Interaction of GABAB-Mediated Inhibition With Voltage-Gated Currents of Pyramidal Cells: Computational Mechanism of a Sensory Searchlight

1998 ◽  
Vol 80 (6) ◽  
pp. 3197-3213 ◽  
Author(s):  
Neil J. Berman ◽  
Leonard Maler
Keyword(s):  
Bipolar Cell ◽  
Excitatory Amino Acid ◽  
Maximum Amplitude ◽  
Pyramidal Cells ◽  
Inhibitory Effect ◽  
Bipolar Cells ◽  
Postsynaptic Potentials ◽  
Voltage Gated ◽  
Conditional Inhibition

Berman, Neil J. and Leonard Maler. Interaction of GABAB-mediated inhibition with voltage-gated currents of pyramidal cells: computational mechanism of a sensory searchlight. J. Neurophysiol. 80: 3197–3213, 1998. This study examines, in the in vitro electrosensory lateral line lobe (ELL) slice preparation, mono- and disynaptic inhibition in pyramidal cells evoked by stimulation of the direct descending pathway from nucleus praeminentialis (Pd). The pathway forms the stratum fibrosum (StF) in the ELL and consists of excitatory fibers from Pd stellate cells that make monosynaptic contact with pyramidal cells and disynaptic inhibitory contacts via local interneurons and of GABAergic inhibitory fibers from Pd bipolar cells. Single or tetanic stimulation (physiological rates of 100–200 Hz) of the StF produced excitatory postsynaptic potentials (EPSPs) or compound EPSPs in ELL pyramidal cells. Slow (>600 ms) and fast inhibitory postsynaptic potentials (IPSPs; 5–50 ms) also were evoked. Application of γ-aminobutyric acid-A (GABAA) antagonists blocked the fast inhibition and dramatically increased the firing rate response to StF tetanic stimuli. GABAA antagonists also increased the amplitude of the slow IPSP. The slow IPSP was reduced by GABAB antagonists. Blockade of excitatory amino acid (EAA) synaptic transmission allowed the monosynaptic bipolar-cell-mediated inhibition to be studied in isolation: EAA antagonists blocked most of the EPSP response to StF stimulation leaving fast and (an increased amplitude) slow IPSP components. The bipolar-cell IPSPs were mediated by GABAA and GABAB receptors as they were sensitive to GABAA and GABAB antagonists. The bipolar-cell IPSPs scaled with stimulation rate (20–400 Hz), reaching a maximum amplitude at 200 Hz. Inhibitory efficacy of bipolar-cell slow IPSPs were tested by their ability to reduce spiking in the face of sustained or brief current pulses. Established spike trains (by sustained injected current) were little affected by the onset of the slow IPSP. Weak brief currents injected during the slow IPSP were strongly inhibited. Strong brief currents could overcome the slow IPSP inhibitory effect. Inhibition was observed to interact with the intrinsic I A-like K+ currents to produce a complex control of cell spiking. Hyperpolarizing inhibition removes inactivation of I A to prevent subsequent inputs from driving the cell to threshold. Established depolarizing inputs, having allowed I A to inactivate, enable the cell to be highly sensitive to further depolarizing input. The term “conditional inhibition” is proposed to describe the general phenomenon where synaptic inhibition interacts with voltage-sensitive intrinsic currents.

scholarly journals Glutamatergic Propagation of GABAergic Seizure-Like Afterdischarge in the Hippocampus In Vitro

2003 ◽  
Vol 90 (4) ◽  
pp. 2746-2751 ◽  
Author(s):  
Yoshikazu Isomura ◽  
Yoko Fujiwara-Tsukamoto ◽  
Masahiko Takada
Keyword(s):  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
In Vitro Study ◽  
Pyramidal Cells ◽  
Inhibitory Effect ◽  
Experimental Models ◽  
Fluoride Ions ◽  
Ca1 Region ◽  
Cortical Regions

