The effect of propofol on ca1 pyramidal cell excitability and gabaa-mediated inhibition in the rat hippocampal slice

Albertson, Timothy E; Walby, William F.; Stark, L. G.; Joy, R. M.

doi:10.1016/0024-3205(96)00243-3

Cited by 37 publications

(19 citation statements)

References 28 publications

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“…Although all the anesthetics tested in the present study, except propofol, were effective at clinical concentrations, similar to our previous reports (7,22), it was required to use concentrations of propofol approximately 10 times larger than clinical serum levels of 2.0 ϫ 10 Ϫ5 mol/L (6,23). In addition, considering the high protein binding of propofol, its effect site concentration may be smaller than clinical serum concentrations.…”

Section: Discussionsupporting

confidence: 70%

“…Propofol suppresses the responses of the AMPA-, kainate-, and NMDA-receptor channels at large concentrations and slightly depresses the NMDA receptor channels at clinical concentrations (4,20). In addition, propofol did not inhibit PS1 in studies using PPS techniques (6,7). The results of these electrophysiologic studies indicate that the effects of propofol on glutamate receptors require considerably larger concentrations than those on GABA A receptors (21).…”

Section: Discussionmentioning

confidence: 89%

“…They concluded that volatile anesthetics have multisite and drug-specific mechanisms. Previous studies have demonstrated that IV anesthetics can inhibit glutamate-mediated excitatory synaptic transmission (4), whereas others have shown that these anesthetics can modulate GABA-mediated inhibition (5,6). Few reports have compared the effects of anesthetics on both excitatory and inhibitory synaptic transmission on the same preparation (7).…”

mentioning

confidence: 97%

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Intravenous Anesthetics Are More Effective than Volatile Anesthetics on Inhibitory Pathways in Rat Hippocampal CA1

Asahi¹,

Hirota²,

Sasaki³

et al. 2006

Anesthesia & Analgesia

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In this study, we have examined the effects of both volatile and IV general anesthetics on excitatory synaptic transmission, with and without recurrent inhibition, to clarify whether excitatory or inhibitory synapses are the major targets of action. Field population spike amplitudes (fPSs) of CA1 pyramidal neurons were recorded in rat hippocampal slices. Schaffer-collateral-commissural fibers (Sch) were stimulated orthodromically, and the evoked fPSs (PS[Sch]) in CA1 area were measured. In addition, the fPSs (PS[Alv+Sch]) elicited by stimulation of the Sch after antidromic stimulation of the alveus hippocampi (Alv) to produce recurrent inhibition were determined. It was observed that sevoflurane (0.5%-5%) and isoflurane (0.5%-5%) primarily inhibited PS[Sch] and also produced additive inhibition on the PS[Alv+Sch] in a concentration-dependent manner. The calculated 50% effective concentration (EC50) values for PS[Sch] and PS[Alv+Sch] were 5.3 vol% and 3.9 vol% (sevoflurane) and 1.7 vol% and 1.1 vol% (isoflurane), respectively. In comparison, thiopental (2.0 x 10(-5)-5.0 x 10(-4) mol/L) reduced both the PS[Sch] and PS[Alv+Sch] in a concentration-dependent manner. The calculated EC50 values for thiopental on PS[Sch] and PS[Alv+Sch] were 3.4 x 10(-4) and 5.7 x 10(-5) mol/L, respectively. Propofol (2.0 x 10(-5)-3.5 x 10(-4) mol/L) had little effect on the PS[Sch] but reduced PS[Alv+Sch] with a calculated EC(50) value of 5.1 x 10(-4) mol/L. The effects of the IV anesthetics with recurrent inhibition were antagonized in the presence of the gamma-aminobutyric acid-A-receptor antagonist bicuculline methiodide. In addition, all anesthetics prolonged recurrent inhibition from 100 ms (sevoflurane and isoflurane) to 400 ms (propofol). The results suggest that sevoflurane and isoflurane inhibit mainly on glutamate-mediated orthodromic pathways, whereas thiopental and propofol enhance gamma-aminobutyric acid-A-mediated recurrent inhibitory pathways in CA1 neurons, thus providing further evidence that the mechanisms of general anesthetics are drug- and pathway-specific.

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Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 89%

mentioning

confidence: 97%

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Intravenous Anesthetics Are More Effective than Volatile Anesthetics on Inhibitory Pathways in Rat Hippocampal CA1

Asahi¹,

Hirota²,

Sasaki³

et al. 2006

Anesthesia & Analgesia

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“…Klor kanalları sinaptik veziküllerde, mitokondride, mikrozomlarda ve diğer hücre içi organellerde bulunmaktadır [10][11][12][13][14] . Aynı zaman da klor kanalları presinaptik terminallerde de yer almaktadır 15- 19 .…”

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The Effect of Radio Frequency Signals on Calcium Dependent Chlorur Channels of Spinal Ganglial Cells

