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Results for “synaptic plasticity”

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At least 649 records · Page 36Linked to original sources
PubMed2004

Long-term synaptic plasticity in deep layer-originated associational projections to superficial layers of rat entorhinal cortex.

Superficial layers of the entorhinal cortex (EC) relay the majority of cortical input projections to the hippocampus, whereas deep layers of the EC mediate a large portion of hippocampal output projections back to other cortical areas, suggesting a functional segregation between superficial and deep layers of the EC as input and output structures of the hippocampus, respectively. However, deep layers of the EC send associational projections to superficial layers, suggesting a potential interaction between neocortical input and hippocampus-processed output in superficial layers. This possibility was investigated by examining whether deep to superficial EC projections support long-term synaptic plasticity, and whether they interact with other pathways in superficial layers in rat medial EC slice preparations. Synaptic responses of the deep-to-superficial layer projections were verified based on field potential profiles, paired-pulse facilitation, physical separation between superficial and deep layers, and pharmacological manipulation. Long-term potentiation (LTP) was reliably induced in the deep-to-superficial layer projections by burst stimulations that emulated theta or sharp wave electroencephalogram (EEG),and it was blocked by an N-methyl-d-aspartate receptor antagonist (D-2-amino-5-phosphonopentanoic acid) and a calcium channel blocker (nifedipine). Prolonged low frequency stimulation induced long-term depression. A weak stimulation of deep layers, which induced a small degree of LTP by itself, generated a much larger degree of LTP when paired with a strong stimulation of superficial layers, indicating that the deep-to-superficial layer projections cooperate with other pathways in the superficial EC to enhance synaptic weights. Our results suggest that neocortical input and hippocampal output information are integrated in superficial layers of the EC.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2006

Synaptic plasticity in CNGA3(-/-) mice: cone bipolar cells react on the missing cone input and form ectopic synapses with rods.

In the mammalian retina, rods and cones connect to distinct sets of bipolar cells. Rods are presynaptic to a single type of rod bipolar cell, whereas cones connect to different types of cone bipolar cells. Synaptic rewiring between cone photoreceptor terminals and rod bipolar cell dendrites has been described as a general result of photoreceptor degeneration. To investigate whether cone bipolar cells also show synaptic plasticity in the absence of cone input, we studied the connectivity of cone bipolar cell dendrites in CNGA3(-/-) mice, a model with specific loss of cone photoreceptor function. Dendritic connections of ON and OFF cone bipolar cells were visualized using specific cell markers or by intracellular injection with fluorescent dyes. The results show that cone bipolar cells in CNGA3(-/-) mice form ectopic synapses with rods. In contrast, cone bipolar cells do not form ectopic synapses with rods in CNGA3(-/-)Rho(-/-) mice, in which both types of photoreceptors are nonfunctional. In analogy with these results, we found that input-deprived rod bipolar cells form ectopic synapses with functional cones in Rho(-/-) mice but not with inoperable cones in the CNGA3(-/-)Rho(-/-) mouse. Our data indicate that the formation of ectopic bipolar cell synapses in the outer plexiform layer requires a functional presynaptic photoreceptor.

Animals↗
PubMed2004

Hippocampal synaptic plasticity in mice devoid of cellular prion protein.

The cellular prion protein plays a role in the etiology of transmissible and inherited spongiform encephalopathies. However, the physiological role of the cellular prion protein is still under debate. Results regarding the synaptic transmission using the same strain of animals where the cellular prion protein gene was ablated are controversial, and need further investigation. In this work, we have studied the hippocampal synaptic transmission in mice devoid of normal cellular prion protein, and have shown that these animals present an increased excitability in this area by the lower threshold (20 Hz) to generate long-term potentiation (LTP) in hippocampal dentate gyrus when compared to wild-type animals. The mice devoid of normal cellular prion protein are also more sensitive to the blocking effects of dizocilpine and 2-amino-5-phosphonopentanoic acid on the hippocampal long-term potentiation generation. In situ hydridization experiments demonstrated overexpression of the mRNAs for the N-methyl-D-aspartate (NMDA) receptor NR2A and NR2B subunits in mice devoid of normal cellular prion protein. Therefore, our results indicate that these animals have an increased hippocampal synaptic plasticity which can be explained by a facilitated glutamatergic transmission. The higher expression of specific N-methyl-d-aspartate receptor subunits may account for these effects.

