scholarly journals Inhibitory postsynaptic potentials in neonatal rat sympathetic preganglionic neurones in vitro.

1989 ◽  
Vol 410 (1) ◽  
pp. 267-281 ◽  
Author(s):  
N J Dun ◽  
N Mo
Keyword(s):  
Neonatal Rat ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials

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.

Inhibitory Interactions Between Ferret Thalamic Reticular Neurons

2002 ◽  
Vol 87 (5) ◽  
pp. 2571-2576 ◽  
Author(s):  
Yousheng Shu ◽  
David A. McCormick
Keyword(s):  
Reversal Potential ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Inhibitory Input ◽  
Inhibitory Interaction ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
Reticular Neurons ◽  
Inhibitory Interactions

The thalamic reticular nucleus (nRt) provides an important inhibitory input to thalamic relay nuclei and is central in the generation of both normal and abnormal thalamocortical activities. Although local inhibitory interactions between these neurons may play an important role in controlling thalamocortical activities, the physiological features of this interaction have not been fully investigated. Here we sought to establish the nature of inhibitory interaction between nRt neurons with intracellular and extracellular recordings in slices of ferret nRt maintained in vitro. In many nRt neurons, intracellular recordings revealed spontaneous inhibitory postsynaptic potentials (IPSPs). In addition, the local excitation of nRt cells with glutamate led to the generation of IPSPs in the intracellularly recorded nRt neuron. These evoked IPSPs exhibited an average reversal potential of −72 mV and could be blocked by picrotoxin, a GABAA-receptor antagonist. These results indicate that nRt neurons interact locally through the activation of GABAA receptor-mediated inhibitory postsynaptic potentials. This lateral inhibition may play an important role in controlling the responsiveness of these cells to cortical and thalamic excitatory inputs in both normal and abnormal thalamocortical function.

Valproate enhances inhibitory postsynaptic potentials in hippocampal neurons in vitro

1987 ◽  
Vol 435 (1-2) ◽  
pp. 213-219 ◽  
Author(s):  
Uli Preisendörfer ◽  
Marc L. Zeise ◽  
Manfred R. Klee
Keyword(s):  
Hippocampal Neurons ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials

Synaptic mechanisms in sympathetic preganglionic neurons

1992 ◽  
Vol 70 (S1) ◽  
pp. S86-S91 ◽  
Author(s):  
N. J. Dun ◽  
S. Y. Wu ◽  
E. Shen ◽  
T. Miyazaki ◽  
S. L. Dun ◽  
...  
Keyword(s):  
Excitatory Amino Acid ◽  
Neonatal Rat ◽  
Excitatory Postsynaptic Potentials ◽  
Sympathetic Preganglionic Neurons ◽  
Postsynaptic Potentials ◽  
Preganglionic Neurons ◽  
Inhibitory Postsynaptic Potentials ◽  
Ventral Roots ◽  
Adult Cat ◽  
Synaptic Mechanisms

Intracellular recordings from sympathetic preganglionic neurons (SPNs) in adult cat and neonatal rat spinal cord slices reveal four types of synaptic potentials, namely, excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), and slow EPSPs in both preparations, and a slow IPSP in cat SPNs. Pharmacological studies show that glutamate or a related excitatory amino acid and glycine are the probable mediators of EPSPs and IPSPs. There may be heterogenous mediators of slow EPSPs; substance P, serotonin, norepinephrine, and epinephrine are all probable mediators of slow EPSPs in subpopulations of SPNs. In the case of slow IPSPs, norepinephrine appears to be the likely transmitter. Finally, stimulation of ventral roots elicits a synaptic potential that appears to be caused by glutamate released from afferent fibers in the ventral roots. Our results indicate that a multitude of synaptic mechanisms exist in the rat SPNs by means of which inputs arising from sensory and supraspinal neurons are processed in a timely and orderly manner, thus ensuring highly organized but differentiated outputs to multiple peripheral target cells.Key words: sympathetic preganglionic neurons, excitatory postsynaptic potentials, inhibitory postsynaptic potentials, slow excitatory postsynaptic potentials, glutamate, glycine.

scholarly journals Synaptic Interactions Underlying Synchronized Inhibition in the Basal Amygdala: Evidence for Existence of Two Types of Projection Cells

2011 ◽  
Vol 105 (2) ◽  
pp. 687-696 ◽  
Author(s):  
Andrei T. Popescu ◽  
Denis Paré
Keyword(s):  
Oscillatory Activity ◽  
Repetitive Firing ◽  
Small Subset ◽  
Projection Neurons ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
Basal Amygdala ◽  
Synaptic Interactions ◽  
Membrane Potential Fluctuations

The basal amygdala (BA) plays a key role in mediating the facilitating effects of emotions on memory. Recent findings indicate that this function depends on the ability of BA neurons to generate coherent oscillatory activity, facilitating synaptic plasticity in target neurons. However, the mechanisms allowing BA neurons to synchronize their activity remain poorly understood. Here, we aimed to shed light on this question, focusing on a slow periodic inhibitory oscillation previously observed in the BA in vitro. Paired patch recordings showed that these large inhibitory postsynaptic potentials (IPSPs) occur almost synchronously in BA projection neurons, that they were typically not preceded by excitatory postsynaptic potentials (EPSPs), and that they had little or no correlate in neighboring amygdala nuclei or cortical fields. The initial phase of the IPSPs was associated with an increase in membrane potential fluctuations at 50–100 Hz. In keeping with this, the IPSPs seen in projection cells were correlated with repetitive firing at 50–100 Hz in presumed interneurons and they could be abolished by picrotoxin. However, the IPSPs were also sensitive to 6-cyano-7-nitroquinoxaline-2,3-dione, implying that they arose from the interplay between glutamatergic and GABAergic BA neurons. In support of this idea, we identified a small subset of projection cells (15%), positively identified as such by retrograde labeling from BA projection sites, that began firing shortly before the IPSP onset and presumably drove interneuronal firing. These results add to a rapidly growing body of data indicating that the BA contains at least two distinct types of projection cells that vary in their relation with interneurons and extra-amygdala targets.

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