Postsynaptic responses of hippocampal neurons to mesencephalic stimulation: Depolarizing potentials and discharge patterns (original) (raw)
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Computer simulations of EPSP-spike (E-S) potentiation in hippocampal CA1 pyramidal cells.
Long-term potentiation of hippocampal excitatory synapses is often accompanied by an increase in the probability of spiking to an EPSP of fixed strength (E-S potentiation). We used computer simulations of a CA1 pyramidal neuron to test the plausibility of the hypothesis that E-S potentiation is caused by changes in dendritic excitability. These changes were simulated by adding "hot spots" of noninactivating voltage-sensitive Ca2+ conductance to various dendritic compartments. This typically caused spiking in response to previously subthreshold synaptic inputs. The magnitude of the simulated E-S potentiation depended on the passive electrical properties of the cell, the excitability of the soma, and the relative locations on the dendrites of the synaptic inputs and hot spots. The specificity of the simulated E-S potentiation was quantified by colocalizing the hot spots with a subset (40 of 80) of the synaptic contacts, denoted "tetanized," and then comparing the effects of the hot spots on these and the remaining (untetanized) synaptic contacts. The simulated E-S potentiation tended to be specific to the tetanized input if the untetanized contacts were, on average, electrically closer to the soma than the tetanized contacts. Specificity was also high if the tetanized and untetanized contacts were segregated to different primary dendrites. The results also predict, however, that E-S potentiation by this mechanism will appear to be nonspecific (heterosynaptic) if the synapses of the untetanized input are sufficiently far from the soma relative to the tetanized synapses. Experimental confirmation of this prediction would support the hypothesis that changes in postsynaptic excitability can contribute to hippocampal E-S potentiation.
Neuroscience, 1994
Long-term potentiation induced by high-frequency stimulation in the CA1 region of the hippocampus exhibits EPSP-spike potentiation. This consists of an increase in population spike amplitude exceeding that predicted by EPSP potentiation alone. This phenomenon is apparently due to an increase in pyramidal cell excitability. Patterns of afferent stimuli which activate pyramidal cells to reproduce the theta rhythm observed in the hippocampus under physiological conditions, have been shown to induce LTP-like enhancement of synaptic responses in vitro. The aim of this study was to investigate the presence of EPSP-spike potentiation and/or changes in pyramidal cell excitability during the long-term potentiation induced in the CA1 region of rat hippocampal slices by theta-like patterns of stimuli: the primed burst and the patterned stimulation. Using extracellular recording, a significant leftward shift in the EPSP-spike relationship was found 30 min after primed burst or patterned stimulation. The magnitude of EPSP-spike potentiation induced by patterned stimulation was similar to that produced by high-frequency stimulation. Both were significantly greater than that induced by a primed burst, indicating that only a subset of pyramidal cells were potentiated by this kind of afferent activation. Modifications in synaptic efficacy and cell excitability brought about by a primed burst were investigated in 25 intracellularly recorded pyramidal cells.
EPSP Amplification and the Precision of Spike Timing in Hippocampal Neurons
Neuron, 2000
pathetic ganglion cells (Cassell and McLachlan, 1986) and in granule cells of the olfactory bulb (Schoppa and 25 rue de Dr Roux 75724 Paris Westbrook, 1999). EPSP shaping by postsynaptic conductances is im-France portant in the integration of subthreshold synaptic signals. In pyramidal cells, for instance, EPSP amplification augments the efficacy of dendritic synapses, so com-Summary pensating for an attenuation of distal events (Andreasen and Lambert, 1998). However, signaling at excitatory The temporal precision with which EPSPs initiate acsynapses also comprises a graded dimension of infortion potentials in postsynaptic cells determines how mation coding that lies in the variability in timing of activity spreads in neuronal networks. We found that synaptically induced firing. At some junctions, including small EPSPs evoked from just subthreshold potentials the Calyx of Held synapse (Brew and Forsythe, 1995) initiated firing with short latencies in most CA1 hippoand synapses terminating on other auditory neurons campal inhibitory cells, while action potential timing (Koyano et al., 1996) and on spinal motoneurons (Fetz in pyramidal cells was more variable due to plateau
The Journal of Physiology, 1998
1. Dual intracellular recordings in the CA1 region of adult rat hippocampal slices and biocytin filling of synaptically connected cells were used to study the excitatory postsynaptic potentials (EPSPs) elicited in basket (n = 7) and bistratified interneurones (n = 7) by action potentials activated in simultaneously recorded pyramidal cells. 2. Interneurones could be subdivided according to their electrophysiological properties into classical fast spiking, burst firing, regular spiking and fast spiking cells with a rounded spike after-hyperpolarization. These physiological classes did not, however, correlate with morphological type. EPSPs were not recorded in regular spiking cells. 3. Average EPSP amplitudes were larger in bistratified cells (range, 0•5-9 mV) than in basket cells (range, 0•15-3•6 mV) and the probability of obtaining a pyramidal cell-interneurone EPSP was also higher for the bistratified cells (1:7) than for the basket cells (1:22). EPSP 10-90% rise times in bistratified cells (0•7-2 ms) and their widths at half-amplitude (3•9-11•2 ms) were slightly longer than in basket cells (rise times, 0•4-1•6 ms; half-widths, 2•2-9•7 ms). 4. The majority of these EPSPs (6 of 8 tested) increased in amplitude and duration with postsynaptic depolarization, although in two (of 4) basket cells the voltage relation was conventional. 5. All EPSPs tested in both basket (n = 7) and bistratified cells (n = 5) decreased in amplitude with repetitive presynaptic firing. The average amplitudes of second EPSPs elicited within 15 ms of the first were between 34 and 94% of the average amplitude of the first EPSP. Third and fourth EPSPs in brief trains were further depressed. This depression was associated with an increase in the incidence of apparent failures of transmission indicating a presynaptic locus.
