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At least 595 records · Page 33Linked to original sources
PubMed2002

Nicotinic receptors and hippocampal synaptic plasticity ... it's all in the timing.

As we learn more about the functional expression of nicotinic receptors in specific brain regions such as the hippocampus, intriguing interactions are being uncovered at the cellular and circuit levels. Recent work from John Dani's laboratory provides important insights into how nicotinic receptors can modify hippocampal synaptic plasticity in both positive and negative ways, and this could help explain the role of nicotinic receptors in learning and memory.

Acetylcholine↗
PubMed1997

Pathway-specific synaptic plasticity: activity-dependent enhancement and suppression of long-term heterosynaptic facilitation at converging inputs on a single target.

To explore mechanisms of long-term, pathway-specific synaptic plasticity, we examined consequences of differential stimulation of Aplysia sensorimotor connections in culture where two sensory neuron (SN) inputs converge on a single target motor cell L7. A single pairing of tetanus in one SN with bath application of 5-HT evoked long-term (24 hr) increase in efficacy of the SN connection given paired stimulation that was comparable in magnitude to the increase in synaptic efficacy evoked with repeated applications of 5-HT. Repeated pairing of tetanus in one SN with applications of 5-HT evoked a significant increase in efficacy of the SN connection given paired stimuli, and significant reduction in facilitation that is normally evoked by repeated applications of 5-HT in the unpaired SN connection. Hyperpolarization of L7 or incubation with APV interfered with both enhancement of facilitation with paired stimulation and suppression of facilitation with unpaired stimulation, but without interfering with long-term facilitation evoked either by repeated applications of 5-HT or by a single pairing. The results suggest that a single connection can undergo at least two forms of activity-dependent, pathway-specific facilitation lasting more than 24 hr. One form, evoked with a single pairing, is initiated and maintained primarily by activity in the presynaptic neuron. The other form, evoked with repeated paired stimuli, requires target-dependent activity that differentially modulates long-term heterosynaptic facilitation at the converging inputs.

2-Amino-5-phosphonovalerate↗
PubMed2006

Dendritic spikes and activity-dependent synaptic plasticity.

Whereas the regenerative nature of action potential conduction in axons has been known since the late 1940s, neuronal dendrites have been considered as passive cables transferring incoming synaptic activity to the soma. The relatively recent discovery that neuronal dendrites contain active conductances has revolutionized our view of information processing in neurons. In many neuronal cell types, sodium action potentials initiated at the axon initial segment can back-propagate actively into the dendrite thereby serving, for the dendrite, as an indicator of the output activity of the neuron. In addition, the dendrites themselves can initiate action-potential-like regenerative responses, so-called dendritic spikes, that are mediated either by the activation of sodium, calcium, and/or N-methyl-D-aspartate receptor channels. Here, we review the recent experimental and theoretical evidence for a role of regenerative dendritic activity in information processing within neurons and, especially, in activity-dependent synaptic plasticity.

Action Potentials↗
PubMed2006

Spatiotemporal asymmetry of associative synaptic plasticity in fear conditioning pathways.

Input-specific long-term potentiation (LTP) in afferent inputs to the amygdala serves an essential function in the acquisition of fear memory. Factors underlying input specificity of synaptic modifications implicated in information transfer in fear conditioning pathways remain unclear. Here we show that the strength of naive synapses in two auditory inputs converging on a single neuron in the lateral nucleus of the amygdala (LA) is only modified when a postsynaptic action potential closely follows a synaptic response. The stronger inhibitory drive in thalamic pathway, as compared with cortical input, hampers the induction of LTP at thalamo-amygdala synapses, contributing to the spatial specificity of LTP in convergent inputs. These results indicate that spike timing-dependent synaptic plasticity in afferent projections to the LA is both temporarily and spatially asymmetric, thus providing a mechanism for the conditioned stimulus discrimination during fear behavior.

Action Potentials↗
PubMedDate not supplied

Perinatal nutritional iron deficiency reduces hippocampal synaptic transmission but does not impair short- or long-term synaptic plasticity.

Studies show that perinatal nutritional iron deficiency (ID) produces learning and memory impairments in humans and animals. This suggests that the functional physiology of learning and cognitive centers in the brain, such as the hippocampus, may be compromised by developmental ID. The present study used electrophysiological brain slice methods to examine multiple measures of hippocampal synaptic efficacy from rats that were subjected to perinatal ID diets or control (CN) diets. Measures of synaptic efficacy were obtained from the first and last synaptic regions of the hippocampal tri-synaptic loop (i.e. the dentate gyrus (DG) and CA1). Rats were placed on ID or CN diets on gestational day 11, and hippocampal brain slices were prepared between postnatal day 25 and 37. Results show that ID slices were not impaired in short-term (i.e. paired-pulse facilitation (PPF)) or long-term measures (i.e. long-term potentiation (LTP)) of synaptic plasticity in either the DG or CA1 areas. Input-output (IO) measures showed that synaptic transmission was reduced in both of these areas in the ID slices when compared with the CN slices. This suggests that ID-induced learning deficits may be the result of reductions in synaptic transmission throughout the hippocampus, and possibly in other learning and memory centers.

