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At least 451 records · Page 25Linked to original sources
PubMed1981

Analysis of miniature spontaneous inhibitory postsynaptic currents (sIPSCs) from current noise in crayfish opener muscle.

Deviating from the normal situation, some crayfish muscle fibres showed spontaneous inhibitory activity: discharge of large inhibitory postsynaptic currents, IPSCs, alternating with long lasting bursts of current noise. Analysis of the bursts of current noise revealed that they are composed of spontaneous miniature unit currents, sIPSCs. In the burst periods the sIPSCs occurred with an average rate of 3.5--10 k Hz and had an amplitude of about alpha = 90 pA at a driving force delta E = 10 mV. The peak conductance gamma alpha = alpha/delta E of the sIPSCs was gamma alpha = 9.2 nS +/- 0.5 (S.D., n = 5) for membrane potentials between E = --60 mV and E = --80 mV. gamma alpha seemed to decrease when the membrane was hyperpolarized. The time constants of decay, tau of the sIPSCs were identical with tau of the IPSCs. Further, tau and its potential dependence agreed with the mean lifetimes of inhibitory postsynaptic channels operated by gamma-aminobutyric acid (GABA) [Dudel et al. 1977, 1980]. Synchronized opening of about 750 inhibitory synaptic channels generates a sIPSC. Analysis of this anomalous bursting inhibitory activity thus yields the size of the inhibitory quantum of transmission, which could not be obtained from IPSCs.

Animals↗
PubMed1998

Properties of depolarization-induced suppression of inhibitory transmission in cultured rat hippocampal neurons.

Properties of depolarization-induced suppression of inhibitory transmission ("DSI") in cultured rat hippocampal neurons were examined, by recording inhibitory postsynaptic currents (IPSCs) evoked by single presynaptic neurons. In about 40% of the inhibitory synapses, transient suppression of IPSCs was induced by applying a depolarizing pulse (to 0 mV, > 2 s) to the postsynaptic neuron, which was identified to be gamma-aminobutyric acid dependent (GABAergic) in some pairs, and to be glutamatergic in some other pairs. This depolarization-induced suppression of IPSCs, "DSI", was Ca2+ dependent, and was associated with an increase in the paired-pulse ratio. Phorbol esters had an occluding effect on DSI when applied to the bath solution, but not to the pipette solution used for the postsynaptic neuron. Application of the opioid receptor antagonist naloxone had no effect on DSI. The present study demonstrates that a pair of cultured hippocampal neurons can exhibit DSI similar to that previously reported to occur in hippocampal slices; this suggests that a dissociated cell culture system can provide a useful model system for the study of DSI. Furthermore, it was found that inhibitory neurons, in addition to excitatory ones, can induce DSI, and that a process sensitive to phorbol esters, but not activation of opioid receptors, is involved in DSI.

Animals↗
PubMed2002

Distribution and kinetic properties of GABAergic inputs to layer V pyramidal cells in rat auditory cortex.

Neocortical layer V is distinguished by both its pyramidal cells and its varied cortical and extracortical projections. Several studies suggest that the layer V pyramidal cell types, intrinsically bursting (IB) and regular spiking (RS) cells, differ both in the circuits in which they participate and in their inhibitory inputs. We quantified differences in inhibitory inputs to RS and IB cells using whole-cell voltage clamp techniques in the auditory cortex. We recorded miniature inhibitory postsynaptic currents (mIPSCs) and spontaneous IPSCs to gain kinetic, amplitude, and frequency information about GABAergic synapses. We then used focal sucrose applications to elicit mIPSC rate increases at the soma or dendrites of both cell types. We also electrically stimulated the axons giving rise to inhibitory synaptic inputs to measure minimally evoked IPSCs occurring at the soma or apical dendrites. We found that spontaneous and evoked IPSCs recorded from the auditory cortex have faster rise and decay kinetics when directly compared with those of the same layer V cells in other sensory cortical areas. We also found that mIPSCs observed in auditory IB and RS cells are different from one another. RS cell mIPSCs are larger and have faster rises and decays than IB cell mIPSCs, but IB cell mIPSCs occur more frequently. Focal sucrose application showed that most IB cell mIPSCs originate in the dendrites and are subject to dendritic filtering while most RS cell mIPSCs originate at the soma and are not filtered. These findings suggest that, first, IB and RS cells process their inputs in fundamentally different ways and, second, auditory cortical RS and IB cells may have specializations that allow them to process inhibitory inputs faster.

