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Hippocampal CA1 Pyramidal Cells (hippocampal + ca1_pyramidal_cell)
Selected AbstractsRegulated expression of HCN channels and cAMP levels shape the properties of the h current in developing rat hippocampusEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2006Rainer Surges Abstract The hyperpolarization-activated current (Ih) contributes to intrinsic properties and network responses of neurons. Its biophysical properties depend on the expression profiles of the underlying hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels and the presence of cyclic AMP (cAMP) that potently and differentially modulates Ih conducted by HCN1, HCN2 and/or HCN4. Here, we studied the properties of Ih in hippocampal CA1 pyramidal cells, the developmental evolution of the HCN-subunit isoforms that contribute to this current, and their interplay with age-dependent free cAMP concentrations, using electrophysiological, molecular and biochemical methods. Ih amplitude increased progressively during the first four postnatal weeks, consistent with the observed overall increased expression of HCN channels. Activation kinetics of the current accelerated during this period, consonant with the quantitative reduction of mRNA and protein expression of the slow-kinetics HCN4 isoform and increased levels of HCN1. The sensitivity of Ih to cAMP, and the contribution of the slow component to the overall Ih, decreased with age. These are likely a result of the developmentally regulated transition of the complement of HCN channel isoforms from cAMP sensitive to relatively cAMP insensitive. Thus, although hippocampal cAMP concentrations increased over twofold during the developmental period studied, the coordinated changes in expression of three HCN channel isoforms resulted in reduced effects of this signalling molecule on neuronal h currents. [source] Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapsesHIPPOCAMPUS, Issue 10 2006Tatiana Kovalenko Abstract Relatively mild ischemic episode can initiate a chain of events resulting in delayed cell death and significant lesions in the affected brain regions. We studied early synaptic modifications after brief ischemia modeled in rats by transient vessels' occlusion in vivo or oxygen,glucose deprivation in vitro and resulting in delayed death of hippocampal CA1 pyramidal cells. Electron microscopic analysis of excitatory spine synapses in CA1 stratum radiatum revealed a rapid increase of the postsynaptic density (PSD) thickness and length, as well as formation of concave synapses with perforated PSD during the first 24 h after ischemic episode, followed at the long term by degeneration of 80% of synaptic contacts. In presynaptic terminals, ischemia induced a depletion of synaptic vesicles and changes in their spatial arrangement: they became more distant from active zones and had larger intervesicle spacing compared to controls. These rapid structural synaptic changes could be implicated in the mechanisms of cell death or adaptive plasticity. Comparison of the in vivo and in vitro model systems used in the study demonstrated a general similarity of these early morphological changes, confirming the validity of the in vitro model for studying synaptic structural plasticity. © 2006 Wiley-Liss, Inc. [source] Analysis and comparison of morphological reconstructions of hippocampal field CA1 pyramidal cellsHIPPOCAMPUS, Issue 3 2005José Ambros-Ingerson Abstract Morphological reconstructions have become a routine and valuable tool for neuroscientists. The accuracy of reconstructions is a matter of considerable interest given that they are widely used in computational studies of neural function. Despite their wide usage, comparisons of reconstructions obtained using various methodologies are lacking. We reviewed reconstructions of hippocampal CA1 pyramidal cells from five published studies and found marked differences in some of the most basic measurements. For four of the five studies means of total cell length clustered in the 11,479,13,417-,m range. The remaining study had a significantly larger value for this index at 16,992 ± 5,788 ,m. Surface area means varied more than 4-fold from 16,074 to 67,102 ,m2. Volume means varied more than 8-fold from 3,828 to 30,384 ,m3. Simulated passive input resistance means varied from 38.0 to 172.1 M,, reflecting the variability in cell dimensions. Estimates of the electrotonic length varied from 1.26 to 1.56. In two reconstructions used in previously published studies, simulated somatic excitatory postsynaptic potentials (EPSPs) varied 2,4-fold in amplitude, time to peak and half-width, for synaptic inputs at similar locations. Substantial jitter on the z -axis was identified as one likely source of the discrepancy in total cell length, while substantial differences in diameter measurements across studies, and sometimes within the same study, accounted for the variability in surface area and volume. While some part of the observed variability is surely due to the diversity of CA1 pyramidal cells, our analysis suggests that a substantial portion stemmed from methodological inconsistencies and from technological limitations. Suggestions are made for improving the quality and usefulness of morphological reconstructions. We conclude that reconstructions across studies have substantial variability in measures that are very relevant to neuronal function. Consequently, modelers are advised to use more than just one reconstructed cell in their simulations of neural function. © 2004 Wiley-Liss, Inc. [source] Bi-directional modulation of fast inhibitory synaptic transmission by leptinJOURNAL OF NEUROCHEMISTRY, Issue 1 2009Natasha Solovyova Abstract The hormone leptin has widespread actions in the CNS. Indeed, leptin markedly influences hippocampal excitatory synaptic transmission and synaptic plasticity. However, the effects of leptin on fast inhibitory synaptic transmission in the hippocampus have not been evaluated. Here, we show that leptin modulates GABAA receptor-mediated synaptic transmission onto hippocampal CA1 pyramidal cells. Leptin promotes a rapid and reversible increase in the amplitude of evoked GABAA receptor-mediated inhibitory synaptic currents (IPSCs); an effect that was paralleled by increases in the frequency and amplitude of miniature IPSCs, but with no change in paired pulse ratio or coefficient of variation, suggesting a post-synaptic expression mechanism. Following washout of leptin, a persistent depression (inhibitory long-lasting depression) of evoked IPSCs was observed. Whole-cell dialysis or bath application of inhibitors of phosphoinositide 3 (PI 3)-kinase or Akt prevented leptin-induced enhancement of IPSCs indicating involvement of a post-synaptic PI 3-kinase/Akt-dependent pathway. In contrast, blockade of PI 3-kinase or Akt activity failed to alter the ability of leptin to induce inhibitory long-lasting depression, suggesting that this process is independent of PI 3-kinase/Akt. In conclusion these data indicate that the hormone leptin bi-directionally modulates GABAA receptor-mediated synaptic transmission in the hippocampus. These findings have important implications for the role of this hormone in regulating hippocampal pyramidal neuron excitability. [source] | ||||||||||