Animals↗
PubMed2001

Synaptic plasticity in the trigeminal principal nucleus during the period of barrelette formation and consolidation.

We examined whether the postsynaptic responses of cells in the principal sensory nucleus of the trigeminal nerve (PrV) are subject to long-term changes in synaptic strength, and if such changes were correlated the whisker-specific patterning during and just after the critical period for pattern formation. We used an in vitro brainstem preparation in which the trigeminal ganglion (TG) and PrV remained attached. By electrically activating TG afferents, we evoked large-amplitude extracellular field potentials. These responses were postsynaptic in origin and blocked by the glutamate antagonist, DNQX. At P1, a time when barrelettes are consolidating, high frequency stimulation of their afferents led to an immediate (<1 min) and long-lasting (> or =90 min) reduction (35%) in the amplitude of the evoked response. At P3-7, when the pattern of barrelettes have stabilized, the same form of tetanus led to an immediate and long-lasting increase (40%) in the amplitude of the response. Both forms of synaptic plasticity were mediated by the activation of L-type Ca(2+) channels. Application of the L-type channel blocker, nitrendipine, led to a complete blockade of any the tetanus induced changes. These associative processes may regulate the patterning and maintenance of whisker-specific patterns in the brainstem trigeminal nuclei.

2-Amino-5-phosphonovalerate↗
PubMed1999

Impaired synaptic plasticity in mice carrying the Huntington's disease mutation.

Cognitive impairment is an early symptom of Huntington's disease (HD). Mice engineered to carry the HD mutation in the endogenous huntingtin gene showed a significant reduction in long-term potentiation (LTP), a measure of synaptic plasticity often thought to be involved in memory. However, LTP could be induced in mutant slices by an 'enhanced' tetanic stimulus, implying that the LTP-producing mechanism is intact in mutant mice, but that their synapses are less able to reach the threshold for LTP induction. Mutant mice showed less post-tetanic potentiation than wild-type animals, and also showed decreased paired pulse facilitation, suggesting that excitatory synapses in HD mutant mice are impaired in their ability to sustain transmission during repetitive stimulation. We show that mutants, while normal in their ability to transmit at low frequencies, released significantly less glutamate during higher frequency synaptic activation. Thus, a reduced ability of Huntington synapses to respond to repetitive synaptic demand of even moderate frequency could result not only in a functional impairment of LTP induction, but could also serve as a substrate for the cognitive symptoms that comprise the early-stage pathology of HD.

Animals↗
PubMed1987

Calcium-promoted translocation of protein kinase C to synaptic membranes: relation to the phosphorylation of an endogenous substrate (protein F1) involved in synaptic plasticity.

The translocation of protein kinase C between membrane and cytosol has been implicated in several cellular processes (Kraft and Anderson, 1983; Wooten and Wrenn, 1984; Akers et al., 1985, 1986; Hirota et al., 1985; Wolf et al., 1986). We desired to identify potential trigger mechanisms underlying the translocation of protein kinase C activity to neural membranes following the synaptic plasticity observed after long-term potentiation (LTP; Akers et al., 1986). Takai et al. (1979) have suggested an important role for calcium in protein kinase C translocation; we have therefore studied the effects of Ca2+ on both the translocation of protein kinase C activity and the in vitro phosphorylation of its endogenous substrate, protein F1, in rat hippocampal synaptosomes. Since identical free Ca2+ levels were maintained in subsequent assays of synaptosomal membranes (SPM) and cytosol preparations, alterations in endogenous enzyme activity and in vitro phosphorylation were due to the Ca2+ present during treatment of synaptosomes, and not to the Ca2+ present during assays of enzymatic activity. This afforded the opportunity to relate directly such enzyme translocation to endogenous substrate phosphorylation. The major findings were as follows: 1. Following treatment of synaptosomes with Ca2+, protein kinase C activity in synaptic membrane and protein F1 in vitro phosphorylation were elevated in a dose-dependent manner. 2. The greatest increment in membrane protein kinase C activity and protein F1 in vitro phosphorylation occurred when Ca2+ was increased from 0.1 to 1.0 microM. Maximal levels of enzyme activity were seen following treatment with 10 microM Ca2+, and minimum levels were observed following treatment with EGTA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Distinct mechanisms of bidirectional activity-dependent synaptic plasticity in superficial and deep layers of rat entorhinal cortex.

