Postsynaptic hyperpolarization increases the strength of AMPA-mediated synaptic transmission at large synapses between mossy fibers and CA3 pyramidal cells

2000 ◽  
Vol 39 (12) ◽  
pp. 2288-2301 ◽  
Author(s):  
Nicola Berretta ◽  
Aleksej V Rossokhin ◽  
Alexander M Kasyanov ◽  
Maxim V Sokolov ◽  
Enrico Cherubini ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Mossy Fibers ◽  
Pyramidal Cells ◽  
Ca3 Pyramidal Cells

Effect of tolbutamide on tetraethylammonium-induced postsynaptic zinc signals at hippocampal mossy fiber-CA3 synapses

2017 ◽  
Vol 95 (9) ◽  
pp. 1058-1063 ◽  
Author(s):  
Fatima C. Bastos ◽  
Vanessa N. Corceiro ◽  
Sandra A. Lopes ◽  
José G. de Almeida ◽  
Carlos M. Matias ◽  
...  
Keyword(s):  
Mossy Fiber ◽  
Mossy Fibers ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Chemical Stimulation ◽  
Term Potentiation ◽  
Voltage Dependent ◽  
Zinc Release ◽  
Ca3 Pyramidal Cells

The application of tetraethylammonium (TEA), a blocker of voltage-dependent potassium channels, can induce long-term potentiation (LTP) in the synaptic systems CA3–CA1 and mossy fiber-CA3 pyramidal cells of the hippocampus. In the mossy fibers, the depolarization evoked by extracellular TEA induces a large amount of glutamate and also of zinc release. It is considered that zinc has a neuromodulatory role at the mossy fiber synapses, which can, at least in part, be due to the activation of presynaptic ATP-dependent potassium (KATP) channels. The aim of this work was to study properties of TEA-induced zinc signals, detected at the mossy fiber region, using the permeant form of the zinc indicator Newport Green. The application of TEA caused a depression of those signals that was partially blocked by the KATP channel inhibitor tolbutamide. After the removal of TEA, the signals usually increased to a level above baseline. These results are in agreement with the idea that intense zinc release during strong synaptic events triggers a negative feedback action. The zinc depression, caused by the LTP-evoking chemical stimulation, turns into potentiation after TEA washout, suggesting the existence of a correspondence between the observed zinc potentiation and TEA-evoked mossy fiber LTP.

scholarly journals Recruitment of an inhibitory hippocampal network after bursting in a single granule cell

2007 ◽  
Vol 104 (18) ◽  
pp. 7640-7645 ◽  
Author(s):  
Masahiro Mori ◽  
Beat H. Gähwiler ◽  
Urs Gerber
Keyword(s):  
Pyramidal Cell ◽  
Granule Cell ◽  
Mossy Fiber ◽  
Mossy Fibers ◽  
Pyramidal Cells ◽  
Network Activity ◽  
Inhibitory Input ◽  
Inhibitory Interneurons ◽  
Failure Rates ◽  
Ca3 Pyramidal Cells

The hippocampal CA3 area, an associational network implicated in memory function, receives monosynaptic excitatory as well as disynaptic inhibitory input through the mossy-fiber axons of the dentate granule cells. Synapses made by mossy fibers exhibit low release probability, resulting in high failure rates at resting discharge frequencies of 0.1 Hz. In recordings from functionally connected pairs of neurons, burst firing of a granule cell increased the probability of glutamate release onto both CA3 pyramidal cells and inhibitory interneurons, such that subsequent low-frequency stimulation evoked biphasic excitatory/inhibitory responses in a CA3 pyramidal cell, an effect lasting for minutes. Analysis of the unitary connections in the circuit revealed that granule cell bursting caused powerful activation of an inhibitory network, thereby transiently suppressing excitatory input to CA3 pyramidal cells. This phenomenon reflects the high incidence of spike-to-spike transmission at granule cell to interneuron synapses, the numerically much greater targeting by mossy fibers of inhibitory interneurons versus principal cells, and the extensively divergent output of interneurons targeting CA3 pyramidal cells. Thus, mossy-fiber input to CA3 pyramidal cells appears to function in three distinct modes: a resting mode, in which synaptic transmission is ineffectual because of high failure rates; a bursting mode, in which excitation predominates; and a postbursting mode, in which inhibitory input to the CA3 pyramidal cells is greatly enhanced. A mechanism allowing the transient recruitment of inhibitory input may be important for controlling network activity in the highly interconnected CA3 pyramidal cell region.

