Entorhinal inputs to hippocampal CA1 and dentate gyrus in the rat: a current-source-density study

1995 ◽  
Vol 73 (6) ◽  
pp. 2392-2403 ◽  
Author(s):  
L. S. Leung ◽  
L. Roth ◽  
K. J. Canning
Keyword(s):  
Dentate Gyrus ◽  
Cell Body ◽  
Granule Cells ◽  
Current Source ◽  
Pyramidal Cells ◽  
Short Latency ◽  
Current Source Density ◽  
Perforant Path ◽  
Stratum Radiatum ◽  
Source Density

1. Laminar profiles of the average evoked potentials and current-source-density analysis were used to study the input provided by the medial perforant path (PP) to the hippocampus in the urethan-anesthetized rat. 2. Stimulation of the PP activated an early latency sink in the middle molecular layer of the dentate gyrus (DG) and in the stratum lacunosum-moleculare in CA1. The DG current sink was generated by excitatory synaptic currents activated by the PP on dentate granule cells. In the normal rat, the peak current sink in the DG was typically five times greater than that of CA1. However, the CA1 sink could be distinguished from the DG sink in several ways: 1) it peaked when the DG sink was subsiding; 2) it showed paired-pulse facilitation, whereas the DG sink did not; and 3) in rats in which the DG was lesioned by local colchicine injection, the DG sink was reduced much more than the CA1 sink. 3. The PP afferents to CA1 required a slightly higher stimulus threshold (> 100 microA) for activation than those projecting to the DG granule cells (< 30 microA). The onset latency of the early CA1 sink (2.5 +/- 0.2 ms, mean +/- SE) was also slightly longer than that of the DG sink (1.7 +/- 0.1 ms), suggesting that the axons of entorhinal layer III cells that project to CA1 have a slightly lower conduction velocity than the axons of the layer II cells that project to the DG. 4. The short-latency current sink activated by the PP in the distal dendritic layers of CA1 was likely provided by excitatory currents at the distal apical dendrites of CA1 pyramidal cells. The accompanying current source was mainly confined to stratum radiatum and appeared not to involve the cell body layer. Thus the electrotonic current spread may not be effective enough to depolarize the cell body or axon hillock. Contribution of interneurons to the above source-sink profile is possible, with the provision that these interneurons must have dendritic processes that span strata radiatum and lacunosum moleculare. 5. Extracellular field recordings provided no evidence that PP evoked a short-latency (< 9 ms) CA1-generated population spike, even with the use of micropipettes filled with mM bicuculline. Similarly, unit recordings in CA1 revealed only long-latency (9-17 ms) unit firing after PP stimulation, corresponding to a late, di/trisynaptic excitation of CA1 via the Schaffer collaterals.(ABSTRACT TRUNCATED AT 400 WORDS)

Hippocampal Interneurons Are Excited Via Serotonin-Gated Ion Channels

1997 ◽  
Vol 78 (5) ◽  
pp. 2493-2502 ◽  
Author(s):  
Lori L. McMahon ◽  
Julie A. Kauer
Keyword(s):  
Ion Channels ◽  
Synaptic Transmission ◽  
Dentate Gyrus ◽  
Granule Cells ◽  
Brain Slices ◽  
Pyramidal Cells ◽  
Stratum Radiatum ◽  
Negative Slope ◽  
Patch Clamp Recording ◽  
Gated Ion Channels

