Isoliquiritigenin, a Chalcone Compound, Enhances Spontaneous Inhibitory Postsynaptic Response

Several investigators of the molluscan nervous system have used TEA, injected into presynptic neurones, to determine whether the connexions made by these neurones are monosynaptic. The increase in spike duration produced by the TEA causes an increase in transmitter release, and hence an increase in the amplitude of the postsynaptic potential if the connexion is direct. If the connexion is indirect, the spike in an intercalated neurone will not be affected by the TEA, and the postsynaptic response will remain constant. Experiments described here show that TEA can cross electrotonic junctions in the gastropod mollusc Planorbis corneus. They also show that each TEA-prolonged presynaptic impulse may produce more than one postsynaptic impulse. A larger postsynaptic potential could therefore be produced by presynaptic injection of TEA in the case of an indirect connexion. This indicates that care must be taken when interpreting the results of experiments using TEA to test for monosynaptic connexions.

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Presynaptic Group II mGluR Inhibition of Short-Term Depression in the Medial Perforant Path of the Dentate Gyrus In Vitro

Journal of Neurophysiology ◽

10.1152/jn.2001.85.6.2509 ◽

2001 ◽

Vol 85 (6) ◽

pp. 2509-2515 ◽

Cited By ~ 20

Author(s):

John Kilbride ◽

Anthony M. Rush ◽

Michael J. Rowan ◽

Roger Anwyl

Keyword(s):

Dentate Gyrus ◽

Metabotropic Glutamate Receptors ◽

State Level ◽

Perforant Path ◽

Dependent Manner ◽

Short Term ◽

Concentration Dependent Manner ◽

Postsynaptic Response ◽

Group Ii

Inhibition of short-term plasticity by activation of presynaptic group II metabotropic glutamate receptors (group II mGluR) was investigated in the medial perforant path of the dentate gyrus in the hippocampus in vitro. Brief trains of stimulation (10 stimuli at 1–200 Hz) evoked short-term depression of field excitatory postsynaptic potentials (EPSPs). The steady-state level of depression, measured after 10 stimuli, was frequency dependent, increasing between 1 and 200 Hz. Activation of group II mGluR by the selective agonist LY354740 did not alter short-term depression evoked by frequencies up to 10 Hz, but did inhibit short-term depression evoked at higher frequencies in a frequency- and concentration-dependent manner. The time-averaged postsynaptic response (EPSP per unit time) was found to increase linearly with frequency up to ∼20 Hz. At higher frequencies, the response plateaued, thereby becoming independent of frequency. Frequencies above this were differentiated only during the transient postsynaptic response that accompanies changes in firing rates. Activation of presynaptically located group II mGluR increased the frequency at which the EPSP per unit time plateaued up to 30–50 Hz.

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Tissue-type Plasminogen Activator (tPA) Modulates the Postsynaptic Response of Cerebral Cortical Neurons to the Presynaptic Release of Glutamate

Frontiers in Molecular Neuroscience ◽

10.3389/fnmol.2016.00121 ◽

2016 ◽

Vol 9 ◽

Cited By ~ 12

Author(s):

Valerie Jeanneret ◽

Fang Wu ◽

Paola Merino ◽

Enrique Torre ◽

Ariel Diaz ◽

...

Keyword(s):

Plasminogen Activator ◽

Cortical Neurons ◽

Tissue Type ◽

Postsynaptic Response ◽

Tissue Type Plasminogen Activator ◽

Type Plasminogen Activator ◽

Cerebral Cortical Neurons ◽

Presynaptic Release

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Relation of Posttetanic Potentiation to Subnormality of Lateral Geniculate Potentials

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1957.188.2.238 ◽

1957 ◽

Vol 188 (2) ◽

pp. 238-244 ◽

Cited By ~ 18

Author(s):

Edward V. Evarts ◽

John R. Hughes

Keyword(s):

Electrical Stimulation ◽

Optic Nerve ◽

Posttetanic Potentiation ◽

Postsynaptic Response ◽

Lateral Geniculate ◽

Decerebrate Cats ◽

Stimulation Of

The lateral geniculate response to electrical stimulation of the optic nerve was recorded in decerebrate cats and in cats anesthetized with Nembutal. Tetanization of the optic nerve at 500/sec. for 20 seconds in nembutalized cats produced a prolonged second subnormality of the geniculate postsynaptic response. Further tetanization during tetanically-induced second subnormality produced posttetanic potentiation (PTP). The degree of PTP (expressed in percentage of the pretetanic level) of the postsynaptic response following a 20-second tetanus was proportional to the degree of second subnormality present at the time the tetanus was applied. PTP was also found to occur during the subnormality which followed a brief train of optic nerve shocks, and during LSD-induced subnormality. PTP of postsynaptic lateral geniculate potentials occurred only rarely in the absence of some form of intentionally induced subnormality.

