation of appropriate excitatory synapses between both cell pairs, but it also reduced the incidence of inappropriate inhibitory synapse formation. The CM-induced plasticity of synaptic connections involved new protein synthesis and transcription and was mediated via receptor tyrosine kinases. Taken together, our data provide the first direct insight into the cellular mechanism underlying trophic factor-induced specificity and plasticity of synaptic connections between soma-soma paired Lymnaea neurons.

Animals↗
PubMed2006

Subplate neurons regulate maturation of cortical inhibition and outcome of ocular dominance plasticity.

Synaptic plasticity during critical periods of development requires intact inhibitory circuitry. We report that subplate neurons are needed both for maturation of inhibition and for the proper sign of ocular dominance (OD) plasticity. Removal of subplate neurons prevents the developmental upregulation of genes involved in mature, fast GABAergic transmission in cortical layer 4, including GABA receptor subunits and KCC2, and thus prevents the switch to a hyperpolarizing effect of GABA. To understand the implications of these changes, a realistic circuit model was formulated. Simulations predicted that without subplate neurons, monocular deprivation (MD) paradoxically favors LGN axons representing the deprived (less active) eye, exactly what was then observed experimentally. Simulations also account for published results showing that OD plasticity requires mature inhibition. Thus, subplate neurons regulate molecular machinery required to establish an adult balance of excitation and inhibition in layer 4, and thereby influence the outcome of OD plasticity.

Animals↗
PubMed2004

Synaptic vesicle pools and plasticity of synaptic transmission at the Drosophila synapse.

Our knowledge on the Drosophila neuromuscular synapse is rapidly expanding. Thus, this synapse offers an excellent model for studies of the molecular mechanism of synaptic transmission and synaptic plasticity. Two synaptic vesicle (SV) pools have been identified and characterized using a fluorescent styryl dye, FM1-43, to stain SVs. They are termed the exo/endo cycling pool (ECP), which corresponds to the readily releasable pool (RRP) defined electrophysiologically, and the reserve pool (RP). These two pools were identified first in a temperature-sensitive paralytic mutant, shibire, and subsequently confirmed in wild-type larvae. The ECP participates in synaptic transmission during low frequency firing of presynaptic nerves and locates in the periphery of presynaptic boutons in the vicinity of release sites, while SVs in the RP spread toward the center of boutons and are recruited only during tetanic stimulation. These two pools are separately replenished by endocytosis. Cyclic AMP facilitates recruitment of SVs from the RP to the ECP. Activation of presynaptic metabotropic glutamate receptors recruits SVs from the RP and enhances SV release by elevation of the cAMP level. Memory mutants that have defects in the cAMP/PKA cascade, dunce and rutabaga, exhibit reduced levels of recruitment of synaptic SVs from the RP to the ECP and have limited short-term synaptic plasticity. SV mobilization between the two pools could be a key step for changes in synaptic efficacy. Since a variety of mutants that have distinct defects in synaptic transmission are available for detailed studies of synaptic function, this direction of approach in Drosophila seems promising.

Animals↗