Previous investigations have suggested that GABA may act actively as an excitatory mediator in the generation of seizure-like (ictal) or interictal epileptiform activity in several experimental models of temporal lobe epilepsy. However, it remains to be known whether or not such GABAergic excitation may participate in seizure propagation into neighboring cortical regions. In our in vitro study using mature rat hippocampal slices, we examined the cellular mechanism underlying synchronous propagation of seizure-like afterdischarge in the CA1 region, which is driven by depolarizing GABAergic transmission, into the adjacent subiculum region. Tetanically induced seizure-like afterdischarge was always preceded by a GABAergic, slow posttetanic depolarization in the pyramidal cells of the original seizure-generating region. In contrast, the slow posttetanic depolarization was no longer observed in the subicular pyramidal cells when the afterdischarge was induced in the CA1 region. Surgical cutting of axonal pathways through the stratum oriens and the alveus between the CA1 and the subiculum region abolished the CA1-generated afterdischarge in the subicular pyramidal cells. Intracellular loading of fluoride ions, a GABAA receptor blocker, into single subicular pyramidal cells had no inhibitory effect on the CA1-generated afterdischarge in the pyramidal cells. Furthermore, the CA1-generated afterdischarge in the subicular pyramidal cells was largely depressed by local application of glutamate receptor antagonists to the subiculum region during afterdischarge generation. The present results indicate that the excitatory GABAergic generation of seizure-like activity seems to be restricted to epileptogenic foci of origin in the seizure-like epilepsy model in vitro.

Neural architecture of the electrosensory lateral line lobe: adaptations for coincidence detection, a sensory searchlight and frequency-dependent adaptive filtering

1999 ◽  
Vol 202 (10) ◽  
pp. 1243-1253 ◽  
Author(s):  
N.J. Berman ◽  
L. Maler
Keyword(s):  
Lateral Line ◽  
Activity Patterns ◽  
Pyramidal Cells ◽  
Coincidence Detection ◽  
Weakly Electric Fish ◽  
In Vivo Studies ◽  
Frequency Dependent ◽  
Postsynaptic Potentials

The electrosensory lateral line lobe (ELL) of weakly electric fish is the only nucleus that receives direct input from peripheral electroreceptor afferents. This review summarises the neurotransmitters, receptors and second messengers identified in the intrinsic circuitry of the ELL and the extrinsic descending direct and indirect feedback pathways, as revealed by recent in vitro and in vivo studies. Several hypotheses of circuitry function are examined on this basis and on the basis of recent functional evidence: (1) fast primary afferent excitatory postsynaptic potentials (EPSPs) and fast granule cell 2 GABAA inhibitory postsynaptic potentials (IPSPs) suggest the involvement of basilar pyramidal cells in coincidence detection; (2) voltage-dependent EPSPs and IPSPs, dendritic spike bursts and frequency-dependent synaptic facilitation support a sensory searchlight role for the direct feedback pathway; and (3) the contributions of distal and proximal inhibition, anti-Hebbian plasticity and beam versus isolated fiber activity patterns are discussed with reference to an adaptive spatio-temporal filtering role for the indirect descending pathway.

scholarly journals VOLTAGE-GATED POTASSIUM CHANNELS CONTROL THE GAIN OF ROD-DRIVEN LIGHT RESPONSES IN MIXED-INPUT ON BIPOLAR CELLS

2020 ◽  
Author(s):  
Christina Joselevitch ◽  
Jan Klooster ◽  
Maarten Kamermans
Keyword(s):  
Potassium Channels ◽  
Bipolar Cell ◽  
Gain Control ◽  
Bipolar Cells ◽  
Transient Signal ◽  
List Type ◽  
Light Responses ◽  
Voltage Gated ◽  
Light Levels ◽  
Slow Kinetics

