Theta pattern stimulation and the induction of LTP: the sequence in which synapses are stimulated determines the degree to which they potentiate (original) (raw)
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Hippocampus, 2016
The hippocampal synapses display a conspicuous ability for long-term plasticity, which is thought to contribute to learning and memory. Previous research has shown that long-term potentiation (LTP) greatly differs between the dorsal (DH) and ventral (VH) CA1 hippocampal synapses when induced by high-frequency stimulation. In this study, using rat hippocampal slices and more physiologically relevant activity patterns based on the frequency of the theta rhythm (i.e. theta-burst stimulation, TBS) we found that the DH compared with the VH displayed a higher ability for induction and stability of NMDA receptor-dependent LTP of the field excitatory postsynaptic potential. Nevertheless, the maximal magnitude of LTP was similar in the two hippocampal segments. Blockade of GABA B receptors prevented the LTP induction by the minimal effective TBS and reduced the magnitude of LTP induced by longer TBS. TBS produced a threefold higher facilitation of the synaptic burst responses in the DH compared with the VH, accompanied by a strong enhancement in the postsynaptic excitation in the DH but mostly depression in the VH. The DH displayed NMDA receptordependent and NMDA receptor-independent facilitation, but the facilitation in the VH was only NMDA receptor-dependent. Also, the TBS-associated activity of GABA B receptors was higher in the DH than in the VH. The different response profiles during TBS could underlie the differences in LTP between the two hippocampal segments. L-type voltage-dependent calcium channels (L-VDCC) and the metabotropic glutamate receptor-5 (mGluR5) equally contributed in DH and VH to compound LTP induced by relatively long TBS. We propose that these dorsoventral differences in synaptic plasticity reflect specializations of the intrinsic circuitry of the hippocampus, that are involved in the distinct information processing performed by the two hippocampal segments and could effectively support the contribution
The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998
Long-term potentiation (LTP), a persistent enhancement of synaptic transmission that may be involved in some forms of learning and memory, is induced at excitatory synapses in the CA1 region of the hippocampus by coincident presynaptic and postsynaptic activity. Although action potentials back-propagating into dendrites of hippocampal pyramidal cells provide sufficient postsynaptic activity to induce LTP under some in vitro conditions, it is not known whether LTP can be induced by patterns of postsynaptic action potential firing that occur in these cells in vivo. Here we report that a characteristic in vivo pattern of action potential generation in CA1 pyramidal cells known as the complex spike burst enables the induction of LTP during theta frequency synaptic stimulation in the CA1 region of hippocampal slices maintained in vitro. Our results suggest that complex spike bursting may have an important role in synaptic processes involved in learning and memory formation, perhaps by pr...
Brain Research, 1992
The efficacy of stimulation patterns consisting of brief high frequency bursts repeated at various intervals to induce long-term potentiation (LTP) at synapses on apical and basai dendrites of CA1 hippocampal neurons was tested in vitro. Both apical and basai dendritic synapses exhibited maximal LTP after bursts repeated at 5-10 Hz, i.e. elose to the frequency of the endogenous hippocampal theta rhythm. As at apical dendritic synapses, LTP at basai dendritic synapses was blocked by an antagonist of NMDA receptors. Basai dendritic LTP was significantly greater in magnitude than apical dendritic LTP, although the reason for this is unknown.
1997
The phenomenon of long-term potentiation is widely used as an experimental model of memory. An approach that has been used to study its underlying mechanisms is to analyse its interaction with presynaptic paired-pulse facilitation. Several studies found no evidence for an interaction in the CA1 hippocampal area, whereas other data, for example from quantal analysis, suggested that presynaptic mechanisms contribute to the maintenance of long-term potentiation. In the present study, initial slopes of field potentials in area CA1 were measured in rat hippocampal slices. ''Conventional'' long-term potentiation was induced by high-frequency (100 Hz) afferent tetanization of the testing input. ''Associative'' long-term potentiation was induced by combining lower frequency (40 Hz) tetanization of a testing input with high-frequency tetanization of a second input. The paired-pulse facilitation ratio decreased in the majority of experiments in which long-term potentiation was induced conventionally, but it decreased, increased or did not change after inducing associative potentiation. Decreases in the paired-pulse facilitation correlated inversely with the initial (pre-tetanic) facilitation ratio. A more detailed regression analysis suggests that this correlation results from two other correlations: (i) that between changes in paired-pulse facilitation and the magnitude of long-term potentiation, and (ii) that between initial paired-pulse facilitation and the magnitude of long-term potentiation. The first correlation prevailed during the initial 10 min following tetanization, while the second prevailed 40-60 min later.