McMahon, Lori L. and Julie A. Kauer. Hippocampal interneurons are excited via serotonin-gated ion channels. J. Neurophysiol. 78: 2493–2502, 1997. Serotonergic neurons of the median raphe nucleus heavily innervate hippocampal GABAergic interneurons located in stratum radiatum of area CA1, suggesting that this strong subcortical projection may modulate interneuron excitability. Using whole cell patch-clamp recording from interneurons in brain slices, we tested the effects of serotonin (5-HT) on the physiological properties of these interneurons. Serotonin produces a rapid inward current that persists when synaptic transmission is blocked by tetrodotoxin and cobalt, and is unaffected by ionotropic glutamate and γ-aminobutyric acid (GABA) receptor antagonists. The 5-HT–induced current was independent of G-protein activation. Pharmacological evidence indicates that 5-HT directly excites these interneurons through activation of 5-HT3 receptors. At membrane potentials negative to −55 mV, the current-voltage ( I-V) relationship of the 5-HT current displays a region of negative slope conductance. Therefore the response of interneurons to 5-HT strongly depends on membrane potential and increases greatly as cells are depolarized. Removal of extracellular calcium, but not magnesium, increases the amplitude of 5-HT–induced currents and removes the region of negative slope conductance, thereby linearizing the I-V relationship. The axons of 5-HT–responsive interneurons ramify widely within CA1; some of these interneurons also project to and arborize extensively in the dentate gyrus. The organization of these inhibitory connections strongly suggests that these cells regulate excitability of both CA1 pyramidal cells and dentate granule cells. As our results indicate that 5-HT may mediate fast excitatory synaptic transmission onto these interneurons, serotonergic inputs can simultaneously modulate the output of both hippocampus and dentate gyrus.

scholarly journals Correction: Status Epilepticus Induced Spontaneous Dentate Gyrus Spikes: In Vivo Current Source Density Analysis

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0136125
Author(s):  
Sean P. Flynn ◽  
Sylvain Barriere ◽  
Rod C. Scott ◽  
Pierre-Pascal Lenck-Santini ◽  
Gregory L. Holmes
Keyword(s):  
Status Epilepticus ◽  
Dentate Gyrus ◽  
Current Source ◽  
Current Source Density ◽  
Source Density ◽  
Current Source Density Analysis ◽  
Density Analysis

scholarly journals Status Epilepticus Induced Spontaneous Dentate Gyrus Spikes: In Vivo Current Source Density Analysis

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0132630
Author(s):  
Sean P. Flynn ◽  
Sylvain Barrier ◽  
Rod C. Scott ◽  
Pierre-Pascal Lenck- Santini ◽  
Gregory L. Holmes
Keyword(s):  
Status Epilepticus ◽  
Dentate Gyrus ◽  
Current Source ◽  
Current Source Density ◽  
Source Density ◽  
Current Source Density Analysis ◽  
Density Analysis

Analysis of synaptic events in the opossum piriform cortex with improved current source-density techniques

1989 ◽  
Vol 61 (4) ◽  
pp. 702-718 ◽  
Author(s):  
R. Rodriguez ◽  
L. B. Haberly
Keyword(s):  
Piriform Cortex ◽  
Current Source ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Superficial Layer ◽  
Current Source Density ◽  
Membrane Currents ◽  
Source Density ◽  
Potential Component ◽  
Association Fibers