AbstractTo achieve high sensitivity at scotopic levels, vision sacrifices spatial and temporal resolution. The detection of dim light, however, depends crucially on the ability of the visual system to speed up rod signals as they advance towards the brain. At higher light levels, gain control mechanisms are necessary to prevent premature saturation of second-order neurons. We investigated how goldfish mixed-input ON bipolar cells (ON mBCs) manage to partially compensate for the intrinsically slow kinetics of rod signals in the dark-adapted state, and at the same time control the gain of rod signals. Rod-driven responses of axotomized ON mBCs become faster and more transient than those of rod horizontal cells as stimulus intensity increases. This transientness has a voltage-dependency consistent with the activation of a voltage-gated K+ conductance. Simulations with NEURON indicate that the voltage-gated K+ channels responsible for speeding up responses are concentrated at the distal tips of the bipolar cell dendrites, close to the glutamate receptors. These channels act as a gain control mechanism, by shunting the effect of tonically hyperpolarized rods onto the ON mBC. Further activation of K+ channels accelerates the ON mBC response by decreasing the membrane time constant as light levels increase. Therefore, the presence of voltage-gated K+ channels at the dendritic tips of ON mBCs extends the dynamic range of these neurons, and at the same time generates a transient signal already at the first visual synapse.Key Points SummaryHere we show that voltage-gated potassium channels can adjust the gain of the rod input to mixed-input ON bipolar cells and generate a transient signal already at the first visual synapse.These channels are activated during the light-induced depolarization, making bipolar cell light responses smaller, faster, and more transient, effects that can be abolished by the K+ channel blocker TEA.Mathematical simulations suggest that these channels are concentrated at the bipolar cell dendritic tips, close to the site of rod input.This kind of gain control happens at all levels in the retina and is especially important for cells that receive mixed input from rods and cones, in order to prevent premature saturation with increasing light levels and remove the temporal redundancy of the photoreceptor signal.

scholarly journals Retinal Bipolar Cell Input Mechanisms in Giant Danio. III. on-off Bipolar Cells and Their Color-Opponent Mechanisms

2005 ◽  
Vol 94 (1) ◽  
pp. 265-272 ◽  
Author(s):  
Kwoon Y. Wong ◽  
John E. Dowling
Keyword(s):  
Glutamate Receptors ◽  
Bipolar Cell ◽  
Excitatory Amino Acid ◽  
Bipolar Cells ◽  
Kainate Receptors ◽  
Kainate Receptor ◽  
Evoked Responses ◽  
Excitatory Amino Acid Transporter ◽  
Cell Components ◽  
Giant Danio

Whole cell patch recording was performed from morphologically identified cone-driven on-off bipolar cells (Cabs) in giant danio retinal slices to study their glutamate receptors and light-evoked responses. Specific agonists were puffed in the presence of cobalt, picrotoxin, and strychnine to identify glutamate receptors on these cells. Most Cabs responded to both the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate receptor agonist kainate and the excitatory amino acid transporter (EAAT) substrate d-aspartate, and both responses were localized to the dendrites. Kainate generated depolarizations whereas d-aspartate had Erev close to ECl and generated hyperpolarizations, indicating that the AMPA/kainate receptors are sign-preserving, whereas the EAATs are sign-inverting. In response to white light, some Cabs gave on bipolar cell-like responses whereas others gave off bipolar cell-like ones, but many cells' responses had both on and off bipolar cell components. In response to appropriately colored center-selective stimuli, many Cabs responded to short and long wavelengths with opposite polarities and were thus double color-opponent. The depolarizing components of the responses to white or colored stimuli were suppressed by the EAAT blocker dl- threo-β-benzyloxyaspartate (TBOA), whereas the hyperpolarizing components were reduced by the AMPA/kainate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX). These results are consistent with the hypothesis that both EAATs and AMPA/kainate receptors are involved in the generation of light-evoked responses in Cabs and that they confer these cells with on and off bipolar cell properties, respectively. Cabs can generate double color-opponent center responses by receiving inputs from certain cones through EAATs and from other cones through AMPA/kainate receptors.

Retinal Bipolar Cell Input Mechanisms in Giant Danio. I. Electroretinographic Analysis

2005 ◽  
Vol 93 (1) ◽  
pp. 84-93 ◽  
Author(s):  
Kwoon Y. Wong ◽  
Alan R. Adolph ◽  
John E. Dowling
Keyword(s):  
Bipolar Cell ◽  
Metabotropic Glutamate Receptor ◽  
Excitatory Amino Acid ◽  
Bipolar Cells ◽  
Kainate Receptors ◽  
Excitatory Amino Acid Transporter ◽  
Group Iii ◽  
Metabotropic Glutamate ◽  
Giant Danio ◽  
D Wave

