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Results for “synaptic plasticity”

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PubMed2004

The selective effect of a protein kinase C inhibitor on synaptic plasticity in defensive behavior command neurons during development of sensitization in the snail.

Studies of defensive behavior command neurons LP11 and RP11 in semi-intact common snail preparations addressed the effects of the protein kinase C antagonist polymyxin B on the effect of nociceptive sensitization. Neurons in control snails responded to application of nociceptive stimuli to the head with membrane depolarization, increases in excitability, and depression of neuron responses to sensory stimulation during the short-term stage, with marked facilitation of responses during the long-term stage of sensitization. Acquisition of sensitization in the presence of polymyxin B resulted in partial suppression of responses to nociceptive stimuli. Changes in command neuron membrane excitability in these conditions, as well as changes in responses to tactile stimulation of the foot and chemical stimulation of the head, were similar to those seen in neurons of sensitized control animals. The inhibitor also had no effect on short-term depression of neuron responses induced by tactile stimulation of the head. In addition, acquisition of sensitization during administration of polymyxin B led to complete suppression of the facilitation of responses to tactile stimulation of the snail's head during the long-term stage of sensitization. It is suggested that in sensitized common snails, protein kinase C is involved in controlling the mechanisms of nociception and is also involved in the mechanisms of selective induction of plasticity in the synaptic inputs of command neurons, which are activated by tactile stimulation of the animal's head.

Action Potentials↗
PubMed1998

Estrogen-mediated structural and functional synaptic plasticity in the female rat hippocampus.

Light and electron microscopic studies have shown that ovarian steroids regulate the density and number of excitatory synaptic inputs to hippocampal pyramidal cells in the adult female rat; elevated levels of estradiol are associated with a higher density of dendritic spine synapses on CA1 pyramidal cells. Electrophysiological analyses indicate that these hormone-induced synapses increase hippocampal excitability as well as the potential for synaptic plasticity. Importantly, correlation of dendritic spine density and sensitivity to synaptic input of individual CA1 pyramidal cells from estradiol-treated and control animals suggests that synapses induced by estradiol may be a specialized subpopulation that contains primarily the NMDA subtype of glutamate receptor. The apparent NMDA receptor specificity of these synapses may be key to understanding their functional significance. Currently, the behavioral consequences of additional spine synapses are unknown. Numerous studies have aimed at correlating hormone-induced changes in hippocampal connectivity with differences in hippocampus-dependent spatial learning ability in mazes, but the results of these efforts have been equivocal. Anatomical, electrophysiological, and behavioral studies of estradiol-mediated hippocampal plasticity are reviewed. In conclusion, it is suggested that standard behavioral tests of hippocampal function are not sufficient to reveal the behavioral consequences of hormone-induced hippocampal plasticity. Rather, understanding the behavioral consequences of estradiol and progesterone effects on hippocampal connectivity may require analysis of the hippocampus' cognitive and spatial information processing functions in relation to alternative biologically relevant behaviors. A (nonexclusive) proposal that hormone-induced hippocampal plasticity may facilitate appropriate prepartum/maternal behavior is discussed.

Animals↗
PubMed1999

Fast burst firing and short-term synaptic plasticity: a model of neocortical chattering neurons.

We present an ionic conductance model of chattering neurons in the neocortex, which fire fast rhythmic bursts in the gamma frequency range (approximately 40 Hz) in response to stimulation [Gray C. M. and McCormick D. A. (1996) Science 274, 109-113]. The bursting mechanism involves a "ping-pong" interplay between soma-to-dendrite back propagation of action potentials and an afterdepolarization generated by a persistent dendritic Na+ current and a somatic Na+ window current. The oscillation period is primarily determined by a slowly inactivating K+ channel and passive membrane properties. The model behavior is compared quantitatively with the experimental data. It is shown that the cholinergic muscarinic receptor activation can transform the model cell's firing pattern from tonic spiking to rapid bursting, as a possible pathway for acetylcholine to promote 40-Hz oscillations in the visual cortex. To explore possible functions of fast burst firing in the neocortex, a hypothetical neural pair is simulated, where a chattering cell is presynaptic to an inhibitory interneuron via stochastic synapses. For this purpose, we use a synapse model endowed with a low release probability, short-term facilitation and vesicle depletion. This synapse model reproduces the behavior of certain neocortical pyramid-to-interneuron synapses [Thomson A. M. et al. (1993) Neuroscience 54, 347-360]. We showed that the burstiness of cell firing is required for the rhythmicity to be reliably transmitted to the postsynaptic cell via unreliable synapses, and that fast burst firing of chattering neurons can provide an exceptionally powerful drive for recruiting feedback inhibition in cortical circuits. From these results, we propose that the fast rhythmic burst firing of neocortical chattering neurons is generated by a calcium-independent ionic mechanism. Our simulation results on the neural pair highlight the importance of characterizing the short-term plasticity of the synaptic connections made by chattering cells, in order to understand their putative pacemaker role in synchronized gamma oscillations of the visual cortex.