Anemia, Iron-Deficiency↗
PubMed1998

Synaptic plasticity in the CA1 area of the hippocampus of scrapie-infected mice.

Using conventional in vitro extracellular field potential recordings we have investigated both short- and long-term synaptic plasticity in the hippocampal CA1 area of mice infected with ME7 scrapie. In agreement with earlier studies, no changes were seen in the properties of the Schäffer collateralevoked field excitatory postsynaptic potential during the early stages of the disease (up to 160 days, post inoculation, d.p.i) after which time the recorded potentials were seen to attenuate. Also, up to this time no changes were seen in either paired-pulse facilitation or post-tetanic potentiation, which are short-term phenomena associated with brief elevations in presynaptic calcium levels. However, there was a significant shift from the ability of slices to maintain long-term potentiation (LTP) from 100 d.p.i. onwards. In all of these experiments short-term potentiation (STP) was preserved, suggesting that from the time that abnormal PrP becomes detectable, or perhaps even earlier, the mechanisms responsible for stabilizing the maintenance phase of LTP are impaired. This result is discussed in terms of the relationship between STP and LTP and how this might be compromised by the conversion of cellular prion protein (PrPC) to the scrapie, protease resistant form of PrP (PrPSc).

Animals↗
PubMed1997

Altered synaptic plasticity in hippocampal CA1 area of apolipoprotein E deficient mice.

In mice with a homozygous or heterozygous deficiency for ApoE as well as in wild-type animals we established synaptic responsiveness in the hippocampal CA1 area following stimulation of the Schaffer/commissural fibers. The maximal population spike amplitude was significantly larger in wild-type animals than in mice lacking the ApoE gene, whereas the facilitation in population spike amplitude after paired pulse stimulation was most pronounced in homozygous mutant mice. Primed burst stimulation induced a lasting increase in population spike amplitude of all three groups. Apart from a more pronounced initial potentiation in the homozygous mutants, primed burst potentiation was comparable in all groups. Subsequent theta burst stimulation resulted in a long-term enhanced synaptic responsiveness which was impaired in heterozygous animals. The data show that both homo- and heterozygous ApoE mutant mice display altered synaptic plasticity in the hippocampal CA1 area.

Animals↗
PubMed2001

Contribution of the neural cell adhesion molecule to neuronal and synaptic plasticity.

The neural cell adhesion molecule (NCAM) and its polysialylated form PSA-NCAM contribute to many aspects of the development and plasticity of the central nervous system. This includes mechanisms of cell differentiation and migration, neurite outgrowth, establishment of specific patterns of synaptic connections, synaptic plasticity and long-term potentiation. How NCAM and PSA-NCAM contribute to regulate all these different mechanisms remains essentially unknown. Adhesive properties appear to be important, but recent studies also point to possible interactions between NCAM and PSA-NCAM with intracellular signalling cascades that are essential to biological functions. Some of these mechanisms are discussed and a hypothesis is proposed based on the existence of cross-talk between these molecules and signalling pathways mediated by growth factors.

Animals↗
PubMed1997

Synaptic plasticity in olfactory memory formation in female mice.

Female mice develop a long-lasting olfactory recognition memory of a partner male at the first relay in the vomeronasal system. In this study the synaptic plasticity relevant to this phenomenon was examined at reciprocal dendrodendritic synapses in the accessory olfactory bulb of female mice by electron microscopy. The size of asymmetrical excitatory synapses (mitral/tufted to granule cells) of the reciprocal synapses was significantly larger in the group of female mice which were subjected to a treatment intended to induce olfactory memory formation than in the control group. It is suggested that olfactory memory formation is associated with a conformational change at the level of synaptic structure of the accessory olfactory bulb.

Analysis of Variance↗
PubMed2003

Cortico-striatal synaptic plasticity in endothelial nitric oxide synthase deficient mice.