Electroretinograms (ERGs) were recorded from the giant danio ( Danio aequipinnatus) to study glutamatergic input mechanisms onto bipolar cells. Glutamate analogs were applied to determine which receptor types mediate synaptic transmission from rods and cones to on and off bipolar cells. Picrotoxin, strychnine, and tetrodotoxin were used to isolate the effects of the glutamate analogs to the photoreceptor–bipolar cell synapse. Under photopic conditions, the group III metabotropic glutamate receptor (mGluR) antagonist (RS)-α-cyclopropyl-4-phosphonophenylglycine (CPPG) only slightly reduced the b-wave, whereas the excitatory amino acid transporter (EAAT) blocker dl- threo-β-benzyl-oxyaspartate (TBOA) removed most of it. Complete elimination of the b-wave required both antagonists. The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate receptor antagonist 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX) blocked the d-wave. Under scotopic conditions, rod and cone inputs onto on bipolar cells were studied by comparing the sensitivities of the b-wave to photopically matched green and red stimuli. The b-wave was >1 log unit more sensitive to the green than to the red stimulus under control conditions. In CPPG or l-AP4 (l-(+)-2-amino-4-phosphonobutyric acid, a group III mGluR agonist), the sensitivity of the b-wave to the green stimulus was dramatically reduced and the b-waves elicited by the 2 stimuli became nearly matched. The d-wave elicited by dim green stimuli, which presumably could be detected only by the rods, was eliminated by NBQX. In conclusion: 1) cone signals onto on bipolar cells involve mainly EAATs but also mGluRs (presumably mGluR6) to a lesser extent; 2) rods signal onto on bipolars by mainly mGluR6; 3) off bipolar cells receive signals from both photoreceptor types by AMPA/kainate receptors.

Role of synaptic excitation in the generation of bursting-induced epileptiform potentials in the endopiriform nucleus and piriform cortex

1993 ◽  
Vol 70 (6) ◽  
pp. 2550-2561 ◽  
Author(s):  
W. H. Hoffman ◽  
L. B. Haberly
Keyword(s):  
Amino Acid ◽  
Positive Feedback ◽  
Excitatory Amino Acid ◽  
Piriform Cortex ◽  
Receptor Activation ◽  
Population Activity ◽  
Postsynaptic Potentials ◽  
Slow Onset ◽  
Bursting Activity

1. The mechanism of generation of epileptiform excitatory postsynaptic potentials (e-EPSPs) induced by bursting activity in vitro was examined in slices of piriform cortex. 2. Previous study revealed that e-EPSPs in piriform cortex are generated in the subjacent endopiriform nucleus, perhaps with a contribution from the claustrum and deep part of layer III of piriform cortex. A puzzling feature of these e-EPSPs was their abrupt origin at long latency with little sign of preceding abnormal activity. 3. Systematic mapping revealed that within spatially restricted regions of the endopiriform nucleus there is an irregular buildup in extracellularly recorded multiunit activity and intracellularly recorded depolarization that precedes the onset of e-EPSPs. Analysis of latency revealed that these “slow-onset” e-EPSPs precede the more widely distributed “abrupt-onset” e-EPSPs, suggesting that they occur at sites of initiation. 4. The hypothesis was tested that the buildup associated with slow-onset e-EPSPs is dependent on synaptically mediated excitation. According to this hypothesis, all-or-none e-EPSPs originate when mutually excitatory (positive feedback) interactions within a population of cells in the endopiriform nucleus become self-regenerative. 5. Predictions from the regenerative positive feedback hypothesis that were successfully verified include the presence of excitatory synaptic connections between cells in the endopiriform nucleus; the consistent prediction of a subsequent e-EPSP from the occurrence of the accelerating buildup in population activity; the occurrence of inhibitory postsynaptic potentials (IPSPs) together with EPSPs during the buildup period; and the blockage of the buildup and e-EPSP by a low concentration of a specific excitatory amino acid antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX). 6. Blockage of e-EPSPs by a concentration of DNQX that was much less than that required to block monosynaptic EPSPs in the endopiriform nucleus indicates that synaptic reverberation is mediated by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) type excitatory amino acid receptors. 7. D-2-amino-5-phosphonovaleric acid (D-APV) reduced the duration and amplitude of e-EPSPs but did not block their occurrence, indicating that N-methyl-D-aspartate (NMDA) receptors have a boosting effect on e-EPSPs but are not required for their generation. This is in contrast to the induction of e-EPSPs by bursting activity for which NMDA receptor activation is required. 8. Outside the region of initiation e-EPSPs propagated through the endopiriform nucleus at a velocity of 0.1 m/s.(ABSTRACT TRUNCATED AT 400 WORDS)