Lack of vesicular zinc in mossy fibers does not affect synaptic excitability of CA3 pyramidal cells in zinc transporter 3 knockout mice

Neuroscience ◽  
2003 ◽  
Vol 116 (1) ◽  
pp. 237-248 ◽  
Author(s):  
V. Lopantsev ◽  
H.J. Wenzel ◽  
T.B. Cole ◽  
R.D. Palmiter ◽  
P.A. Schwartzkroin
Keyword(s):  
Knockout Mice ◽  
Mossy Fibers ◽  
Pyramidal Cells ◽  
Zinc Transporter ◽  
Ca3 Pyramidal Cells

Seizures Induce Simultaneous GABAergic and Glutamatergic Transmission in the Dentate Gyrus-CA3 System

2000 ◽  
Vol 84 (6) ◽  
pp. 3088-3090 ◽  
Author(s):  
Rafael Gutiérrez
Keyword(s):  
Dentate Gyrus ◽  
Mossy Fibers ◽  
Pyramidal Cells ◽  
Inhibitory Response ◽  
Excitatory Postsynaptic Potential ◽  
Postsynaptic Potential ◽  
Ca3 Pyramidal Cells ◽  
Neuronal Sprouting ◽  
Kindled Seizures ◽  
Synaptic Responses

Monosynaptic and polysynaptic responses of CA3 pyramidal cells (PC) to stimulation of the dentate gyrus (DG) are normally blocked by glutamate receptor antagonists (GluRAs). However, after kindled seizures, GluRAs block the monosynaptic excitatory postsynaptic potential (EPSP) and isolate a monosynaptic inhibitory postsynaptic potential (IPSP), suggesting that mossy fibers release GABA. However, kindling epilepsy induces neuronal sprouting, which can underlie this fast inhibitory response. To explore this possibility, the synaptic responses of PC to DG stimulation were analyzed in kindled epileptic rats, with and without seizures, and in nonepileptic rats, immediately after a single pentylenetetrazol (PTZ)-induced seizure, in which sprouting is unlikely to have occurred. Excitatory and inhibitory synaptic responses of PC to DG stimulation were blocked by GluRAs in control cells and in cells from kindled nonseizing rats, confirming that inhibitory potentials are disynaptically mediated. However, a fast IPSP could be evoked in kindled epileptic rats and in nonepileptic rats after a single PTZ-induced seizure. The same response was induced after rekindling the epileptic nonseizing rats. This IPSP has an onset latency that parallels that of the control EPSP and is not altered under low Ca2+ medium or halothane perfusion. In addition, it was reversibly depressed byl(+)-2-amino-4-phosphonobutyric acid (l-AP4), which is known to inhibit transmitter release from mossy fibers. These results demonstrate that seizures, and not the synaptic rearrangement due to an underlying epileptic state, induce the emergence of fast inhibition in the DG-CA3 system, and suggest that the mossy fibers underlie this plastic change.

Origin of the Apparent Asynchronous Activity of Hippocampal Mossy Fibers

1997 ◽  
Vol 78 (1) ◽  
pp. 24-30 ◽  
Author(s):  
Darrell A. Henze ◽  
Nathaniel N. Urban ◽  
German Barrionuevo
Keyword(s):  
Mossy Fiber ◽  
Molecular Layer ◽  
Mossy Fibers ◽  
Pyramidal Cells ◽  
Antidromic Activation ◽  
Stratum Lucidum ◽  
Hippocampal Area ◽  
Ca3 Pyramidal Cells ◽  
Area Ca3

Henze, Darrell A., Nathaniel N. Urban, and German Barrionuevo. Origin of the apparent asynchronous activity of hippocampal mossy fibers. J. Neurophysiol. 78: 24–30, 1997. Fiber volleys (FVs) from the stratum lucidum of rat hippocampal area CA3 were recorded extracellularly from in vitro slices in the presence of 10 mM kynurenic acid. In agreement with previous work, bulk stimulation of the dentate gyrus (DG) near the hilar border leads to an asynchronous FV. Transection of the stratum lucidum between the DG stimulation site and the CA3 recording site reduced or eliminated the early components of the asynchronous FV, indicating that they are of mossy fiber (MF) origin. In contrast, moving the stimulating electrode away from the hilus toward the hippocampal fissure reduced or eliminated the late components of the FV. Subsequently, we found that bulk stimulation on the DG/hilar border induces an antidromic population spike in CA3 pyramidal cells. Finally, the MFs and associational collaterals have differentconduction velocities (0.51 and 0.37 m/s, respectively; temperature =33°C). From these data, we conclude that the late components of the asynchronous FV are due to antidromic activation of CA3 collaterals that have been shown to be present in the DG and hilus. A corollary of these findings is that bulk stimulation on the DG/hilar border can lead to at least two different monosynaptic inputs to CA3 pyramidal cells: the MFs and the antidromically activated associational collaterals. We suggest that when MF synaptic responses are being evoked with the use of bulk stimulation, stimulating electrodes should be placed in the outer molecular layer of the DG to prevent the activation of hilar-projecting associational collaterals. This procedure should be added to the previously proposed criteria for preventing polysynaptic contamination of the intracellularly recorded evoked MF synaptic response.

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