Nitric oxide (NO) is a retrograde messenger involved in the processes of learning and memory. The role of the endothelial isoform of nitric oxide synthase (eNOS) in striatal synaptic plasticity was investigated in eNOS-deficient (eNOS(-/-)) and wild type (WT) mice. Tetanic stimulation of cortical afferents in WT mice evoked either long-term potentiation (LTP), or long-term depression (LTD) of cortico-striatal transmission. Both these plasticity related phenomena were NMDA-receptor-dependent; LTD was blocked by sulpiride, a dopamine D2-receptor antagonist. LTP occurrence in slices from eNOS(-/-) mice was significantly reduced when compared with WT mice. The NOS inhibitor NL-ARG reduced the occurrence of LTP and increased the occurrence of LTD in WT mice, resembling the balance of LTP/LTD in eNOS(-/-) mice. Impairment of NO-synthesis thus shifts striatal plasticity towards LTD. This indicates a possible involvement of eNOS from endothelia in neuronal modulation.

Animals↗
PubMed1996

Synaptic plasticity in the caudate nucleus of patients with Parkinson's disease.

The loss of dopaminergic neurons from the substantia nigra in Parkinson's disease (PD) may provoke a reorganization of cellular interactions in the nigrostriatal pathway. Indeed, a plasticity of putative corticostriatal synapses has been evidenced in the striatum of rats with a 6-hydroxy-dopamine-induced lesion of the substantia nigra. However, to our knowledge, synaptic plasticity in the striatum has not previously been investigated in human PD. In this study, we have analysed, at electron microscope level, the morphological characteristics of the synapses formed by afferents in asymmetric contact with dendritic spines of neurons in the caudate nucleus of three patients with PD and three matched controls. The length of the postsynaptic densities and the number of perforated synapses were both significantly increased (24 and 88%, respectively) in the PD patients; the size of these afferents and the surface area occupied by their mitochondria also showed an increase (24 and 50%, respectively), although not statistically significant. The size and density of dendritic spines and the size of postsynaptic density perforations were unchanged. These data indicate the presence of plasticity of the putative corticostriatal synapses in PD and suggest a hyperactivity of cortical afferents to GABAergic neurons.

Aged↗
PubMed2005

[The role of Alzheimer amyloid plaques in the mechanisms of neuron synaptic plasticity disturbance].

The authors studied hippocampal microscopic sections taken from transgenic mice expressing non-mutated human amyloid precursor protein (APP695), and age-matched non-transgenic control mice. The aim of the study was to reveal individual effects of plaque-like amyloid of aged (25.5 months) transgenic mice and diffuse amyloid of non-transgenic mice (verified by immunohistochemistry and Congo Red fluorescence) on synaptic plasticity. In vitro extracellular recording of excitatory postsynaptic potentials from hyppocampal CA1 area revealed impairment of input/output characteristics and long-term potentiation, and a several-millisecond delay of initial post-tetanic traces in aged transgenic vs. control mice. The results show that amyloid plaques (not diffuse amyloid) may be one of the causes of synaptic dysfunction in Alzheimer disease.

Alzheimer Disease↗
PubMed1994

Glutamate receptor phosphorylation and synaptic plasticity.

The recent findings that glutamate receptors are phosphorylated and functionally modulated by protein kinases has provided evidence that phosphorylation of these receptors may play a critical role in mechanisms of synaptic plasticity.

Animals↗
PubMed1999

Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice.

We investigated synaptic communication and plasticity in hippocampal slices from mice overexpressing mutated 695-amino-acid human amyloid precursor protein (APP695SWE), which show behavioral and histopathological abnormalities simulating Alzheimer's disease. Although aged APP transgenic mice exhibit normal fast synaptic transmission and short term plasticity, they are severely impaired in in-vitro and in-vivo long-term potentiation (LTP) in both the CA1 and dentate gyrus regions of the hippocampus. The LTP deficit was correlated with impaired performance in a spatial working memory task in aged transgenics. These deficits are accompanied by minimal or no loss of presynaptic or postsynaptic elementary structural elements in the hippocampus, suggesting that impairments in functional synaptic plasticity may underlie some of the cognitive deficits in these mice and, possibly, in Alzheimer's patients.

Aging↗
PubMed2006

The role of synaptic ion channels in synaptic plasticity.

The nervous system receives a large amount of information about the environment through elaborate sensory routes. Processing and integration of these wide-ranging inputs often results in long-term behavioural alterations as a result of past experiences. These relatively permanent changes in behaviour are manifestations of the capacity of the nervous system for learning and memory. At the cellular level, synaptic plasticity is one of the mechanisms underlying this process. Repeated neural activity generates physiological changes in the nervous system that ultimately modulate neuronal communication through synaptic transmission. Recent studies implicate both presynaptic and postsynaptic ion channels in the process of synapse strength modulation. Here, we review the role of synaptic ion channels in learning and memory, and discuss the implications and significance of these findings towards deciphering the molecular biology of learning and memory.

Animals↗
PubMedDate not supplied

Tetraethylammonium-induced synaptic plasticity in rat neocortex.