Single cell shape and population densities of indoleamine-accumulating and displaced bipolar cells in Reeves' turtle retina

1990 ◽  
Vol 238 (1293) ◽  
pp. 351-367 ◽  
Keyword(s):  
Cell Density ◽  
Bipolar Cell ◽  
Lucifer Yellow ◽  
Outer Nuclear Layer ◽  
Bipolar Cells ◽  
Cell Labelling ◽  
Specific Cell ◽  
Inner Plexiform Layer ◽  
Central Retina

Two types of bipolar cell in the Geoclemys reevesii retina were studied quantitatively by means of specific cell labelling with an indoleamine derivative (5, 6-dihydroxytryptamine, 5, 6-DHT), a nucleic acid stain (4, 6-diamidino-2-phenylindole, DAPI) and Lucifer yellow CH. Indoleamine-accumulating (IA ) bipolar cells were selectively labelled with 5, 6-DHT applied intraocularly. After the cells accumulated 5, 6-DHT, the indoleamine fluorescence was photoconverted to diaminobenzidine products to allow observation of morphological details. Close examination of many cells (cell number; n = 120) showed that the IA bipolar cells consist of a single morphological type whose axon collaterals ramify sublaminae 1, 4 and 5 respectively. This terminal branching pattern corresponds to cells that hyperpolarize when their receptive field centres are illuminated (Weiler 1981). The density of IA bipolar cells was highest in the visual streak (4130 cells mm -2 ) and lowest at the peripheral margin (1970 cells mm -2 ). By applying a small amount of DAPI to the eye, nuclei located in the most proximal row of the outer nuclear layer were labelled selectively. By using selective intracellular dye injection into DAPI-labelled cells under fluorescence microscope (Tauchi & Masland 1984, 1985), these cells were found to have Landolt’s clubs and single descending axons. Dye injections into more than fifty DAPI-labelled somata showed that they belonged exclusively to displaced bipolar cells. These comprised at least two subtypes that differ in the ramification pattern of their axon terminals within the inner plexiform layer: one was monostratified, whereas the other was bistratified. The displaced bipolar cell density was as high as 9400 cells mm -2 in the central retina, falling to 2000 cells mm -2 in the superior margin. In vitro Lucifer labelling revealed that the overall bipolar cell density in the central retina was as high as 39300 cells mm -2 . Both the conventionally located and displaced bipolar cells were included in this population. About 11% of the total bipolar cell population consisted of IA bipolar cells. Assuming that one half of the conventionally located bipolar cells are the centre-hyperpolarizing type, IA bipolar cells represent approximately 28% of the total. As displaced bipolar cells represent almost one quarter of the total bipolar population, the dislocation of their somata stands out morphologically, inviting investigation of possible functional correlates.

Zinc enhances GABAergic transmission in rat neocortical neurons

1993 ◽  
Vol 70 (3) ◽  
pp. 1264-1269 ◽  
Author(s):  
F. M. Zhou ◽  
J. J. Hablitz
Keyword(s):  
Action Potentials ◽  
Excitatory Amino Acid ◽  
Input Resistance ◽  
Synaptic Activity ◽  
Membrane Properties ◽  
Repetitive Firing ◽  
Resting Membrane Potential ◽  
Gamma Aminobutyric Acid ◽  
Postsynaptic Potentials

1. Intracellular recordings were made in layer II-III neurons of rat neocortical slices maintained in vitro. The effect of bath application of zinc (50-300 microM) on evoked synaptic activity and passive membrane properties was examined. 2. Excitatory postsynaptic potentials (EPSPs) mediated by N-methyl-D-aspartate (NMDA) and non-NMDA receptors were recorded in response to electrical stimulation. Zinc did not affect either type of EPSP. Resting membrane potential, repetitive firing properties, and input resistance were not altered by zinc. 3. Inhibitory postsynaptic potentials (IPSPs) were enhanced after zinc application. Zinc also induced generation of large amplitude spontaneous gamma-aminobutyric acid-A (GABAA)- and GABAB-mediated IPSPs. Postsynaptic responses to iontophoretically applied GABA were unaffected. In the presence of zinc, GABAergic synaptic potentials could result in generation of action potentials. 4. Directly evoked IPSPs recorded in the presence of the excitatory amino acid receptor blockers 6-cyano-7-nitroquinoxaline-2,3-dione and 2-amino-5-phosphonovaleric acid were enhanced by zinc. Under these conditions spontaneous IPSPs with superimposed action potentials were present. Baclofen, in the presence of zinc, reduced the amplitude of evoked IPSPs. 5. These results indicate that zinc may be an endogenously occurring neuromodulator. Zinc appears to enhance GABAergic IPSPs by increasing the excitability of inhibitory interneurons, thus resulting in increased GABA release.