Experimental Neurology, 1983
The mechanisms of paired-pulse potentiation of the CA 1 pyramidal cell population were examined by determining input-output relations for control and potentiated responses originating from the activation of radiatum fibers in the hippocampal slice preparation. Two types of potentiation for synchronously discharging pyramidal cells (population spike) were observed. In the first type, the potentiation of the population spike was found to be a combination of synaptic and extrasynaptic factors. This form of potentiation was observed in 16 of 28 slices. In the second type, the potentiation of the population spike was attributed entirely to the potentiation of summated dendritic depolarizations (population EPSP). This synaptic process of potentiation was observed in 12 of 28 slices. The involvement of only extrasynaptic mechanisms in the paired-pulse potentiation of the population spike was not observed. For the potentiation originating from a combination of synaptic and extrasynaptic mechanisms, 60% of the potentiation of the population spike was a result of synaptic factors and 40% could be attributed to extrasynaptic factors. These results support the concept that alterations in the excitability of postsynaptic neurons serve as a component of the mechanisms of paired-pulse potentiation in the radiatum fiber-CA1 pyramidal cell system.
Neuroscience, 1998
In the CA1 area of the hippocampus, low frequency and tetanic conditioning stimuli are known to trigger long-term depression and potentiation of synaptic responses respectively and to produce irreversible excitatory postsynaptic potential/spike potentiation, i.e. an increase of the probability of discharge of the neurons. Using simultaneous extracellular recordings in stratum radiatum and stratum pyramidale in the CA1 area of the rat hippocampus, brief application of the K + channel blocker tetraethylammonium resulted both in long-term potentiation of synaptic responses and in excitatory postsynaptic potential/spike potentiation that could be reversed by subsequent low frequency or tetanic stimuli. Excitatory postsynaptic potential/spike potentiation and its subsequent reversal by an electrical conditioning stimulus were found to have an N-methyl--aspartate receptor-independent component. We conclude that the reversal of excitatory postsynaptic potential/spike potentiation can occur and that it does not require the induction of long-term modification of synaptic responses. 1998 IBRO.
Quantal analysis of paired-pulse facilitation in guinea pig hippocampal slices
Neuroscience Letters, 1987
Intracellular excitatory postsynaptic potentials (EPSPs) were recorded in area CA~ of hippocampal slices from guinea pigs. With paired-pulse stimulation of stratum radiatum, the second stimulus (interval of 40 50 ms) produced an EPSP with enlarged amplitude. Two methods of quantal analysis showed an increase in quantal content of the facilitated EPSP and a smaller increase in quantal size. The correlation between amplitudes of the first and second EPSP was usually insignificant. The results favour a presynaptic location of the mechanisms of the paired-pulse facilitation and suggest increases in the average of transmitter quanta released by presynaptic volley as well as increases in the amount of transmitter in each quantum. Paired-pulse facilitation (PPF) is an increase in amplitude of the second excitatory postsynaptic potential (EPSP) with paired stimulation [5]. Quantal analysis was applied to PPF at neuromuscular and spinal cord synapses [5, 8, 9, 19] and an increase was shown in the mean quantal content (m) without changes in the quantal size (v). The result was considered a strong support for a presynaptic location of the underlying mechanisms. PPF is particularly prominent for hippocampal responses [1, 4, 10], but quantal analysis was used only in a few studies. Principally m was found to be changed in EPSPs evoked by near-threshold stimuli in the hippocampus of unanaesthetized rabbits but v also increased [2, 14, 16, 17]. However, the number of neurones studied was small, a single method of quantal analysis was used, and some features of the stimulation procedure might suggest influences of inhibitory PSPs on v estimation. The slice preparation provides a better possibility for quantal analysis. With recordings of EPSPs, presumably elicited by activation of single mossy fibers, Yamamoto [18] found increase in m in 3 CA3 neurones without changes in v. This author used Poisson equations which can influence the estimate of v changes [2, 14]. The aim of the present study was to reconsider mechanisms of PPF using the slice prepa