Animals↗
PubMed2005

Synaptic plasticity at the cerebellum input stage: mechanisms and functional implications.

The mf-GrC relay provides the case of a synapse at which elementary neurotransmission mechanisms are particularly well understood allowing a precise investigation of synaptic plasticity. An interesting consequence is that a presynaptic mechanism of LTP could be precisely documented on the basis of quantal analysis. By being presynaptically expressed, LTP becomes instrumental to regulation of short-term synaptic dynamics thereby controlling time-dependent transformations of the incoming mossy fiber input. It is unknown to what extent these considerations could be generalized, but early observations were provided for comparable concepts and mechanisms in neocortical synapses (Tsodyks and Markram, 1997). Although several aspects remain to be investigated, mf-GrC LTP provides a wide substrate for information storage in the cerebellum. In the rat cerebellum, there are 10(11) GrCs and 4 times as many mf-GrC synapses. Mathematical models have suggested that mf-GrC LTP improves mutual information transfer, and that the combination of synaptic and non-synaptic changes improves sparse representation of the mf input (Schweighofer et al., 2000; Philipona et al., 2003). Moreover, mf-GrC LTP could play a key role in regulating neurotransmission dynamics, implementing adaptability in delay lines early envisioned by Breitenberg (1967) and then revisited by Medina and Mauk (2002). These observations challenge the simple view of spatial pattern separation proposed by Marr (1969). The potential consequences of mf-GrC LTP need to be further investigated and confronted with computational models of the cerebellar network.

Afferent Pathways↗
PubMed2001

Developmentally restricted synaptic plasticity in a songbird nucleus required for song learning.

We provide evidence here of long-term synaptic plasticity in a songbird forebrain area required for song learning, the lateral magnocellular nucleus of the anterior neostriatum (LMAN). Pairing postsynaptic bursts in LMAN principal neurons with stimulation of recurrent collateral synapses had two effects: spike timing- and NMDA receptor-dependent LTP of the recurrent synapses, and LTD of thalamic afferent synapses that were stimulated out of phase with the postsynaptic bursting. Both types of plasticity were restricted to the sensory critical period for song learning, consistent with a role for each in sensory learning. The properties of the observed plasticity are appropriate to establish recurrent circuitry within LMAN that reflects the spatiotemporal pattern of thalamic afferent activity evoked by tutor song. Such circuit organization could represent a tutor song memory suitable for reinforcing particular vocal sequences during sensorimotor learning.

Afferent Pathways↗
PubMed2004

Stability of synaptic plasticity in the adult rat visual cortex induced by complex environment exposure.

Studies have demonstrated the effects of complex environment (EC) housing on brain plasticity both during postnatal development and in adulthood, but it is not clear how long these plastic changes persist nor what happens when environmental exposure is discontinued. Here we examined layer IV in the visual cortex of adult male rats for the: (1) effects of EC housing on synaptic plasticity, and (2) persistence of the synaptic changes after withdrawal from the complex environment. Fifty-eight adult male Long Evans rats were assigned to either: EC, socially paired housing (SC), or individual housing (IC). These rats remained in their assigned environment for 30 days. After 30 days, all rats in SC and some animals from the EC and IC groups were removed and perfused. The remaining animals in EC were then assigned to either remain in EC (ECEC) or be subsequently housed in IC (ECIC) for another 30 days. Similarly, rats in the IC group either remained in IC (ICIC) or were subsequently housed in EC (ICEC) for another 30 days. Electron microscopy results showed that all rats exposed to EC had significantly more synapses/neuron compared to SC, IC, and ICIC animals. Longer exposure to EC (ECEC) did not result in statistically more synapses per neuron; however, decreased neuron volume was seen. EC-induced synaptic changes persisted for an additional 30 days after withdrawal from EC (ECIC) confirming that EC-induced plastic changes occur in the brain regardless of age and indicating that once changes occur they tend to persist.

