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At least 487 records · Page 27Linked to original sources
PubMed2002

Dynamically interacting processes underlie synaptic plasticity in a feedback pathway.

Descending feedback is a common feature of sensory systems. Characterizing synaptic plasticity in feedback inputs is essential for delineating the role of feedback in sensory processing. In this study, we demonstrate that multiple interacting processes underlie the dynamics of synaptic potentiation in one such sensory feedback pathway. We use field recording and modeling to investigate the interaction between the transient high-magnitude potentiation (200-300%) elicited during tetanic stimulation of the feedback pathway and the lower magnitude posttetanic potentiation (PTP; ~30%) that slowly decays on cessation of the tetanus. The amplitude of the observed transient potentiation is graded with stimulus frequency. In contrast, the induction of PTP has a stimulus frequency threshold between 1 and 5 Hz, and its amplitude is independent of stimulus frequency. We suggest that the threshold for PTP induction may be linked to a minimum level of sustained potentiation (MSP) during repetitive trains of stimuli. We have developed a novel model that describes the interaction between the transient plasticity observed during train stimulation and the generation of PTP. The model combines a multiplicative, facilitation-depression-type (FD) model that describes the transient plasticity, with an enzymatic network that describes the dynamics of PTP. The model links transient plasticity to PTP through an input term that reflects MSP. The stratum fibrosum-pyramidal cell (StF-PC) synapse investigated in this study is the terminus of a feedback pathway to the electrosensory lateral line lobe (ELL) of a weakly electric gymnotiform fish. Dynamic plasticity at the StF-PC synapse may contribute to the putative role of this feedback pathway as a sensory searchlight.

Action Potentials↗
PubMed2005

ATP hydrolysis is required for the rapid regulation of AMPA receptors during basal synaptic transmission and long-term synaptic plasticity.

ATP hydrolysis is critical for many cellular processes; however, the acute requirement for ATP hydrolysis in synaptic transmission and plasticity in neurons is unknown. Here we studied the effects of postsynaptically applying the non-hydrolyzable ATP analogue adenosine 5'-[beta,gamma-methylene]triphosphate (AMP-PCP) into hippocampal CA1 pyramidal cells in hippocampal slices. The effects of this manipulation were investigated on basal transmission and on two forms of long-term synaptic plasticity, long-term potentiation (LTP) and long-term depression (LTD). AMP-PCP caused an increase in basal AMPA receptor (AMPAR)-mediated transmission, which occurred rapidly within minutes of infusing the drug. This effect was selective for AMPARs, since pharmacologically isolated NMDAR-mediated synaptic currents did not exhibit this run up. In two-pathway experiments infusion of AMP-PCP blocked the induction of both LTD and LTP. These findings show an acute and selective role for ATP hydrolysis in regulating AMPAR function both during basal transmission and long-term synaptic plasticity. Recent evidence indicates that AMPARs are selectively and acutely regulated by the ATPase N-ethylmaleimide-sensitive factor (NSF), which forms part of a multi-protein complex with AMPARs. Our data are consistent with the idea that such a mechanism that can acutely bi-directionally regulate AMPAR function at synapses and requires ATP hydrolysis is necessary for rapid activity-dependent changes in synaptic strength.

Adenosine Triphosphate↗
PubMed1992

K(+)-channel blockers restore synaptic plasticity in the neuromuscular junction of dunce, a Drosophila learning and memory mutant.

The effects of K(+)-channel blockers on synaptic transmission in dunce (dnc), a Drosophila learning and memory mutant, were investigated. Larvae dnc mutants lack facilitation and post-tetanic potentiation (PTP) at their motor end-plates; dnc mutants are also deficient in a form of phosphodiesterase, and exhibit abnormally high levels of cyclic adenosine 3',5'-monophosphate (cAMP). A two-microelectrode voltage-clamp was used to record end-plate currents and spontaneous end-plate currents from longitudinal ventrolateral third-instar larval muscle. The K(+)-channel blockers 3,4-diaminopyridine (3,4-DAP) and tetraethylammonium (TEA), at micromolar concentrations, caused a reversible decrease in end-plate current amplitudes both in wild-type and mutant end-plates. In the presence of blockers, a period of high-frequency stimulation (tetanus) of the nerve gave way to a transient increase in the end-plate currents of dnc mutants resembling facilitation and PTP in normal end-plates; 3,4-DAP and TEA also restored facilitation and PTP in normal end-plates after incubation with a non-hydrolysable analogue of cAMP (8Br-cAMP). It is suggested that a specific K+ conductance might be relevant to the lack of synaptic plasticity at the dnc neuromuscular synapses.