Animals↗
PubMed2005

Analysis of the excitatory and inhibitory components of postsynaptic currents recorded in pyramidal neurons and interneurons in the rat hippocampus.

Postsynaptic currents recorded from interneurons and pyramidal cells in hippocampal slices by local voltage clamping were found to be the sum of excitatory (EPSC) and inhibitory (IPSC) components. An approach allowing quantitative assessment of the amplitude and time course of EPSC and IPSC without pharmacological blockade of the major postsynaptic receptors involved in generating these currents was developed. The approach is based on the existence of a significant difference between reversion potentials of cationic and anionic currents and the presence of a linear zone in the voltage-current characteristics of responses to excitatory and inhibitory transmitters. Comparison of the results of this calculation-based method with those of classical pharmacological analysis of the excitatory and inhibitory components of postsynaptic currents showed them to be virtually identical, which allows synaptic currents in defined neurons to be studied without altering the state of synaptic connections throughout the brain slice. IPSC was found to make a smaller contribution to the total postsynaptic current recorded in interneurons as compared with pyramidal neurons in rat hippocampal field CA1.

Animals↗
PubMed1992

Norepinephrine activates potassium conductance in neurons of the turtle cerebral cortex.

Whole-cell voltage and current clamp recordings were obtained from cortical neurons of the pond turtle, Pseudemys scripta elegans. Norepinephrine (NE) induced an outward current in 50% of pyramidal neurons. This current had a reversal potential of -88.3 +/- 3.2 mV, consistent with a K+ conductance increase, and had a mean amplitude of 18.3 +/- 7.2 pA at -40 mV. The ionic dependence and pharmacological analyses are both consistent with alpha 2 adrenergic receptor stimulation. Inhibition of Na(+)-dependent action potentials with TTX did not diminish the NE-induced K+ conductance, indicating that NE acts directly on the postsynaptic neuron. In addition to effects on postsynaptic conductance, NE dramatically decreased the amplitude of spontaneous inhibitory postsynaptic currents (IPSCs) in 55% of pyramidal neurons. The decrease in spontaneous IPSCs was observed both in those neurons which exhibited an increase in K+ conductance in response to NE administration (81%) and in those which did not (33%). Thus, NE modulates neuronal excitability both directly by activating a postsynaptic K+ conductance and indirectly by decreasing spontaneous IPSCs.

Action Potentials↗
PubMed1992

Ethanol enhances synaptically evoked GABAA receptor-mediated responses in cerebral cortical neurons in rat brain slices.

Previous intracellular electrophysiological studies on rat hippocampal brain slices have shown very little effect of acute ethanol application on synaptically evoked GABAA receptor-mediated responses recorded in CA1 pyramidal neurons. The present study was designed to compare the effects of ethanol on pyramidal neurons in the hippocampus and cerebral cortex. Using conventional intracellular microelectrodes (60-80 M omega) to impale cortical neurons in brain slices, 80 mM ethanol application did not affect the membrane input impedance nor evoked EPSPs, but significantly affected the resting membrane potential (usually a 2-5 mV hyperpolarization). When stimulus-evoked GABAA-mediated IPSCs were studied using whole-cell recordings from cortical neurons voltage-clamped at depolarizing potentials, monophasic IPSCs were evoked that were blocked by bicuculline, increased by pentobarbital, and enhanced by ethanol superfusion in a dose dependent manner over the range of 20-160 mM. Hippocampal IPSCs recorded under identical conditions were not enhanced by ethanol. Parallel studies of GABA-stimulated 36Cl- flux measurements in microsacs prepared from hippocampal, cerebral cortical and cerebellar tissue demonstrated that ethanol significantly enhanced (30-50%) 36Cl- flux in microsacs derived from the cerebral cortex and cerebellum, but not in microsacs prepared from the hippocampus. These results demonstrate that there are clear brain region-dependent differences in the way that GABAA receptor function is altered by acute ethanol, and that these differences are apparent not only as an enhancement of responses to exogenous GABA, but also as a facilitation of the responses to endogenous GABA released from inhibitory nerve terminals during synaptic activation.