Recordings were obtained from neurons in layer II/III of slices of rat frontal cortex maintained in vitro. We investigated whether brief application of the potassium channel blocker tetraethylammonium (TEA), which induces a novel form of synaptic plasticity in the CA1 region of the hippocampus referred to as LTPK, evokes similar responses in neocortex. Consistent with previous findings, TEA produced a persistent enhancement of excitatory transmission, which was independent of NMDA receptor activation but required the activation of nifedipine-sensitive voltage-dependent Ca2+ channels (VDCC), presumably the L-type. We also observed a persistent enhancement of presumptive CI(-)-dependent GABAA receptor-mediated transmission. Enhancement of excitatory and inhibitory synaptic transmission did not require activation of synapses with electrical stimulation during TEA application. The enhancement of excitatory, but not inhibitory synaptic transmission, was blocked when the Ca2+ chelator 1,2-bis(2-aminophenoxy)-ethane N,N,N',N'-tetraacetic acid (BAPTA) was included in the recording electrode. Under voltage clamp conditions that minimized the activation of L-type channels robust enhancement of both excitatory and inhibitory transmission was still observed. No enhancement of excitatory synaptic transmission was observed in the presence of NiCl2, a putative T-type channel blocker. The possible involvement of kinase activation was studied by including the non-specific and competitive kinase inhibitor (+/-)-1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7) in the patch pipette. H-7 retarded the time course and reduced the magnitude of the enhancement of excitatory transmission. These results suggest that TEA-induced enhancement of excitatory transmission in the neocortex requires entry of Ca2+ into the postsynaptic neuron via VDCCs and possibly the activation of a kinase.

Animals↗
PubMed2004

Rapid synaptic plasticity of glutamatergic synapses on dopamine neurons in the ventral tegmental area in response to acute amphetamine injection.

Drugs of abuse activate the reward circuitry of the mesocorticolimbic system, and it has been hypothesized that drug exposure triggers synaptic plasticity of glutamatergic synapses onto dopamine (DA) neurons of the ventral tegmental area. Here, we show that just a 2 h in vivo exposure to amphetamine is sufficient to potentiate these synapses, measured as an increase in the synaptic AMPAR/NMDAR ratio. We tested the prediction that an increase in GluR1-containing AMPA receptors would result in an increase in GluR1 homomeric receptors at synapses, but were unable to observe any evidence of the predicted rectification in DA neurons from animals treated with amphetamine. We also examined the possibility of increased AMPA receptor insertion in the membrane, but did not detect a significant increase in biotinylated surface GluR1. We conclude that amphetamine induces rapid changes in synaptic AMPAR/NMDAR ratios, suggesting that potentiation of glutamatergic synapses is a relatively early event in the series of neuroadaptations in response to drugs of abuse.

2-Amino-5-phosphonovalerate↗
PubMed2001

Isoflurane blocks synaptic plasticity in the mouse hippocampus.

BACKGROUND: The volatile anesthetic isoflurane depresses glutamatergic transmission. In this study, the authors investigated the effects of isoflurane on the induction of long-term potentiation (LTP) and long-term depression (LTD) in slices from the juvenile and adult mouse hippocampus. Both forms of synaptic plasticity involve the activation of glutamate receptors. METHODS: Field excitatory postsynaptic potentials and excitatory postsynaptic currents from neurons in the CA1 area were evoked by stimulation of the Schaffer collateral-commissural pathway. Two independent synaptic inputs were stimulated. Clinically relevant concentrations (0.2-0.3 mM) of isoflurane were added to the perfusion solution. RESULTS: Field excitatory postsynaptic potentials from slices of juvenile and adult mice were depressed to 37.3 +/- 6.1% and 58.3 +/- 7.4%, respectively, and excitatory postsynaptic currents were reduced to 36.7 +/- 5.4% by isoflurane. A brief tetanic stimulation (100 Hz, 1 s) induced stable LTP of field excitatory postsynaptic potentials. In the presence of isoflurane, tetanization failed to induce LTP. The effect of isoflurane on LTP induction was reversible and could be prevented by antagonizing gamma-aminobutyric acid type A receptors (GABAA). Low-frequency stimulation (1 Hz/900 pulses) induced LTD. In the presence of isoflurane, low-frequency stimulation failed to induce LTD. CONCLUSIONS: The prevention of the isoflurane-induced depression of LTP by the GABAA antagonist picrotoxin suggests an involvement of GABAA receptors. An enhancement of the efficacy of GABA-mediated inhibitory synaptic transmission prevents the depolarization of the postsynaptic membrane during tetanus, necessary for the induction of use-dependent alteration of synaptic strength. An impairment of these processes may be a cause for the transient loss of recall and cognitive impairment after anesthesia in juvenile and adult brains.

Aging↗