4-Aminopyridine↗
PubMed2002

Dose-dependent effects of prenatal ethanol exposure on synaptic plasticity and learning in mature offspring.

BACKGROUND: We have observed profound deficits in hippocampal synaptic plasticity and one-trial learning in offspring whose mothers drank moderate quantities of ethanol during pregnancy. In the present study, we examined the question of whether lower maternal blood ethanol concentrations (BECs) could produce functional deficits in offspring. METHODS: Rat dams consumed either a 2%, 3%, or 5% ethanol liquid diet throughout gestation. Three other groups of dams were pair-fed a 0% ethanol liquid diet, and a seventh group consumed lab chow ad libitum. Adult offspring from each diet group were assigned either to studies of evoked [3H]-D-aspartate (D-ASP) release from hippocampal slices or spatial learning studies using the Morris Water Task. RESULTS: Consumption of the 2%, 3%, and 5% ethanol liquid diets produced mean peak maternal BECs of 7, 30 and 83 mg/dL, respectively. Consumption of these ethanol diets had no effect on offspring birthweight, litter size or neonatal mortality. Likewise, evoked D-ASP release from hippocampal slices and performance on a standard version of the Morris Water Task were not affected by prenatal ethanol exposure. By contrast, activity-dependent potentiation of evoked D-ASP release from slices and one-trial learning on a "moving platform" version of the Morris Water Task were markedly reduced in offspring whose mothers consumed the 5% ethanol liquid diet. Intermediate deficits in these two parameters were observed in offspring from the 3% ethanol diet group, whereas offspring from the 2% ethanol diet group were not statistically different than controls. CONCLUSIONS: We conclude that the threshold for eliciting subtle, yet significant learning deficits in offspring prenatally exposed to ethanol is less than 30 mg/dL. This BEC is roughly equivalent to drinking 1 to 1.5 ounces of ethanol per day.

Age Factors↗
PubMed1993

Estrogen induces synaptic plasticity in adult primate neurons.

The number of axosomatic synapses, the length of the synaptic plates and the perimeter of the post synaptic neuronal perikarya were assessed on thin sections from the infundibular hypothalamic nucleus and from the ventrobasal thalamus of 3 adult ovariectomized African green monkeys that were treated with estradiol valerate and of 3 control animals that were injected with vehicle. Estradiol valerate treatment resulted in a 61% [corrected] decrease in the number of axosomatic synapses in the infundibular hypothalamic nucleus. The length of the synaptic plates and the perimeter of the postsynaptic cells were not affected by the hormonal treatment. The decrease in the number of axosomatic synaptic inputs in the infundibular hypothalamic nucleus was accompanied by a significant increase in the glial ensheathing of neuronal somas. No effect of the hormonal treatment was detected in the ventrobasal thalamus. The results indicate that estrogen may induce glial and synaptic plasticity in the hypothalamus of adult primates.

Animals↗
PubMed1999

Synaptic plasticity and learning and memory: LTP and beyond.

Long-term potentiation (LTP) of synaptic activity is by far the most popular and widely researched model of synaptic plastic changes that might occur during learning. Numerous recent reports, however, have not found a correlation between the inducibility of LTP in the hippocampus and the ability of animals to learn hippocampus-dependent tasks. For example, some experiments with gene deletion (knockout) mice strains have shown that in some strains LTP is not inducible in the dentate gyrus, in area CA3, or CA1, but the animals are still able to learn spatial tasks. This apparent mismatch has rejuvenated the discussion concerning whether LTP is a good model for mechanisms that underlie memory formation in the nervous system. This review analyzes the conditions under which LTP is induced or learning takes place and suggests reasons for the mismatches that can occur and what we can learn from them. High-frequency stimulation protocols and in vitro assays cannot be seen to resemble natural firing patterns or conditions found in the brain. More physiological experimental conditions, especially in vivo recording in awake animals, could lead the way to the development of improved models of learning mechanisms that better correlate with learning abilities of animals.

