Corticosterone-induced decrease of inhibitory postsynaptic potentials in rat hippocampal pyramidal neurons in vitro depends on cytosolic factors

1996 ◽  
Vol 215 (2) ◽  
pp. 83-86 ◽  
Author(s):  
A. Teschemacher ◽  
M.L. Zeise ◽  
W. Zieglgänsberger
Keyword(s):  
Pyramidal Neurons ◽  
Hippocampal Pyramidal Neurons ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
Cytosolic Factors

scholarly journals Heterogeneity in Use-Dependent Depression of Inhibitory Postsynaptic Potentials in the Rat Neostriatum In Vitro

1997 ◽  
Vol 77 (1) ◽  
pp. 427-434 ◽  
Author(s):  
Gabriele Radnikow ◽  
Jutta Rohrbacher ◽  
Ulrich Misgeld
Keyword(s):  
Aminobutyric Acid ◽  
Medium Spiny Neurons ◽  
Stimulus Interval ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
Spiny Neurons ◽  
Neostriatal Slices ◽  
Minimal Stimulation ◽  
Paired Pulse Depression

Radnikow, Gabriele, Jutta Rohrbacher, and Ulrich Misgeld. Heterogeneity in use-dependent depression of inhibitory postsynaptic potentials in the rat neostriatum in vitro. J. Neurophysiol. 77: 427–434, 1997. “Minimal stimulation” was applied to evoke responses in an “all-or-none” fashion in presumed medium spiny neurons of rat neostriatal slices in the presence of antagonists for glutamatergic excitation. For comparison, responses were evoked in the same cells by compound stimulation. Bicuculline (30 μM) blocked responses evoked by minimal stimulation, indicating that they were γ-aminobutyric acid-A (GABAA)-receptor-mediated inhibitory postsynaptic potentials (IPSPs), whereas responses evoked by compound stimulation were only reduced in amplitude. Likewise, R(−)baclofen (1–20 μM) blocked IPSPs evoked by minimal stimulation in all but one cell. On the contrary, responses evoked by compound stimulation were always reduced in amplitude but never blocked. Paired-pulse depression (PPD) of averaged responses to minimal and compound stimulation was observed at a stimulus interval of 300 ms. The GABAB receptor antagonist CGP55845A (0.5 μM) had no effect on PPD evoked by compound stimulation but abolished PPD evoked by minimal stimulation. In a second set of experiments, the two stimulation paradigms were used to evoke responses in neostriatal slices continuously bathed in R(−)baclofen (10–20 μM). In R(−)baclofen a strong PPD was evoked by minimal and by compound stimulation. The amplitude of the response to compound stimulation increased on application of CGP55845A (0.5 μM). At the same time, PPD evoked by compound stimulation decreased. On the contrary, IPSP amplitude and PPD evoked by minimal stimulation remained unchanged. We conclude that two types of GABAergic terminals exist in the rat neostriatum, only one of which is regulated by GABAB receptors. However, the other class of terminals, not regulated by GABAB receptors, displays a much more pronounced PPD.

scholarly journals Neurochemical mechanisms of the cerebroprotective action of spiro[indole-3,1'-pyrrol [3,4-с] pyrrol] derivative

2015 ◽  
Vol 13 (1) ◽  
pp. 56-61
Author(s):  
Ol'ga Vital'yevna Khodakovskaya ◽  
Dmitriy Vladimirovich Evdokimov ◽  
Sergey Yur'yevich Shtrygol' ◽  
Igor' Igorevich Abramets ◽  
Leonid Borisovich Braverman ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Nmda Receptors ◽  
Pyramidal Neurons ◽  
Neuroprotective Effect ◽  
Weak Effect ◽  
Code Number ◽  
Postsynaptic Potentials ◽  
Neurochemical Mechanisms

The mechanisms of the neuroprotective effect of 3,2’-spiro-pyrrolo-2-оxindole derivative (code number R-86) were investigated in hippocampal sections of rats by measuring the amplitude of postsynaptic potentials in pyramidal neurons. In vitro R-86 reduced the responces to NMDA-receptors activation as well as hydrogen peroxide-induced injury, being not active in anoxia and neuroglycopenia. When systemically administered, R-86 exerted weak effect in anoxia and neuroglycopenia and decreased steroid-induced neurotoxicity.

Metrifonate Decreases sI AHP in CA1 Pyramidal Neurons In Vitro

2001 ◽  
Vol 85 (1) ◽  
pp. 319-322 ◽  
Author(s):  
John M. Power ◽  
M. Mathew Oh ◽  
John F. Disterhoft
Keyword(s):  
Pyramidal Neurons ◽  
Slow Component ◽  
Cell Voltage ◽  
Current Clamp ◽  
Hippocampal Pyramidal Neurons ◽  
Tail Current ◽  
Electrode Current ◽  
Ca1 Pyramidal Neurons ◽  
Age Related

Metrifonate, a cholinesterase inhibitor, has been shown to enhance learning in aging rabbits and rats, and to alleviate the cognitive deficits observed in Alzheimer's disease patients. We have previously determined that bath application of metrifonate reduces the spike frequency adaptation and postburst afterhyperpolarization (AHP) in rabbit CA1 pyramidal neurons in vitro using sharp electrode current-clamp recording. The postburst AHP and accommodation observed in current clamp are the result of four slow outward potassium currents (s I AHP, I AHP, I M, and I C) and the hyperpolarization activated mixed cation current, I h. We recorded from visually identified CA1 hippocampal pyramidal neurons in vitro using whole cell voltage-clamp technique to better isolate and characterize which component currents of the AHP are affected by metrifonate. We observed an age-related enhancement of the slow component of the AHP tail current (s I AHP), but not of the fast decaying component of the AHP tail current ( I AHP, I M, and I C). Bath perfusion of metrifonate reduced s I AHP at concentrations that cause a reduction of the AHP and accommodation in current-clamp recordings, with no apparent reduction of I AHP, I M, and I C. The functional consequences of metrifonate administration are apparently mediated solely through modulation of the s I AHP.

scholarly journals Transient oxytocin signaling primes the development and function of excitatory hippocampal neurons

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Silvia Ripamonti ◽  
Mateusz C Ambrozkiewicz ◽  
Francesca Guzzi ◽  
Marta Gravati ◽  
Gerardo Biella ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Hippocampal Pyramidal Neurons ◽  
Excitatory Transmission ◽  
Oxytocin Receptors ◽  
Synapse Density ◽  
Protein Components ◽  
And Function

Beyond its role in parturition and lactation, oxytocin influences higher brain processes that control social behavior of mammals, and perturbed oxytocin signaling has been linked to the pathogenesis of several psychiatric disorders. However, it is still largely unknown how oxytocin exactly regulates neuronal function. We show that early, transient oxytocin exposure in vitro inhibits the development of hippocampal glutamatergic neurons, leading to reduced dendrite complexity, synapse density, and excitatory transmission, while sparing GABAergic neurons. Conversely, genetic elimination of oxytocin receptors increases the expression of protein components of excitatory synapses and excitatory synaptic transmission in vitro. In vivo, oxytocin-receptor-deficient hippocampal pyramidal neurons develop more complex dendrites, which leads to increased spine number and reduced γ-oscillations. These results indicate that oxytocin controls the development of hippocampal excitatory neurons and contributes to the maintenance of a physiological excitation/inhibition balance, whose disruption can cause neurobehavioral disturbances.

Sign in / Sign up

Export Citation Format

Share Document