The entorhinal cortex plays a key role in processing memory information in the brain; superficial layers relay information to, and deep layers receive information from, the hippocampus. The cellular mechanisms of memory are thought to include a number that produce long-term potentiation (LTP) and depression (LTD) of synaptic strength. Our work presents evidence that LTP and LTD occur simultaneously at memory-relevant synapses. We report here that low frequency stimulation generates NMDA receptor-dependent LTD in Wistar rat superficial (layers II and III), and LTP in the deep entorhinal cortex layers (layers V and VI). LTP in deep layers is masked by simultaneously occurring voltage-gated calcium channel-dependent LTD. Our data support a novel mechanism for the sliding-threshold (BCM) model of synaptic plasticity: The sliding thresholds for induction of LTP and LTD in entorhinal cortex deep layers will be driven by the relative activation state of NMDA receptors and voltage-gated calcium channels. The co-expression of LTD and LTP at presynaptic sites in the entorhinal cortex deep layers reveals an intriguing mechanism for differential processing of synaptic information, which may underlie the vast dynamic capacity for information storage by this cortical structure.

Animals↗
PubMed2005

Deficits in cortico-striatal synaptic plasticity and behavioral habituation in rats with portacaval anastomosis.

Hepatic encephalopathy is characterized by disturbances of motor and cognitive functions involving the basal ganglia. So far no standards for assessment of neuropsychiatric abnormalities (disorders of sleep, mood, anxiety and personality) in subclinical hepatic encephalopathy have been defined. Using an animal model of mild (subclinical) hepatic encephalopathy we investigated now striatum-related behaviors and cortico-striatal synaptic plasticity in rats 2 months after introduction of a portacaval shunt and sham-operated matched controls. In a novel open field portacaval shunt rats displayed less locomotor activity; unlike controls they also showed no habituation to the field and no recall of the field environment after 24 h, indicative of cognitive deficit. The elevated-plus maze test indicated no differences in fear/anxiety in the portacaval shunt animals. Tetanic stimulation of cortical afferents in magnesium-free solution evoked an N-methyl-D-aspartate-dependent long-term potentiation in sham-operated animals. In portacaval shunt animals long-term potentiation was significantly impaired. Histamine, a potent modulator of cortico-striatal transmission, induced a larger long-term depression of field potentials in control compared with portacaval shunt rats. In conclusion, a combination of electrophysiological and behavioral approaches has revealed functional changes in cortico-striatal transmission. These data are relevant for understanding the mechanisms of motor and cognitive dysfunctions in hepatic encephalopathy patients and for the development of precise psychometric tests, evaluating cognitive deficits in subclinical hepatic encephalopathy.

Animals↗
PubMedDate not supplied

Hippocampal memory modification induced by pattern completion and spike-timing dependent synaptic plasticity.

One of the roles of the hippocampus is viewed as modifying episodic memory so that it can contribute to form semantic memory. In this paper, we show that pattern completion ability of the hippocampal CA3 and symmetric spike timing-dependent synaptic plasticity (STDP) induce memory modification so that the hippocampal CA3 can memorize invariable parts of repetitive episodes as essential elements and forget variable parts of them as unnecessary ones.

Animals↗
PubMed1997

Hippocampal interneurons express a novel form of synaptic plasticity.