Animals↗
PubMed2005

Activity-dependent synaptic plasticity in the central nucleus of the amygdala.

Much evidence indicates that fear conditioning involves potentiation of some thalamic inputs to the lateral amygdala (LA). In turn, the LA would excite more neurons in the central nucleus (CE), leading to the generation of fear responses via their brainstem and hypothalamic projections. However, the posterior thalamus not only projects to LA but also to the medial sector of CE (CEm), suggesting that CEm might also be a site of plasticity. To test whether CEm also exhibits activity-dependent synaptic plasticity, we performed whole-cell recordings of CEm neurons in amygdala slices and stimulated thalamic axons coursing through the internal capsule and, as a control, the basolateral (BL) nucleus. High-frequency stimulation of thalamic inputs led to a long-lasting potentiation of thalamic responses, whereas BL-evoked responses remained unchanged. This thalamic long-term potentiation (LTP) developed even when slices were prepared with a cut severing the connections between the LA and CEm but was greatly reduced when an NMDA receptor antagonist was added to the perfusate shortly before and during LTP induction. Yet, intracellular dialysis with the NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate did not prevent induction of the thalamic LTP, suggesting that presynaptic NMDA receptors are required for its induction. Consistent with this, the thalamic LTP also developed when the cells were dialyzed with a calcium chelator or kept hyperpolarized during induction. Finally, this thalamic LTP was associated with reduced amounts of paired-pulse facilitation, suggesting that it is expressed presynaptically. These results are consistent with the idea that the CEm plays an active role in fear conditioning.

2-Amino-5-phosphonovalerate↗
PubMed2004

[Vital investigation of the genome activity and neuronal synaptic plasticity in snail in the course of learning].

Vital investigation of genome activity and its role in mechanisms of long-term synaptic plasticity formation were studied in LP11 neuron (command neurone of defence behaviour) during sensitisation (simple form of learning) in semi-intact preparation of snail Helix lucorum. Genome activity was investigate by means of specific fluorescent dye SYTO 16 and image analysis system. It was found that application of sensitizing stimulation (10% quinine solution) onto the snail head initiate two-phase changes in neural responses evoked by tactile or chemical stimulation. Depression of neural responses was obtained during short-term phase (during 1 hour after sensitization) and facilitation of neural responses--during long-term phases (over 1 hour). At the same time (15-20 min after learning), a significant increase in SYTO 16 fluorescent level was found in nucleus site LP11 neurone. Initial SYTO 16 fluorescence level was registered in 4-5 hours after sensitization. If the sensitization was produced during actinomycin D application (inhibitor of RNA synthesis, 20 microM) then facilitation of neural responses evoked by sensory stimulation were suppressed during long-term phase of sensitization and was the same as in control sensitized snails during short-term phase of learning. Increase in SYTO 16 fluorescence level in nucleus region site of LP11 neurone was completely prevented in sensitization during actinomycin D application. If actinomycin D was applied 30 min after sensitization (1 hour after first sensitizing stimulation) then synaptic facilitation and fluorescent dynamics was the same as in control sensitized snails. Our experimental data showed that nociceptive sensitization development was followed by quick (15-20 min) DNA activation and long-term synaptic facilitation (1 hour after sensitization), while induction of the processes was suppressed by inhibitor of RNA synthesis during short time interval (during 1 hour of learning).

Animals↗
PubMed2001

Proteolysis of glutamate receptor-interacting protein by calpain in rat brain: implications for synaptic plasticity.