Erdoğan¹,

Ipekçioğlu²

2009

Kafkas Univ Vet Fak Derg

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Makale Kodu (Article Code): 2009/097-A ÖzetBu araştırma ile küresel mobil iletişim sistemlerinden (GSM: Global system for mobil communications) yayılan radyo frekans dalgalarının rat spinal ganglion sinir hücreleri hücre zarında bulunan kalsiyum bağımlı klor kanallarına etkisinin araştırılması amaçlanmıştır. Bu amaçla 20 adet 2 günlük Wistar sıçanlardan elde edilen ve kültür ortamında hazırlanan spinal ganglion sinir hücreleri kullanılmıştır. Hazırlanan çözelti içinde bulunan sinir hücreleri 5 santim mesafede 10 V/m elektrik alan şiddetinde 900 Mhz. frekansında toplam 6 dakika radyo frekansa maruz bırakıldı. Patch kenetleme tekniği ile hücre klor kanal akımlarında meydana gelen değişiklikler kaydedildi. Kayıtların analizinde ortama uygulanan radyo frekans sinyalinin, kalsiyum bağımlı klor kanallarının akımlarında ve membran potansiyelinde anlamlı değişimler oluşturmadığı gözlenmiştir.Anahtar sözcükler: Radyo frekans sinyali, Patch kenetleme tekniği, Spinal ganglion sinir hücresi The Effect of Radio Frequency Signals on Calcium Dependent Chlorur Channels of Spinal Ganglial Cells SummaryThis study is intended to predict the effect of radio frequency waves of global mobile communication systems (GSM: Global system for mobile communication systems) on the calcium dependent chlorur channels of rat dorsal root ganglia neural cell membranes. For this purpose the spinal ganglia cells from 20 Wistar rats which were 2 days old and those prepared in culture media were used. The nerve cells were radiated by 10V/m electric field strength at 900 Mhz. from a distance of 5 cm for six minutes. Changes in cell current were recorded by patch clamp techniques. In the analysis of the records the applied radio frequency signal was not found to change the currents of calcium dependent chlorur channels and the membrane potential meaningfully. The analysis of recordings does not show any meaningful change in the currents of calcium dependent chlorur channels and the membrane potential of the spinal ganglia cells after exposure to a 900 Mhz radiofrequency field.

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“…Because previous investigations have showed nonsynaptic mechanisms of epilepsy (de Almeida et al, 2008), we hypothesize that the responses of neurons to the excitatory inputs could change during different epileptic stages, and the epileptic activity could be sustained by intrinsic features and not by external inputs. Therefore, by using paired-pulse orthodromic and antidromic stimulations (Albertson et al, 1996;Cunha-Reis et al, 2004), we investigated the changes of evoked responses in the hippocampal CA1 region in vivo when the γ-aminobutyric acid (GABA) receptor antagonist picrotoxin (PTX) was used to block the inhibitory synaptic transmission. The results of the investigation can provide important information for the development of new clinical treatments for epilepsy disease.…”

Section: Introductionmentioning

confidence: 99%

Changes of paired-pulse evoked responses during the development of epileptic activity in the hippocampus

Feng

Zheng

Tian

et al. 2011

J. Zhejiang Univ. Sci. B

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Dysfunction of inhibitory synaptic transmission can destroy the balance between excitatory and inhibitory synaptic inputs in neurons, thereby inducing epileptic activity. The aim of the paper is to investigate the effects of successive excitatory inputs on the epileptic activity induced in the absence of inhibitions. Paired-pulse orthodromic and antidromic stimulations were used to test the changes in the evoked responses in the hippocampus. Picrotoxin (PTX), γ-aminobutyric acid (GABA) type A (GABA A ) receptor antagonist, was added to block the inhibitory synaptic transmission and to establish the epileptic model. Extracellular evoked population spike (PS) was recorded in the CA1 region of the hippocampus. The results showed that the application of PTX induced a biphasic change in the paired-pulse ratio of PS amplitude. A short latency increase of the second PS (PS2) was later followed by a reappearance of PS2 depression. This type of depression was observed in both orthodromic and antidromic paired-pulse responses, whereas the GABAergic PS2 depression [called paired-pulse depression (PPD)] during baseline recordings only appeared in orthodromic-evoked responses. In addition, the depression duration at approximately 100 ms was consistent with a relative silent period observed within spontaneous burst discharges induced by prolonged application of PTX. In conclusion, the neurons may ignore the excitatory inputs and intrinsically generate bursts during epileptic activity. The depolarization block could be the mechanisms underlying the PPD in the absence of GABA A inhibitions. The distinct neuronal responses to stimulations during different epileptic stages may implicate the different antiepileptic effects of electrical stimulation.

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The effect of propofol on ca1 pyramidal cell excitability and gabaa-mediated inhibition in the rat hippocampal slice

Cited by 37 publications

References 28 publications

Intravenous Anesthetics Are More Effective than Volatile Anesthetics on Inhibitory Pathways in Rat Hippocampal CA1

Intravenous Anesthetics Are More Effective than Volatile Anesthetics on Inhibitory Pathways in Rat Hippocampal CA1

The Effect of Radio Frequency Signals on Calcium Dependent Chlorur Channels of Spinal Ganglial Cells

Changes of paired-pulse evoked responses during the development of epileptic activity in the hippocampus

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