Animals↗
PubMed2000

Cyclosporin ameliorates traumatic brain-injury-induced alterations of hippocampal synaptic plasticity.

Although traumatic brain injury (TBI) often results in impaired learning and memory functions, the underlying mechanisms are unknown and there are currently no treatments that can preserve such functions. We studied plasticity at CA3-CA1 synapses in hippocampal slices from rats subjected to controlled cortical impact TBI. Long-term potentiation (LTP) of synaptic transmission was markedly impaired, whereas long-term depression (LTD) was enhanced, 48 h following TBI when compared to unoperated and sham control rats. Post-TBI administration of cyclosporin A, a compound that stabilizes mitochondrial function, resulted in a highly significant amelioration of the impairment of LTP and completely prevented the enhancement of LTD. Our data suggest that alterations in hippocampal synaptic plasticity may be responsible for learning and memory deficits resulting from TBI and that agents such as cyclosporin A that stabilize mitochondrial function may be effective treatments for TBI.

Action Potentials↗
PubMed2005

Local translational control in dendrites and its role in long-term synaptic plasticity.

Local protein synthesis in dendrites has emerged as a key mechanism contributing to enduring forms of synaptic plasticity. Although the translational capability of dendrites has been appreciated for over 20 years, it is only recently that significant progress has been made in elucidating mechanisms that contribute to its regulation. It is clear from work over the last few years that the control of translation in dendrites is complex, involving a host of unique (and often surprising) mechanisms that can operate together or in parallel to tightly control gene expression in time and space. Here, we discuss the strategies used by neurons to regulate translation in dendrites and how these are implemented in the service of long-term information storage.

Animals↗
PubMed2006

Kinase suppressor of Ras1 compartmentalizes hippocampal signal transduction and subserves synaptic plasticity and memory formation.

The ERK/MAP kinase cascade is important for long-term memory formation and synaptic plasticity, with a myriad of upstream signals converging upon ERK activation. Despite this convergence of signaling, neurons routinely activate appropriate biological responses to different stimuli. Scaffolding proteins represent a mechanism to achieve compartmentalization of signaling and the appropriate targeting of ERK-dependent processes. We report that kinase suppressor of Ras (KSR1) functions biochemically in the hippocampus to scaffold the components of the ERK cascade, specifically regulating the cascade when a membrane fraction of ERK is activated via a PKC-dependent pathway but not via a cAMP/PKA-dependent pathway. Specificity of KSR1-dependent signaling also extends to specific downstream targets of ERK. Behaviorally and physiologically, we found that the absence of KSR1 leads to deficits in associative learning and theta burst stimulation-induced LTP. Our report provides novel insight into the endogenous scaffolding role of KSR1 in controlling kinase activation within the nervous system.

Adrenergic beta-Agonists↗
PubMed1997

Noradrenergic regulation of synaptic plasticity in the hippocampal CA1 region.

The effects of norepinephrine (NE) and related agents on long-lasting changes in synaptic efficacy induced by several patterns of afferent stimuli were investigated in the CA1 region of rat hippocampal slices. NE (10 microM) showed little effect on the induction of long-term potentiation (LTP) triggered by theta-burst-patterned stimulation, whereas it inhibited the induction of long-term depression (LTD) triggered by 900 pulses of 1-Hz stimulation. In nontreated slices, 900 pulses of stimuli induced LTD when applied at lower frequencies (1-3 Hz), and induced LTP when applied at a higher frequency (30 Hz). NE (10 microM) caused a shift of the frequency-response relationship in the direction preferring potentiation. The effect of NE was most prominent at a stimulus frequency of 10 Hz, which induced no changes in control slices but clearly induced LTP in the presence of NE. The facilitating effect of NE on the induction of LTP by 10-Hz stimulation was blocked by the beta-adrenergic receptor antagonist timolol (50 microM), but not by the alpha receptor antagonist phentolamine (50 microM), and was mimicked by the beta-agonist isoproterenol (0.3 microM), but not by the alpha1 agonist phenylephrine (10 microM). The induction of LTD by 1-Hz stimulation was prevented by isoproterenol but not by phenylephrine, indicating that the activation of beta-receptors is responsible for these effects of NE. NE (10 microM) also prevented the reversal of LTP (depotentiation) by 900 pulses of 1-Hz stimulation delivered 30 min after LTP induction. In contrast to effects on naive (nonpotentiated) synapses, the effect of NE on previously potentiated synapses was only partially mimicked by isoproterenol, but fully mimicked by coapplication of phenylephrine and isoproterenol. In addition, the effect of NE was attenuated either by phentolamine or by timolol, indicating that activation of both alpha1 and beta-receptors is required. These results show that NE plays a modulatory role in the induction of hippocampal synaptic plasticity. Although beta-receptor activation is essential, alpha1 receptor activation is also necessary in determining effects on previously potentiated synapses.