Animals↗
PubMed1995

Effects of metabotropic glutamate receptor agonists on excitatory and inhibitory transmissions in cultured rat hippocampal neurons.

Effects of the metabotropic glutamate receptor agonist, trans-ACPD (tACPD), on the excitatory and the inhibitory transmissions were examined with cultured rat hippocampal neurons, by recording monosynaptic excitatory (EPSCs) and inhibitory postsynaptic currents (IPSCs) evoked by electrical stimulation of single presynaptic neurons. EPSCs were suppressed reversibly by application of 100 microM tACPD in almost all the tested neuron pairs with excitatory connections. Effects of tACPD on IPSCs were variable. Application of tACPD did not affect IPSCs in 15 pairs, suppressed them in eight pairs and enhanced them in the remaining eight pairs out of 31 neuron pairs with inhibitory connections. The study demonstrated that in the hippocampus the activation of metabotropic glutamate receptors modulated the inhibitory transmission differently at different synapses, whereas it always suppressed the excitatory transmission.

Animals↗
PubMed1996

Preferential enhancement of inhibitory synaptic transmission by CS-722 in the ventral horn neurons of neonatal rat spinal cord.

We studied the modulatory effect of (R)-4-chloro-2-(2-hydroxy-3-morpholinopropyl)-5-phenyl-4-isoxaz olin-3-one hydrochloride (CS-722), a centrally acting muscle relaxant, on synaptic transmission in the ventral horn neurons of neonatal rat lumbar spinal cord in slices using whole cell recording techniques. Pharmacologically isolated excitatory or inhibitory postsynaptic currents (EPSCs and IPSCs) were evoked by stimulating neighboring neurons. CS-722 preferentially enhanced IPSCs with little effects on EPSCs. Moreover, CS-722 reduced paired pulse facilitation of gamma-aminobutyric acid (GABA)-mediated IPSCs, suggesting its action on the presynaptic terminal. Preferential facilitatory effects on inhibitory synaptic transmission seem to be one of the mechanisms underlying muscle relaxation of this compound.

Animals↗
PubMed1995

An immunological enrichment method for epithelial cells from peripheral blood.

The ability of primary tumours to metastasize accounts for the majority of cancer deaths. The emergence of circulating carcinoma cells in the peripheral blood is supposed to be an indicator for cancer cell spread. We have focused on this phenomenon in order to develop a sensitive technique for enriching epithelial derived cells on the basis of a two-layer density gradient and subsequent immune magnetic cell sorting. Epithelial cells are possess a cytoskeleton containing an assembly of intermediate filaments. During carcinogenesis these filaments do not undergo modifications of antibody binding epitopes such as occur in the protein domains of surface markers. We have developed a two-layer density gradient in which the epithelial cells form a single density band. This was demonstrated by recovery experiments using [3H]thymidine-labelled epithelial cells which showed epithelial cells were enriched within this first step by a factor of 20. In a second step the MACS system was applied. Cells were stained with a performed FITC-conjugated mouse anti-human cytokeratin antibody bound to a rat anti-mouse antibody coupled to superparamagnetic particles (immune paramagnetic separation complex; IPSC) and subjected to high gradient magnetic fields. The two-step procedure was confirmed by dispersing 50 epithelial cells in 5 x 10(5), 5 x 10(6), 5 x 10(7), 5 x 10(8), 5 x 10(9) peripheral blood leucocytes. Specific binding of the preformed IPSC was demonstrated by flow cytometry, confocal laser, fluorescent and electron microscopy. The specificity of the method was further proved by dual staining with IPSC and anti-human PSA antibody of epithelial prostatic cells separated from peripheral blood in vitro. By means of this double-step separation method it was possible to isolate up to 15-20 cells out of 50 epithelial cells originally suspended into 5 x 10(7) to 5 x 10(9) human peripheral blood leucocytes. This represented an enrichment factor between 20,000 and 200,000, depending on the initial cell number. The immunologically captured epithelial cells can be used for further cytogenetic investigations such as in situ hybridization (ISH) and/or polymerase chain reaction (PCR) to detect cancer cell specific gene aberrations. This sensitive combined buoyant density immune magnetic cell separation technique is capable of detecting free carcinoma cells in the peripheral blood.