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Synaptic plasticity in visual cortex: comparison of theory with experiment

Journal of Neurophysiology ◽

10.1152/jn.1991.66.5.1785 ◽

1991 ◽

Vol 66 (5) ◽

pp. 1785-1804 ◽

Cited By ~ 64

Author(s):

E. E. Clothiaux ◽

M. F. Bear ◽

L. N. Cooper

Keyword(s):

Nonlinear Function ◽

Monocular Deprivation ◽

Noise Pattern ◽

Postsynaptic Response ◽

Synaptic Modification ◽

Fixed Set ◽

Input Activity ◽

Visual Contour ◽

Noise Input ◽

Binocular Deprivation

1. The aim of this work was to assess whether a form of synaptic modification based on the theory of Bienenstock, Cooper, and Munro (BCM) can, with a fixed set of parameters, reproduce both the kinetics and equilibrium states of experience-dependent modifications cortex. 2. According to the BCM theory, the connection strength of excitatory geniculocortical synapses varies as the product of a measure of input activity (d) and a function (phi) of the summed postsynaptic response. For all postsynaptic responses greater than spontaneous but less than a critical value called the ,modification threshold- (theta), phi has a negative value. For all postsynaptic responses greater than theta, phi has a positive value. A novel feature of the BCM theory is that the value of theta is not fixed, but rather ,slides- as a nonlinear function of the average postsynaptic response. 3. This theory permits precise specification of theoretical equivalents of experimental situations, allowing detailed, quantitative comparisons of theory with experiment. Such comparisons were carried out here in a series of computer simulations. 4. Simulations are performed by presenting input to a model cortical neuron, calculating the summed postsynaptic response, and then changing the synaptic weights according to the BCM theory. This process is repeated until the synaptic weights reach an equilibrium state. 5. Two types of geniculocortical input are simulated: ,pattern- and ,noise.- Pattern input is assumed to correspond to the type of input that arises when a visual contour of a particular orientation is presented to the retina. This type of input is said to be ,correlated- when the two sets of geniculocortical fibers relaying information from the two eyes convey the same patterns at the same time. Noise input is assumed to correspond to the type of input that arises in the absence of visual contours and, by definition, is uncorrelated. 6. By varying the types of input available to the two sets of geniculocortical synapses, we simulate the following types of visual experience: 1) normal binocular contour vision, 2) monocular deprivation, 3) reverse suture, 4) strabismus, 5) binocular deprivation, and 6) normal contour vision after a period of monocular deprivation. 7. The constraints placed on the set of parameters by each type of simulated visual environment, and the effects that such constraints have on the evolution of the synaptic weights, are investigated in detail.(ABSTRACT TRUNCATED AT 400 WORDS)

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Postsynaptic Response Kinetics Are Controlled by a Glutamate Transporter at Cone Photoreceptors

Journal of Neurophysiology ◽

10.1152/jn.1998.79.1.190 ◽

1998 ◽

Vol 79 (1) ◽

pp. 190-196 ◽

Cited By ~ 35

Author(s):

Lubor Gaal ◽

Botond Roska ◽

Serge A. Picaud ◽

Samuel M. Wu ◽

Robert Marc ◽

...

Keyword(s):

Voltage Dependence ◽

Light Flash ◽

Horizontal Cell ◽

Glutamate Transporter ◽

Light Response ◽

Horizontal Cells ◽

Cone Photoreceptors ◽

Postsynaptic Response ◽

Glutamate Concentration ◽

Voltage Dependent

Gaal, Lubor, Botond Roska, Serge A. Picaud, Samuel M. Wu, Robert Marc, and Frank S. Werblin. Postsynaptic response kinetics are controlled by a glutamate transporter at cone photoreceptors. J. Neurophysiol. 79: 190–196, 1998. We evaluated the role of the sodium/glutamate transporter at the synaptic terminals of cone photoreceptors in controlling postsynaptic response kinetics. The strategy was to measure the changes in horizontal cell response rate induced by blocking transporter uptake in cones with dihydrokainate (DHK). DHK was chosen as the uptake blocker because, as we show through autoradiographic uptake measurements, DHK specifically blocked uptake in cones without affecting uptake in Mueller cells. Horizontal cells depolarized from about −70 to −20 mV as the exogenous glutamate concentration was increased from ∼1 to 40 μM, so horizontal cells can serve as “glutamate electrodes” during the light response. DHK slowed the rate of hyperpolarization of the horizontal cells in a dose-dependent way, but didn't affect the kinetics of the cone responses. At 300 μM DHK, the rate of the horizontal cell hyperpolarization was slowed to only 17 ± 8.5% (mean ± SD) of control. Translating this to changes in glutamate concentration using the slice dose response curve as calibration in Fig. 2 , DHK reduced the rate of removal of glutamate from ∼0.12 to 0.031 μM/s. The voltage dependence of uptake rate in the transporter alone was capable of modulating glutamate concentration: we blocked vesicular released glutamate with bathed 20 mM Mg2+ and then added 30 μM glutamate to the bath to reestablish a physiological glutamate concentration level at the synapse and thereby depolarize the horizontal cells. Under these conditions, a light flash elicited a 17-mV hyperpolarization in the horizontal cells. When we substituted kainate, which is not transported, for glutamate, horizontal cells were depolarized but light did not elicit any response, indicating that the transporter alone was responsible for the removal of glutamate under these conditions. This suggests that the transporter was both voltage dependent and robust enough to modulate glutamate concentration. The transporter must be at least as effective as diffusion in removing glutamate from the synapse because there is only a very small light response once the transporter is blocked. The transporter, via its voltage dependence on cone membrane potential, appears to contribute significantly to the control of postsynaptic response kinetics.[Figure: see text]

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