Neurophysiological analysis of long-term potentiation in mammalian brain
Behavioural Brain Research, 1995
Long-term potentiation (LTP) is a persistent increase in postsynaptic response following a high-frequency presynaptic activation. Characteristic LTP features, including input specificity and associativity, make it a popular model to study memory mechanisms. Mechanisms of LTP induction and maintenance are briefly reviewed. Increased intracellular Ca 2+ concentration is shown to be critical for LTP induction. This increase is believed to be based on Ca 2 + influx secondary to activation of N-methyl-D-aspartate (NMDA) subtype of glutamate receptors. Existence of other sources of Ca 2 + increase and other critical factors is now becoming evident. They include voltage-dependent Ca 2 + channels, Ca 2 + intracellular stores, metabotropic glutamate receptors, 'modulatory' transmitters. An example of an involvement of voltage-dependent Ca 2 ÷ channels is potentiation induced by intracellular depolarizing pulses. LTP can be divided into decremental earlier (E-LTP) and non-decremental late (L-LTP) phases which explains some inconsistencies in studies of LTP mechanisms. E-LTP is suggested to be based on a transient increase in presynaptic release probabilities. A hypothesis is considered which explains L-LTP by suggesting that Ca 2 + activates structural changes leading to an increase in the synaptic gap resistance. This enhances positive synaptic electrical feedback and augments release probability. The hypothesis predicts specific morphological changes, synchronous transmitter release of two or several quanta in some central synapses and the amplification of such synchronization following LTP induction. Data are discussed which maintain these predictions.
Theory for Characterization of Hippocampal Long-Term Potentiation Induced by Time-Structured Stimuli
Journal of the Physical Society of Japan, 1997
We theoretically investigate long-term potentiation (LTP) in the hippocampus using a simple model of a neuron stimulated by three different time-structured input signals (regular, Markov, and chaotic). The synaptic efficacy change is described taking into account both N-methyl-D-aspartate (NMDA) and non-NMDA receptors. The experimental results are successfully explained by our neuron model, and the remarkable fact that the chaotic stimuli in the nonstationary regime produce the largest LTP is discussed.
Neuroscience Letters, 1999
Long-term potentiation (LTP) is a popular model for the synaptic changes that may occur during learning and memory; it involves a strengthening of synaptic response and is readily induced in the hippocampus, an area of the brain implicated in learning and memory. Previous research on LTP has focused on`early' components of the hippocampal circuitry, that is, the dentate gyrus and areas CA1 and CA3. This paper examines the plasticity of the CA1-subiculum pathway; we extend our previous work in this area demonstrating that the projection from area CA1 to subiculum sustains theta-patterned stimulus-induced LTP in vivo. We show that this pathway remains potentiated over a long period (3 h). Furthermore, once this projection is potentiated, it seems resistant to further episodes of high-frequency stimulation. We discuss the implications of these ®ndings for theories of hippocampal-cortical interaction during the biological consolidation of memory. q
NeuroReport, 1998
We examine here, for the first time, the nature of PPF in the CA1-subiculum projection. PPF peaks at a 5 0 ms interstimulus interval (ISI) and is evident at ISIs from 10 to 500 ms. There is no PPF effect at a 100 0 ms ISI. PPF decreases in magnitude post-LTP induction across the middle range of ISI values tested (30, 50 and 10 0 ms). There is a positive correlation between initial PPF values and LTP; this correlation increases as the ISI increases. Initial values and the change in PPF post-LTP are also negatively correlated . NeuroRepor t9: 4109-4113