Activation of the calcium-dependent protease calpain has been proposed to be a key step in synaptic plasticity in the hippocampus. However, the exact pathway through which calpain mediates or modulates changes in synaptic function remains to be clarified. Here we report that glutamate receptor-interacting protein (GRIP) is a substrate of calpain, as calpain-mediated GRIP degradation was demonstrated using three different approaches: (i) purified calpain I digestion of synaptic membranes, (ii) calcium treatment of frozen-thawed brain sections, and (iii) NMDA-stimulated organotypic hippocampal slice cultures. More importantly, calpain activation resulted in the disruption of GRIP binding to the GluR2 subunit of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors. Because GRIP has been proposed to function as an AMPA receptor-targeting and synaptic-stabilizing protein, as well as a synaptic-organizing molecule, calpain-mediated degradation of GRIP and disruption of AMPA receptor anchoring are likely to play important roles in the structural and functional reorganization accompanying synaptic modifications in long-term potentiation and long-term depression.

Animals↗
PubMed1993

Electroconvulsive stimulation and synaptic plasticity in the rat.

The effects of repeated, spaced, electroconvulsive stimulation (ECS) on rodent hippocampal synaptic plasticity was investigated in vivo. Long-term potentiation (LTP) was induced in intact rats using high-frequency perforant path stimulation, and measured by recording extracellular excitatory field potentials and population spikes evoked in the dentate gyrus by low-frequency stimulation before and after LTP induction. LTP induction appeared to be inhibited in animals which had received ECS. However, inspection and analysis of absolute excitatory postsynaptic potential and population spike size before LTP induction in ECS treated animals suggested that LTP may have already been induced as a consequence of seizure activity, reducing the degree to which further potentiation could be elicited experimentally.

Analysis of Variance↗
PubMed2004

A role for monomeric G-proteins in synaptic plasticity in the rat dentate gyrus in vitro.

Recent studies have implicated Ras signalling in synaptic plasticity. In this study we have investigated a role for the low molecular weight G proteins Ras, Rap, Ra1 and Rac in long-term potentiation and depression using Clostridium Sordelli Lethal Toxin-82 (LT-82), which inactivates Ras, Rap, Ra1 and Rac, and manumycin A, a Ras inhibitor. Perfusion of hippocampal slices with LT-82 (200 ng/ml) attenuated LTP (83+/-10%, n=5, P<0.01, compared with controls of 160+/-11% at 60 min post HFS, n=5). LT-82 had no effect on LTD (63+/-1% at 100 ng/ml, n=5 and 66+/-1% at 200 ng/ml, n=4, compared to controls of 56+/-6%, n=6). Manumycin A (2 microM) had no effect on LTP (162+/-2%, n=5, compared to controls of 167+/-13%, n=5), but significantly attenuated LTD (88+/-6%, n=5, P<0.01, compared to controls of 63+/-9%, n=7). LT-82 (200 ng/ml) significantly increased the amplitude of the isolated NMDA-EPSP at 60 min post-drug application (240+/-40%, n=5, P<0.01, compared with controls of 100+/-4%, n=5). However, manumycin A, had no significant effect on NMDAR-EPSP amplitude (92+/-2%, n=5, compared with controls). These results demonstrate an important role for Ras in LTD and a role for Rap, Ra1 and Rac in LTP.

Animals↗
PubMed2003

Synaptic plasticity in the amygdala: comparisons with hippocampus.

Long-term potentiation (LTP) is a widely studied form of synaptic plasticity, and a considerable amount of evidence indicates that it could be involved in learning and memory. Intensive investigation of this phenomenon in the hippocampus has yielded tremendous insight into the workings of synapses in the mammalian central nervous system, but important questions remain to be answered. The most important of these are: (1) whether LTP is the basis of learning and memory, and (2) how similar are the induction, maintenance, and expression mechanisms in the rest of the brain to those in the hippocampus. Because the most important strategy for linking LTP to learning involves disrupting the mechanisms of LTP and examining the consequences on behavior, it is likely that the first question cannot be answered until the second has been addressed. Recent evidence indicates that although the general processes have much in common, significant differences exist among forebrain structures, including the hippocampus, basolateral amygdala, and ventral striatum. It is clear that the roles of receptors and calcium channels, kinases, and transcription factors vary within these structures, reflecting the different functions of these brain regions.

Amygdala↗
PubMed2001

Dopamine-dependent synaptic plasticity in striatum during in vivo development.