Animals↗
PubMed1992

Comparison of the effect of the GABA uptake blockers, tiagabine and nipecotic acid, on inhibitory synaptic efficacy in hippocampal CA1 neurones.

The action of the novel gamma-aminobutyric acid (GABA) uptake blocker, tiagabine, has been studied on isolated GABAergic fast inhibitory postsynaptic potentials (IPSP) and currents (IPSC) in rat hippocampal CA1 pyramidal cells in the slice preparation. Tiagabine (20-50 microM) had little effect on the peak amplitude of the IPSC, but caused a robust increase in the half-width (by 109 +/- 15%). These results contrasted with those obtained using the established uptake blocker, nipecotic acid (100 microM to 1 mM), which reduced the amplitude of the IPSC by 35 +/- 6% and caused only a modest prolongation of the recovery phase. These effects, which were poorly reversible, are probably explained by the fact that nipecotic acid is a substrate for the GABA-uptake carrier and can act as a false transmitter. Tiagabine is not transported by the GABA carrier and results with this substance demonstrate the role of uptake in determining the kinetics of activation of GABAA receptors. Tiagabine is proposed as the blocker of choice for the GABA uptake system.

Animals↗
PubMed1994

Contributions of multiple calcium channel types to GABAergic transmission in rat cultured hippocampal neurons.

Effects of Ca2+ channel blockers on GABAergic transmission were examined with rat cultured hippocampal neurons. The GABAergic synaptic currents (IPSCs) evoked by electrical stimulation of single presynaptic neurons were recorded from voltage-clamped postsynaptic neurons. The amplitude of IPSCs was not changed by 10 microM nifedipine (L-type Ca2+ channel blocker), but was decreased irreversibly to 37% of control by 1 microM omega-conotoxin GVIA (N-type blocker, CgTX), to 67% by 0.1 microM omega-agatoxin IVA (P-type blocker, AGTX), and to 1% by both toxins. From these data and the Ca(2+)-dependence of IPSCs, the contributions of CgTX-sensitive and AGTX-sensitive Ca2+ channels to the transmission were estimated at 59% and 36%, respectively.

Animals↗
PubMed1995

Baclofen inhibits GABAergic transmission after treatment with type-specific calcium channel blockers in cultured rat hippocampal neurons.

Effects of the GABAB agonist baclofen on GABAergic transmission were examined before and after treatment with N-type (CgTX) and P-type (AGTX) Ca2+ channel blockers in cultured rat hippocampal neurons. Baclofen reduced GABAergic synaptic currents (IPSCs) without affecting the postsynaptic sensitivity to GABA. The presynaptic inhibition by baclofen was not blocked by Ba2+, a K+ channel blocker. IPSCs were reduced by treatment with either CgTX or AGTX, and completely abolished by treatment with both toxins. Both IPSCs after treatment with CgTX and those after AGTX treatment were similarly reduced by baclofen. The results indicate that both the transmission mediated by AGTX-sensitive Ca2+ channels and that by CgTX-sensitive Ca2+ channels are sensitive to baclofen, suggesting that activation of presynaptic GABAB receptors might inhibit both types of Ca2+ channels contributing to the GABAergic transmission in the hippocampus.

Animals↗
PubMed1995

Desensitized states prolong GABAA channel responses to brief agonist pulses.

We studied the role of desensitization at inhibitory synapses by comparing nonequilibrium GABAA channel gating with inhibitory postsynaptic currents (IPSCs). Currents activated by brief pulses of 1-10 mM GABA to outside-out patches from cultured hippocampal neurons mimicked GABA-mediated IPSCs. Although the average open time of single GABAA channels following brief pulses was less than 10 ms, channels entered long (tau = 38-69 ms) closed states and subsequently reopened. Movement through these states resulted in paired-pulse desensitization. The time required for deactivation after removal of agonist also increased in proportion to the extent of desensitization. These results suggest that visits to desensitized states buffer the channel in bound conformations and underlie the expression of long-lasting components of the IPSC. Reopening after GABAA receptor desensitization may thus enhance inhibitory synaptic transmission by prolonging the response to a brief synaptic GABA transient.