1. The piriform cortex of the opossum was studied by current source-density (CSD) analysis of field potentials to determine the laminar and temporal distribution of synaptic currents evoked by lateral olfactory tract (LOT) stimulation. 2. Extracellular conductivity was measured as a function of depth at high resolution and incorporated into CSD computations. Inclusion of the conductivity term resulted in relatively subtle changes in the shapes of CSD profiles. Resolution and accuracy of CSD computations was further improved by use of a new smoothing approach and averaging of multiple potential profiles obtained at the same site. 3. The CSD depth profile resulting from LOT stimulation revealed six major synaptic events that were consistently present at anterior, middle, and posterior sites: one during the first (A1) peak of the initial surface negative dichrotic field potential component, three during the second (B1) peak, one during the surface positive field potential component (period 2), and one during the second surface negative component (period 3). In addition, CSD profiles were computed for the population spike generated by synchronous discharge of action potentials. Depths of the net inward and outward membrane currents underlying these events were correlated with the cortical lamination as determined histologically by placement of small dye marks. 4. In agreement with previous reports it is concluded that the large inward membrane current in layer Ia during the A1 wave underlies a monosynaptic EPSP evoked in distal apical dendritic segments of pyramidal cells by afferent fibers. This EPSP displays a marked paired shock facilitation. 5. Based on anatomic and physiological considerations it is concluded that the three spatially and temporally distinct inward membrane currents (sinks) that were observed in layers III, superficial Ib, and mid- to deep-Ib during the B1 wave, underlie disynaptic EPSPs resulting from direct synaptic interactions between pyramidal cells. It is postulated that the layer III sink is generated in basal dendrites largely via local axon collaterals, the superficial layer Ib sink in intermediate apical dendritic segments by association fibers originating in the anterior piriform cortex, and the deep Ib sink in proximal apical segments by association fibers originating largely in the posterior piriform cortex. 6. The latencies of the layer Ia and superficial layer Ib sinks (presumed mono- and large disynaptic EPSPs, respectively) increased from anterior to posterior. Amplitude of the superficial Ib sink relative to the Ia sink increased from anterior to posterior.(ABSTRACT TRUNCATED AT 400 WORDS)

Current-Source Density Analysis in the Rat Olfactory Bulb: Laminar Distribution of Kainate/AMPA- and NMDA-Receptor-Mediated Currents

1999 ◽  
Vol 81 (1) ◽  
pp. 15-28 ◽  
Author(s):  
Vassiliki Aroniadou-Anderjaska ◽  
Matthew Ennis ◽  
Michael T. Shipley
Keyword(s):  
Nmda Receptor ◽  
Olfactory Bulb ◽  
Granule Cell ◽  
Granule Cells ◽  
Current Source ◽  
Field Potential ◽  
Current Source Density ◽  
Source Density ◽  
Tufted Cells ◽  
Apical Dendrites

Aroniadou-Anderjaska, Vassiliki, Matthew Ennis, and Michael T. Shipley. Current-source density analysis in the rat olfactory bulb: laminar distribution of kainate/AMPA- and NMDA-receptor-mediated currents. J. Neurophysiol. 81: 15–28, 1999. The one-dimensional current-source density method was used to analyze laminar field potential profiles evoked in rat olfactory bulb slices by stimulation in the olfactory nerve (ON) layer or mitral cell layer (MCL) and to identify the field potential generators and the characteristics of synaptic activity in this network. Single pulses to the ON evoked a prolonged (≥400 ms) sink (S1ON) in the glomerular layer (GL) with corresponding sources in the external plexiform layer (EPL) and MCL and a relatively brief sink (S2ON) in the EPL, reversing in the internal plexiform and granule cell layers. These sink/source distributions suggested that S1ON and S2ON were generated in the apical dendrites of mitral/tufted cells and granule cells, respectively. The kainate/AMPA-receptor antagonist CNQX (10 μM) reduced the early phase of S1ON, blocked S2ON, and revealed a low amplitude, prolonged sink at the location of S2ON in the EPL. Reduction of Mg2+, in CNQX, enhanced both the CNQX-resistant component of S1ON and the EPL sink. This EPL sink reversed below the MCL, suggesting it was produced in granule cells. The NMDA-receptor antagonist APV (50 μM) reversibly blocked the CNQX-resistant field potentials in all layers. Single pulses were applied to the MCL to antidromically depolarize the dendrites of mitral/tufted cells. In addition to synaptic currents of granule cells, a low-amplitude, prolonged sink (S1mcl) was evoked in the GL. Corresponding sources were in the EPL, suggesting that S1mcl was generated in the glomerular dendritic tufts of mitral/tufted cells. Both S1mcl and the granule cell currents were nearly blocked by CNQX (10 μM) but enhanced by subsequent reduction of Mg2+; these currents were blocked by APV. S1mcl also was enhanced by γ-aminobutyric acid-A-receptor antagonists applied to standard medium; this enhancement was reduced by APV. ON activation produces prolonged excitation in the apical dendrites of mitral/tufted cells, via kainate/AMPA and NMDA receptors, providing the opportunity for modulation and integration of sensory information at the first level of synaptic processing in the olfactory system. Granule cells respond to input from the lateral dendrites of mitral/tufted cells via both kainate/AMPA and NMDA receptors; however, in physiological concentrations of extracellular Mg2+, NMDA-receptor activation does not contribute significantly to the granule cell responses. The glomerular sink evoked by antidromic depolarization of mitral/tufted cell dendrites suggests that glutamate released from the apical dendrites of mitral/tufted cells may excite the same or neighboring mitral/tufted cell dendrites.

