A depolarizing inhibitory postsynaptic potential activated by synaptically released γ-aminobutyric acid under physiological conditions in rat hippocampal pyramidal cells

1988 ◽  
Vol 66 (8) ◽  
pp. 1100-1102 ◽  
Author(s):  
Paul Perreault ◽  
Massimo Avoli
Keyword(s):  
High Intensity ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Rat Hippocampus ◽  
Aminobutyric Acid ◽  
Afferent Stimulation ◽  
Inhibitory Postsynaptic Potential ◽  
Physiological Conditions ◽  
Ca1 Pyramidal Neurons ◽  
Postsynaptic Potential

We report that CA1 pyramidal neurons of the rat hippocampus respond to high intensity afferent stimulation by generating a late depolarizing potential that typically occurs between the early (fast) inhibitory postsynaptic potential (IPSP) and the late (slow) IPSP. This potential is reminiscent of the response seen after the application of 4-aminopyridine and can be blocked by bicuculline, indicating that GABAA receptors are involved in its generation.

Group I mGluRs Increase Excitability of Hippocampal CA1 Pyramidal Neurons by a PLC-Independent Mechanism

2002 ◽  
Vol 88 (1) ◽  
pp. 107-116 ◽  
Author(s):  
David R. Ireland ◽  
Wickliffe C. Abraham
Keyword(s):  
Metabotropic Glutamate Receptors ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Receptor Subtypes ◽  
Ca1 Pyramidal Neurons ◽  
Group I ◽  
Hippocampal Ca1 ◽  
Group I Mglurs ◽  
Induced Changes

Previous studies have implicated phospholipase C (PLC)-linked Group I metabotropic glutamate receptors (mGluRs) in regulating the excitability of hippocampal CA1 pyramidal neurons. We used intracellular recordings from rat hippocampal slices and specific antagonists to examine in more detail the mGluR receptor subtypes and signal transduction mechanisms underlying this effect. Application of the Group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG) suppressed slow- and medium-duration afterhyperpolarizations (s- and mAHP) and caused a consequent increase in cell excitability as well as a depolarization of the membrane and an increase in input resistance. Interestingly, with the exception of the suppression of the mAHP, these effects were persistent, and in the case of the sAHP lasting for more than 1 h of drug washout. Preincubation with the specific mGluR5 antagonist, 2-methyl-6-(phenylethynyl)-pyridine (MPEP), reduced but did not completely prevent the effects of DHPG. However, preincubation with both MPEP and the mGluR1 antagonist LY367385 completely prevented the DHPG-induced changes. These results demonstrate that the DHPG-induced changes are mediated partly by mGluR5 and partly by mGluR1. Because Group I mGluRs are linked to PLC via G-protein activation, we also investigated pathways downstream of PLC activation, using chelerythrine and cyclopiazonic acid to block protein kinase C (PKC) and inositol 1,4,5-trisphosphate-(IP3)-activated Ca2+ stores, respectively. Neither inhibitor affected the DHPG-induced suppression of the sAHP or the increase in excitability nor did an inhibitor of PLC itself, U-73122. Taken together, these results argue that in CA1 pyramidal cells in the adult rat, DHPG activates mGluRs of both the mGluR5 and mGluR1 subtypes, causing a long-lasting suppression of the sAHP and a consequent persistent increase in excitability via a PLC-, PKC-, and IP3-independent transduction pathway.

Inhibitory processes of hippocampal CA1 pyramidal neurons following kindling-induced epilepsy in the rat

1985 ◽  
Vol 63 (7) ◽  
pp. 872-878 ◽  
Author(s):  
M. W. Oliver ◽  
J. J. Miller
Keyword(s):  
Pyramidal Neurons ◽  
Epileptiform Activity ◽  
Pyramidal Cells ◽  
Repetitive Stimulation ◽  
Membrane Properties ◽  
Stratum Radiatum ◽  
Inhibitory Processes ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Ca1 ◽  
Stimulation Of

To determine the alterations in cellular function which may contribute to the chronic predisposition of neuronal tissue to epileptiform activity, the membrane properties and inhibitory processes of hippocampal CA1 pyramidal cells were investigated using in vitro slices prepared from commissural-kindled rats. No changes were observed in resting membrane potential, input resistance, spike amplitude, and membrane time constant of "kindled" CA1 pyramidal neurons when compared with controls. There were also no differences between control and kindled preparations in the amplitude of recurrent inhibitory postsynaptic potentials (IPSP) and in the duration of inhibition produced by either alvear (Alv) or stratum radiatum (SR) stimulation. Irrespective of group, repetitive stimulation of the Alv reduced the amplitude of the recurrent IPSP but failed to induce seizurelike activity. On the other hand, repetitive stimulation of SR frequently produced a neuronal burst discharge even though the duration and to some extent the amplitude of orthodromic inhibition was increased. On the basis of these data, it may be suggested that chronic changes in CA1 pyramidal cell membrane properties and transient reductions of inhibitory processes do not underlie the enhanced sensitivity of these neurons to seizure activity associated with kindling.

Effects of berberine on potassium currents in acutely isolated CA1 pyramidal neurons of rat hippocampus

2004 ◽  
Vol 999 (1) ◽  
pp. 91-97 ◽  
Author(s):  
Fang Wang ◽  
Gang Zhao ◽  
Lan Cheng ◽  
Hong-Yi Zhou ◽  
Li-Ying Fu ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Potassium Currents ◽  
Rat Hippocampus ◽  
Ca1 Pyramidal Neurons

scholarly journals Heterosynaptic metaplastic regulation of synaptic efficacy in CA1 pyramidal neurons of rat hippocampus

Hippocampus ◽  
2004 ◽  
Vol 14 (8) ◽  
pp. 1011-1025 ◽  
Author(s):  
Didier Le Ray ◽  
David Fernández De Sevilla ◽  
Ana Belén Porto ◽  
Marco Fuenzalida ◽  
Washington Buño
Keyword(s):  
Pyramidal Neurons ◽  
Rat Hippocampus ◽  
Synaptic Efficacy ◽  
Ca1 Pyramidal Neurons

scholarly journals Long‐term high‐intensity sound stimulation inhibits Ih in CA1 pyramidal neurons.

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Júnia Lara Deus ◽  
Alexandra Olímpio Siqueira Cunha ◽  
César Celis Ceballos ◽  
Ricardo Xavier Leão
Keyword(s):  
High Intensity ◽  
Pyramidal Neurons ◽  
Sound Stimulation ◽  
Ca1 Pyramidal Neurons
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