Animals↗
PubMed2005

Bidirectional regulations for glutamate and GABA release in the hippocampus by alpha7 and non-alpha7 ACh receptors.

In the assay of glutamate and gamma-aminobutyric acid (GABA) with a high-performance liquid chromatography, spontaneous release of glutamate and GABA from rat hippocampal slices was significantly enhanced by mecamylamine, an inhibitor of non-alpha7 ACh receptors, or alpha-bungarotoxin, an inhibitor of alpha7 ACh receptors in the absence of tetrodotoxin (TTX), but not in the presence of TTX. Nicotine significantly enhanced glutamate and GABA release in the absence of TTX, that is abolished by mecamylamine or alpha-bungarotoxin, while it had no effect on the release in the presence of TTX. In the recording of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor-mediated excitatory postsynaptic currents (AMPA-EPSCs) and GABA(A) receptor-mediated inhibitory postsynaptic currents (GABA(A)-IPSCs) from CA1 pyramidal neurons of rat hippocampal slices, nicotine did not affect the rate and amplitude of AMPA-EPSCs and AMPA-miniature EPSCs. In contrast, nicotine significantly increased the rate of GABA(A)-IPSCs, without affecting the amplitude, but such effect was not obtained with GABA(A)-miniature IPSCs. The collective results suggest that alpha7 and non-alpha7 ACh receptors expressed in the hippocampus, activated under the basal conditions, inhibit release of glutamate and GABA controlled through multi-synaptic relays, but that otherwise, those receptors, highly activated by nicotine, stimulate both the release, with a part of GABA released from interneurons transmitting to CA1 pyramidal neurons. Furthermore, the results also suggest that alpha7 and non-alpha7 ACh receptors do not have potency sufficiently to modulate glutamate and GABA release controlled by single synapses.

Animals↗
PubMed2004

Fentanyl inhibits GABAergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus.

Fentanyl citrate is a synthetic opiate analgesic often used clinically for neonatal anesthesia. Although fentanyl significantly depresses heart rate, the mechanism of inducing bradycardia remains unclear. One possible site of action is the cardioinhibitory parasympathetic vagal neurons in the nucleus ambiguus (NA), from which originates control of heart rate and cardiac function. Inhibitory synaptic activity to cardiac vagal neurons is a major determinant of their activity. Therefore, the effect of fentanyl on GABAergic neurotransmission to parasympathetic cardiac vagal neurons was studied using whole-cell patch clamp electrophysiology. Application of fentanyl induced a reduction in both the frequency and amplitude of GABAergic IPSCs in cardiac vagal neurons. This inhibition was mediated at both pre- and postsynaptic sites as evidenced by a dual decrease in the frequency and amplitude of spontaneous miniature IPSCs. Application of the selective micro-antagonist CTOP abolished the fentanyl-mediated inhibition of GABAergic IPSCs. These results demonstrate that fentanyl acts on micro-opioid receptors on cardiac vagal neurons and neurons preceding them to reduce GABAergic neurotransmission and increase parasympathetic activity. The inhibition of GABAergic effects may be one mechanism by which fentanyl induces bradycardia.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2005

The interaction of noradrenaline with sevoflurane on GABA(A) receptor-mediated inhibitory postsynaptic currents in the rat hippocampus.

Little is known about the interaction of noradrenaline with volatile anesthetics in inhibitory synaptic transmission. The purpose of the present study was to investigate the interactions of noradrenaline and sevoflurane on inhibitory synaptic transmission mediated by GABA(A) receptors in the rat hippocampus. Pharmacologically isolated GABA(A) receptor-mediated IPSCs were recorded with whole-cell patch-clamp techniques in pyramidal neurons of the CA1 region of rat hippocampal slices. The actions of noradrenaline, noradrenaline analog, sevoflurane, and the interactions of these agents on the frequency and kinetics of spontaneous GABA(A) receptor-mediated IPSCs were studied. Noradrenaline (10 microM) caused an increase in the frequency of action potential-dependent sIPSCs. These effects were completely reversed by the addition of tetrodotoxin (1 microM), suggesting that noradrenaline produces the discharge of GABAergic interneurons innervating on pyramidal cells via adrenoceptors. Although sevoflurane (0.40 mM, 20 min) slightly depressed the amplitude of sIPSCs, sevoflurane significantly prolonged the decay time constant to 451.1 +/- 89.0% of control (n = 9, P < 0.001) without affecting the rise time. In addition, sevoflurane increased the frequency of sIPSCs up to 3-fold. However, pretreatment of cadmium, multiple Ca channel blocker, abolished sevoflurane effects on the frequency whereas the effects on the decay were still observed. Application of both noradrenaline and sevoflurane produced a significant increase of the IPSC frequency than that of noradrenaline alone or sevoflurane alone with prolonged decays. These results provide evidence that both agents have additive effects on GABAergic synaptic transmission at the central nervous system via different mechanisms.