Afferent Pathways↗
PubMedDate not supplied

Ca2+ and synaptic plasticity.

A major effort in neuroscience is directed towards understanding the roles of Ca2+ signalling in the induction of synaptic plasticity. Here, we summarize the evidence concerning Ca2+ signalling, paying particular attention to CA1 excitatory synapses, and its relationship to the induction of long-term potentiation and long-term depression. We discuss the ways in which synaptic activation can elevate Ca2+ postsynaptically and how dendritic spines may act as a Ca2+ compartment which can both isolate and integrate Ca2+ signals.

Animals↗
PubMed1999

latheo, a Drosophila gene involved in learning, regulates functional synaptic plasticity.

Mutations in the latheo (lat) gene disrupt associative learning in Drosophila , but a role for LAT in regulating neuronal function has not been demonstrated. Here, we report that LAT plays a central role in regulating Ca2(+)- and activity-dependent synaptic plasticity. Immunological localization of the LAT protein indicates it is present at synaptic connections of the larval neuromuscular junction (NMJ) and is enriched in presynaptic boutons. Basal synaptic transmission amplitude at the lat mutant NMJ is elevated 3- to 4-fold, and Ca2+ dependence of transmission is significantly reduced. Multiple forms of synaptic facilitation and posttetanic potentiation (PTP) are strongly depressed or absent at the mutant synapse. Our results suggest that LAT is a novel presynaptic protein with a role in the Ca2(+)-dependent synaptic modulation mechanisms necessary for behavioral plasticity.

Animals↗
PubMed2002

Short-term synaptic plasticity, simulation of nerve terminal dynamics, and the effects of protein kinase C activation in rat hippocampus.

Phorbol esters are hypothesised to produce a protein kinase C (PKC)-dependent increase in the probability of transmitter release via two mechanisms: facilitation of vesicle fusion or increases in synaptic vesicle number and replenishment. We used a combination of electrophysiology and computer simulation to distinguish these possibilities. We constructed a stochastic model of the presynaptic contacts between a pair of hippocampal pyramidal cells that used biologically realistic processes and was constrained by electrophysiological data. The model reproduced faithfully several forms of short-term synaptic plasticity, including short-term synaptic depression (STD), and allowed us to manipulate several experimentally inaccessible processes. Simulation of an increase in the size of the readily releasable vesicle pool and the time of vesicle replenishment decreased STD, whereas simulation of a facilitation of vesicle fusion downstream of Ca(2+) influx enhanced STD. Because activation of protein kinase C with phorbol ester enhanced STD of EPSCs in rat hippocampal slice cultures, we conclude that an increase in the sensitivity of the release process for Ca(2+) underlies the potentiation of neurotransmitter release by PKC.

Algorithms↗
PubMed2003

Mechanisms of synaptic plasticity: from membrane to intracellular AMPAR trafficking.

Brief periods of repetitive neural firing onto adjacent neurons can lead to changes in synaptic plasticity, that is, changes in the make-up of macromolecular complexes located at synapses. This process includes the regulated trafficking of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) to synaptic membranes. Little is known, however, about how the AMPARs are regulated before they are shuttled to the membrane. Greger et al. have found that the length of the cytoplasmic tails of constituent subunits of a given AMPAR is determined by editing [at a glutamine (Q) or an arginine (R) codon] near their C termini. Tail length, in turn, dictates whether AMPARs will be retained or quickly released from the endoplasmic reticulum.

Animals↗
PubMed2003

Synaptic plasticity and functionality at the cone terminal of the developing zebrafish retina.