Changes in inhibitory neurotransmission in the CA1 region and dentate gyrus in a chronic model of temporal lobe epilepsy

1995 ◽  
Vol 74 (2) ◽  
pp. 829-840 ◽  
Author(s):  
P. S. Mangan ◽  
D. A. Rempe ◽  
E. W. Lothman
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Dentate Gyrus ◽  
Temporal Lobe ◽  
Granule Cells ◽  
Pyramidal Cells ◽  
Stratum Radiatum ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Stratum Lacunosum Moleculare ◽  
Reversal Potentials

1. In this report we compare changes in inhibitory neurotransmission within the CA1 region and the dentate gyrus (DG) in a model of chronic temporal lobe epilepsy (TLE). Extracellular and intracellular recordings were obtained in combined hippocampal-parahippocampal slices > or = 1 mo after a period of self-sustaining limbic status epilepticus (SSLSE) induced by continuous hippocampal stimulation. 2. Polysynaptic inhibitory postsynaptic potentials (IPSPs) were induced by positioning electrodes to activate specific afferent pathways and evoking responses in the absence of glutamate receptor antagonists [D(-)-2-amino-5-phosphonovaleric acid (APV) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)]. Polysynaptic IPSPs were evoked in CA1 pyramidal cells from electrodes positioned in stratum radiatum and in stratum lacunosum/moleculare. Polysynaptic IPSPs were evoked in DG granule cells from electrodes positioned over the perforant path located in the subiculum. Monosynaptic IPSPs were induced by positioning electrodes within 200 microns of the intracellular recording electrode (near site stimulation) and stimulating in the presence of APV and CNQX to block ionotropic glutamate receptors. Monosynaptic IPSPs were evoked in CA1 pyramidal cells with electrodes positioned in the stratum lacunosum/moleculare and stratum pyramidale. Monosynaptic IPSPs were evoked in DG granule cells with electrodes positioned in the stratum moleculare. 3. Population spike (PS) amplitudes were employed to assure that a full range of stimulus strengths, from subthreshold for action potentials to an intensity giving maximal-amplitude PSs, was used to elicit polysynaptic IPSPs in CA1 pyramidal cells in both post-SSLSE and control slices. In control tissue, polysynaptic IPSPs were biphasic, composed of early and late events. In post-SSLSE tissue, polysynaptic IPSPs were markedly diminished. The diminution of polysynaptic IPSPs was detected at all levels of stimulus intensity. Both early IPSPs [mediated by gamma-aminobutyric acid-A (GABAA) receptors] and late IPSPs (mediated by GABAB receptors) were diminished. Polysynaptic IPSPs were diminished with both stratum radiatum and with stratum lacunosum/moleculare stimulation. 4. Reversal potentials for either polysynaptic early or polysynaptic late IPSPs evoked in CA1 pyramidal cells by stratum radiatum stimulation were not different in slices from post-SSLSE animals as compared with control animals. Likewise, reversal potentials for either polysynaptic early or polysynaptic late IPSPs evoked by stratum lacunosum/moleculare stimulation did not differ in the two groups. These findings excluded changes in driving force as an explanation for the diminished amplitude of IPSPs in CA1 pyramidal cells in the post-SSLSE model.(ABSTRACT TRUNCATED AT 400 WORDS)

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