Individual GABAergic interneurons in hippocampus can powerfully inhibit more than a thousand excitatory pyramidal neurons. Therefore, control of interneuron excitability provides control over hippocampal networks. We have identified a novel mechanism in hippocampus that weakens excitatory synapses onto GABAergic interneurons. Following stimulation that elicits long-term potentiation at neighboring synapses onto excitatory cells, excitatory synapses onto inhibitory interneurons undergo a long-term synaptic depression (interneuron LTD; iLTD). Unlike most other forms of hippocampal synaptic plasticity, iLTD is not synapse specific: stimulation of an afferent pathway triggers depression not only of activated synapses but also of inactive excitatory synapses onto the same interneuron. These results suggest that high frequency afferent activity increases hippocampal excitability through a dual mechanism, simultaneously potentiating synapses onto excitatory neurons and depressing synapses onto inhibitory neurons.

Afferent Pathways↗
PubMed2001

Synaptic plasticity and nicotine addiction.

Nicotine, the main addictive component of tobacco, activates and desensitizes nicotinic acetylcholine receptors (nAChRs). In that way, nicotine alters normal nicotinic cholinergic functions. Among the myriad of psychopharmacological effects that underlie the addiction process, nicotine influences nAChR participation in synaptic plasticity. This influence has particular importance in the mesocorticolimbic dopamine system, which serves during the reinforcement of rewarding behaviors.

Animals↗
PubMed2000

Activity-dependent morphological synaptic plasticity in an adult neurosecretory system: magnocellular oxytocin neurons of the hypothalamus.

Oxytocin and vasopressin neurons, located in the supraoptic and paraventricular nuclei of the hypothalamus, send their axons to the neurohypophysis where the neurohormones are released directly into the general circulation. Hormone release depends on the electrical activity of the neurons, which in turn is regulated by different afferent inputs. During conditions that enhance oxytocin secretion (parturition, lactation, and dehydration), these afferents undergo morphological remodelling which results in an increased number of synapses contacting oxytocin neurons. The synaptic changes are reversible with cessation of stimulation. Using quantitative analyses on immunolabelled preparations, we have established that this morphological synaptic plasticity affects both inhibitory and excitatory afferent inputs to oxytocin neurons. This review describes such synaptic modifications, their functional significance, and the cellular mechanisms that may be responsible.

Adult↗
PubMed2003

Tyrosine kinases, synaptic plasticity and memory: insights from vertebrates and invertebrates.

Tyrosine kinases were first characterized in terms of their function during development. Over the past decade, it has become clear that tyrosine phosphorylation also plays an important role in the adult mammalian nervous system. This article reviews three different families of tyrosine kinase signaling cascades: the Trk receptor tyrosine kinases, the Src family of non-receptor tyrosine kinases and the Eph receptor tyrosine kinases. Each of these cascades has been implicated in both adult synaptic plasticity and memory formation. Evidence from invertebrate systems also demonstrates a role for tyrosine kinase signaling in the induction of long-term memory, suggesting that molecular mechanisms of memory formation are conserved across species.

Animals↗
PubMed2003

Effects of stimulus frequency and age on bidirectional synaptic plasticity in the dentate gyrus of freely moving rats.

We investigated the frequency-dependent transition from homosynaptic long-term depression (LTD) to long-term potentiation (LTP) at the lateral perforant pathway/dentate gyrus synapse in adult (90 days of age) and immature (15 days of age) awake, freely moving rats. Dentate-evoked field potentials were recorded and analyzed using the population spike amplitude and the field EPSP slope measures following sustained stimulation (900 pulses) of the lateral perforant pathway at various frequencies (1, 3, 7, 30, 50, or 200 Hz). Our results indicate that both the strength and the direction (LTP or LTD) of synaptic plasticity vary as a function of activation frequency: sustained low-frequency stimulation ranging from 1 to 7 Hz results in depression of activated synapses, whereas high-frequency stimulation (30-200 Hz) produces potentiation. In addition, a significant (P < 0.01) ontogenetic shift in the frequency of transition from LTD to LTP was observed; the transition frequency in immature animals was significantly lower than that obtained in adult animals. These observations agree strongly with the prediction of the Bienenstock-Cooper-Munro theory of synapse modification, indicating perhaps a neurophysiological basis for this theoretical model of learning in the dentate gyrus of awake behaving rats.