Summation of excitatory postsynaptic potentials in hippocampal pyramidal cells

1983 ◽  
Vol 50 (6) ◽  
pp. 1320-1329 ◽  
Author(s):  
I. A. Langmoen ◽  
P. Andersen
Keyword(s):  
Dendritic Tree ◽  
Pyramidal Cells ◽  
Equilibrium Potential ◽  
Excitatory Postsynaptic Potentials ◽  
Benzyl Penicillin ◽  
Postsynaptic Potentials ◽  
Simultaneous Activation ◽  
The Individual ◽  
Hippocampal Pyramidal Cells

The summation of excitatory postsynaptic potentials (EPSPs) generated in separate parts of the dendritic tree of hippocampal pyramidal cells has been investigated using the in vitro slice preparation. Two separate inputs with known synaptic location were used. The EPSP produced by simultaneous activation of the two inputs (observed sum) was compared to the algebraic sum of the individual EPSPs. Small-amplitude EPSPs (0.5-1.5 mV) added linearly. The shortest distance between the two synaptic groups was 75 micron. With larger amplitudes (greater than 2.5 mV), the EPSP summated nonlinearly. The nonlinear summation was reduced by moderate hyperpolarizations (2-10 mV) of the soma membrane. Also, large EPSPs (greater than 2.5 mV) summated linearly when the peak of the summed EPSP was brought close to the equilibrium potential for the inhibitory postsynaptic potential (IPSP) (EIPSP). When the EPSP peak was made more negative than the EIPSP, summation was again nonlinear but the algebraic sum was now smaller than the observed EPSP sum, i.e., the direction of the nonlinearity was reversed. EPSP summation was linear after the IPSP had been blocked by benzyl penicillin application. We conclude that separate EPSPs in hippocampal pyramids (minimal separation, 75 micron) add linearly but that the addition of an IPSP may complicate this picture. No evidence was found for interaction between the different populations of excitatory synapses.

Dual role of norepinephrine in the hippocampal CA1 region of the rat: inhibition and disinhibition

1988 ◽  
Vol 66 (6) ◽  
pp. 814-819 ◽  
Author(s):  
Patrick P.-H. Leung ◽  
James J. Miller
Keyword(s):  
Pyramidal Neurons ◽  
Epileptiform Activity ◽  
Pyramidal Cells ◽  
Inhibitory Effect ◽  
Stratum Radiatum ◽  
Inhibitory Interneurons ◽  
Spike Response ◽  
Paired Pulse ◽  
Ca1 Region

Norepinephrine (NE) has been shown to produce either an inhibitory or an excitatory influence on CA1 pyramidal neurons of the hippocampus depending on the dosage. It was suggested that NE, in addition to exerting a direct inhibitory effect on pyramidal cells, may also act upon recurrent inhibitory interneurons to produce a disinhibition of the pyramidal cells. The present study was undertaken to examine the effect of NE on alveus-evoked inhibition, presumably mediated by the basket cell interneurons innervating the pyramidal cells. Experiments were carried out on the in vitro hippocampal slice preparation and inhibition was assessed by the percent reduction of the stratum radiatum evoked population spike response when preceded by a conditioning pulse delivered to the alveus to activate the inhibitory interneurons via the recurrent collaterals of the pyramidal cells. Paired pulse stimulation resulted in inhibition of the stratum radiatum evoked test response with conditioning-test intervals up to 60 ms. NE (50 μM) perfusion resulted in a significant and reversible reduction of the alveus-evoked recurrent inhibition. Intracellular recordings using a similar paired pulse paradigm corroborated the extracellular data well. The possible roles of NE in the physiological functioning and pathophysiology of epileptiform activity of the hippocampus are discussed.

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