The neurotransmitters dopamine (DA) and glutamate in the striatum play key roles in movement and cognition, and they are implicated in disorders of the basal ganglia such as Parkinson's disease. Excitatory synapses in striatum undergo a form of developmental plasticity characterized by a decrease in glutamate release probability. Here we demonstrate that this form of synaptic plasticity is DA and DA D2 receptor dependent. Analysis of spontaneous synaptic responses indicates that a presynaptic mechanism involving inhibition of neurotransmitter release underlies the developmental plasticity. We suggest that a major role of DA in the striatum is to initiate mechanisms that regulate the efficacy of excitatory striatal synapses, producing a decrease in glutamate release.

Animals↗
PubMed1997

Control of gonadotropin feedback: the possible role of estrogen-induced hypothalamic synaptic plasticity.

The preovulatory gonadotropin surge is a critical event in reproduction. Although many explanations have been given for the inhibition--disinhibition cycle referred to as positive feedback, none are completely satisfactory. Recent evidence indicates that the preovulatory surge of gonadotropin is induced, in part, by the disengagement of inhibitory synaptic connections in the hypothalamic arcuate nucleus. This disinhibition of gonadotropin-releasing hormone secretion results in a massive release by the estrogen-sensitized pituitary gonadotrophs. Investigations are presently under way to determine whether other areas of the hypothalamus are involved in this estrogen-induced synaptic plasticity.

Animals↗
PubMed1994

Estrous cycle-associated axosomatic synaptic plasticity upon estrogen receptive neurons in the rat preoptic area.

This study examined the hypothesis that synaptic relationships change on a daily basis in the anterior preoptic area of the intact, cycling female rat. Specifically, the anteroventral periventricular nucleus (AVPv) was chosen for analysis due to its abundant estrogen- and progesterone-receptive neurons and its critical role in the control of gonadotropin secretion. Ultrastructural analysis revealed that in the 24 h between proestrus and estrus, there was a 39% increase in axosomatic synapses upon AVPv neurons. In the subsequent 24 h to metestrus, the number of synapses decreased by 22%. Additional data showed that ovariectomy resulted in more axosomatic synapses in the AVPv relative to proestrus (46%) and metestrus (35%). Another component of the study investigated synaptic relationships on estrogen receptor-immunoreactive (ER-ir) and non-ER-ir neurons across the estrous cycle. ER-ir neurons received significantly more synaptic input at proestrus and estrus than did non-ER-ir neurons. At metestrus and following ovariectomy, no significant differences were present. The present study indicates that estrous cycle-associated synaptic plasticity occurs in the AVPv and lends further support to the critical role of this nucleus in regulation of gonadotropin secretion. Moreover, it provides the first evidence that ER- and non-ER-ir neurons are differentially innervated.

Animals↗
PubMed2001

Stores not just for storage. intracellular calcium release and synaptic plasticity.

Activation of most excitatory synapses of central neurons produces calcium release signals from intracellular stores. Synaptically evoked calcium release from stores is frequently triggered by the binding of glutamate to metabotropic receptors and the subsequent activation of IP(3) receptors in spines and dendrites. There is increasing evidence for the presence of local calcium signals caused by calcium-induced calcium release (CICR) through activation of ryanodine or IP(3) receptors. Recent work on mutant mice indicates that store signaling determines activity-dependent synaptic plasticity.

Animals↗
PubMed2006

[Cholesterol is an important molecule in the processes of the synaptic plasticity and degeneration of neurons].

The importance of homeostasis of neural tissue to neuron functioning, the synaptic plasticity of the hippocampus, and laboratory animals' behavior was demonstrated by the authors earlier. A range of experimental data evidences that cholinergic neurotransmission, ionotropic and metabotropic receptors, excessive tau phosphorylation, alterations in amyloid-beta biochemistry, oxidative reactions, and other features of neurodegenerative processes depend on the precise regulation of cerebral cholesterol metabolism. Such results suggest that disturbances in cholesterol homeostasis are the common primary cause of the sporadic and familial forms of Alzheimer's disease, Down syndrome, Niemann-Pick disease type C, and explain the similarity of neurodegenerative signs in different degenerative diseases of the nervous system. The present work was introduced at an annual conference of American Society for Neuroscience, and is available as a scientific report at www.neurobiologyoflipids.org/content/3/7/.

Alzheimer Disease↗