Previous studies have analyzed photoreceptor development, some inner retina cell types, and specific neurotransmitters in the zebrafish retina. However, only minor attention has been paid to the morphology of the synaptic connection between photoreceptors and second order neurons even though it represents the transition from the light sensitive receptor to the neuronal network of the visual system. Here, we describe the appearance and differentiation of pre- and postsynaptic elements at cone synapses in the developing zebrafish retina together with the maturation of the directly connecting second order neurons and a dopaminergic third order feedback-neuron from the inner retina. Zebrafish larvae were examined at developmental stages from 2 to 7dpf (days postfertilization) and in the adult. Synaptic maturation at the photoreceptor terminals was examined with antibodies against synapse associated proteins. The appearance of synaptic plasticity at the so-called spinule-type synapses between cones and horizontal cells was assessed by electron microscopy, and the maturation of photoreceptor downstream connection was identified by immunocytochemistry for GluR4 (AMPA-type glutamate receptor subunit), protein kinase beta(1) (mixed rod-cone bipolar cells), and tyrosine hydroxylase (dopaminergic interplexiform cells). We found that developing zebrafish retinas possess first synaptic structures at the cone terminal as early as 3.5dpf. Morphological maturation of these synapses at 3.5-4dpf, together with the presence of synapse associated proteins at 2.5dpf and the maturation of second order neurons by 5dpf, indicate functional synaptic connectivity and plasticity between the cones and their second order neurons already at 5dpf. However, the mere number of spinules and ribbons at 7dpf still remains below the adult values, indicating that synaptic functionality of the zebrafish retina is not entirely completed at this stage of development.

Animals↗
PubMed1994

Gene targeting and synaptic plasticity.

Gene targeting is revealing new molecular functions by creating very specific developmental, physiological and behavioral perturbations, and providing new insights into biochemical pathways underlying synaptic plasticity. Recent studies of mice carrying mutations in genes thought to be involved in modulating synaptic transmission have been subject to integrated biochemical, physiological and behavioral analyses.

Animals↗
PubMed2002

The effects of galanin on long-term synaptic plasticity in the CA1 area of rodent hippocampus.

Learning and memory involve complex changes in neuronal excitability including long-lasting synaptic plasticity of glutamatergic synapses. The observation that the neuropeptide galanin affects performance in a number of behavioural models predicts that galanin should affect synaptic processes underlying learning. The present study in rat and mouse hippocampal slices now demonstrates that galanin inhibits long-term potentiation induced by both tetanic and theta-burst stimulation in both apical and basal dendrites of CA1 pyramidal neurones but does not affect long-term depression. This selective effect on long-term potentiation does not appear to be mediated through inhibition of N-methyl-D-aspartate or metabotropic glutamate receptor function, but likely resides downstream of receptor activation, possibly at the level of the kinase cascade that converts short-term into long-term potentiation. Our results indicate possible mechanisms by which the neuropeptide galanin may act at the molecular level to influence learning and memory in vertebrates.

Animals↗
PubMed2005

Effect of chronic intermittent restraint stress on hippocampal expression of marker proteins for synaptic plasticity and progenitor cell proliferation in rats.

Chronic restraint stress may change hippocampal mRNA levels of markers for synaptic plasticity such as synaptophysin, growth-associated protein 43 (GAP-43), and brain-derived neurotrophic factor (BDNF). In order to examine the relation between that stressor and those biochemical markers on protein level as well as the Ki-67 protein, a marker of progenitor cell proliferation, we subjected rats to chronic intermittent restraint stress for 6 h per day for 14 days excluding the weekends. This stress intensity caused a significant increase in adrenal gland weight and decrease in body weight gain. However, we did not find significant alteration of protein expression levels for synaptophysin, GAP-43, and BDNF by using Western blot analysis. Unlike these findings, the hippocampal protein expression of Ki-67 was significantly reduced by using both Western blot and immunohistochemical analyses. This reduction of Ki-67 expression in chronically stressed rats was correlated with increased adrenal gland weight and decreased body weight gain. All marker proteins used did not show any changes of hippocampal expression level after a single restraint stress session of 3 h. In conclusion, chronic intermittent restraint stress caused changes in the physiological stress response in rats, and a decrease of hippocampal progenitor cells using the Ki-67 protein as marker which indicates a suppression of adult neurogenesis. The results might contribute to understand the relationship between stress and cellular neurobiology of depression, since chronic antidepressant treatment have been shown to increase adult neurogenesis in the rat hippocampus.

Animals↗