Action Potentials↗
PubMed1986

Phorbol ester promotes growth of synaptic plasticity.

Iontophoretic application of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) to the intact rat hippocampus enhances potentiation produced by subsequent high frequency stimulation of the perforant path. The decay of the enhanced population spike amplitude recorded in the hilar dentate gyrus was prevented in animals receiving ejections of TPA, as compared to controls which decayed to baseline values within 2 h following high frequency stimulation. In fact, growth of the potentiated response was observed beginning at 45 min. Similar results were observed with the population excitatory postsynaptic potential slope, a measure of the synaptic response. Since tumour-promoting phorbol esters are known to translocate and activate protein kinase C (PKC) and PKC is translocated to the membrane following hippocampal potentiation, a role for membrane-associated PKC in the regulation of synaptic plasticity is suggested.

Action Potentials↗
PubMed1993

Altered synaptic plasticity and memory formation in nitric oxide synthase inhibitor-treated rats.

Nitric oxide (NO) is a messenger molecule that is produced in the brain from the metabolism of L-arginine to L-citrulline. Growing evidence suggests a physiological role for NO in long-term potentiation (LTP). Since LTP is a form of synaptic plasticity thought to be involved in learning and memory, we have tested whether inhibition of endogenous NO production affects memory capacities of rats. We found that the NO synthase [L-arginine, NADPH:oxygen oxidoreductase (nitric oxide-forming), EC 1.14.13.39] inhibitor N omega-nitro-L-arginine, at doses blocking LTP in hippocampal slices, impairs spatial learning in a radial arm maze and olfactory memory in a social recognition test. In contrast, N omega-nitro-L-arginine left shock-avoidance learning unaffected. These results indicate that NO is involved in some but not all forms of memory and further support the existence of a causal link between LTP and spatial learning.

Amino Acid Oxidoreductases↗
PubMed2003

Compatibility of bidirectional synaptic plasticity on hippocampo-prefrontal cortex pathway in rats.

The hippocampo-prefrontal cortex pathway reportedly expresses long-term potentiation (LTP) and depression (LTD) in anesthetized rats. We examined whether there were any effects governing the induction of LTD after prior induction of LTP, or vice versa. Induction in sequence of LTP and LTD resulted in significantly stable changes of about 140 and 70% of a common control for 1 h each. The reversed sequence, LTD and LTP, showed a mirror image of about 65 and 135% of control, which were not different from the respective changes in the first sequence (P>0.3 for each). The correlation coefficient between changes was significantly positive in the first sequence and weakly negative in the reverse. These results indicate that this pathway can express compatibility of bidirectional synaptic plasticity while historical changes remain covert.

Animals↗
PubMedDate not supplied

[NO-Ergic transmission and NO as a volume transmitter. Effect of NO on mechanisms of synaptic plasticity and epileptogenesis].

Nitric oxide (NO) is a universal intercellular messenger and the only molecule known so far, which satisfies all requirements of the volume (extrasynaptic) neurotransmitter. The effect of NO on target cells is so read in the four-dimensional coordinate system by combining both the spatial and the temporal components of the nervous activity. In this review, the authors, based on literature data and own studies, present a detailed analysis of properties of NO as a volume neurotransmitter at formation of phenomena of synaptic plasticity in norm and pathology. An evaluation is given of cytotoxic and neuroprotective effects of NO under conditions of the brain tissue ischemia and phenomena of hyperexcitability in foci of epileptiform activity. It is emphasized that the long-term potentiation and long-term depression, phenomena of physiological plasticity, can be transformed into pathological plasticity at disturbances of equilibrium between neuroprotective and neurotoxic effects of NO.

Animals↗