Action Potentials↗
PubMed2006

Inhibitory synaptic transmission in area postrema neurons of the rat showing robust presynaptic facilitation mediated by nicotinic ACh receptors.

Inhibitory synaptic transmission and its modulation in neurons of the area postrema (AP), one of autonomic nuclei in the medulla, were studied using whole-cell patch-electrodes applied to slices from rats on postnatal days 10-24. When glycine (100 microM) or GABA (10 microM) was applied to AP neurons from a "Y tube", large outward currents that showed reversal potential of - 67 mV (approximate Cl- equilibrium potential estimated) were induced. At a holding potential of - 10 mV, application of high K+ to the AP neurons evoked massive inhibitory postsynaptic currents (IPSCs) in the neurons. Most of the evoked synaptic currents were blocked by bicuculline, while the remaining currents were sensitive to strychnine, indicating that the major inhibitory transmission in the area postrema was GABAergic. When nicotine (5-100 microM) was applied to AP neurons, robust IPSCs having GABAergic identity were evoked. Even in the presence of tetrodotoxin, nicotine could induce GABAergic IPSCs, most of which, however, disappeared in the presence of 5 mM Mg2+. Presynaptic facilitation was also induced by other nicotinic agonists, including cytisine, 1,1-dimethyl-4-phenyl-piperazinium iodide, ACh and choline. The nicotine-induced presynaptic facilitation was inhibited by mecamylamine and slightly inhibited by dihydro-beta-erythroidine or alpha-Bungarotoxin. These results indicate that nicotinic receptors are expressed at GABAergic presynaptic terminals in the area postrema and induce Ca2+ influx to trigger vesicular release. The major nicotinic receptors involved are thought to be heteromeric subtypes such as alpha3beta4 receptors, which may regulate inhibitory transmission potently responding to endogenous or exogenous nicotinic agents appeared in this area.

Animals↗
PubMed2003

Partial hippocampal kindling increases GABAB receptor-mediated postsynaptic currents in CA1 pyramidal cells.

In previous studies, we showed that partial hippocampal kindling decreased the efficacy of the presynaptic GABAB receptors on both GABAergic and glutamatergic terminals of CA1 neurons in hippocampal slices in vitro. In this study, GABAB receptor-mediated inhibitory postsynaptic currents (GABAB-IPSCs) were assessed by whole-cell recordings in CA1 pyramidal neurons in hippocampal slices of male Long-Evans rats. The peak GABAB-IPSC evoked by a brief train of supramaximal stratum radiatum stimuli (20 pulses of 300 Hz) in the presence of picrotoxin (0.1 mM) and kynurenic acid (1 mM) was larger in neurons of kindled (65.9 +/- 5.2 pA, N=42 cells) than control (45.8 +/- 4.8 pA, N=32 cells) rats (P<0.01). Adding GABA uptake blocker nipecotic acid (1 mM) or GABAB receptor agonist baclofen (0.01 mM) in the perfusate induced outward currents that were blocked by GABAB receptor antagonist CGP 55845A (1 microM). The peak outward current induced by nipecotic acid was larger in neurons of the kindled (55.4 +/- 5.7 pA, N=30) than the control group (39.8 +/- 4.5 pA, N=28) (P<0.05). However, the magnitude of the baclofen-induced current was not different between kindled (90.8 +/- 6.9 pA, N=29) and control (87.2 +/- 5.9 pA, N=21) groups (P>0.05). We concluded that partial hippocampal kindling increased GABAB-IPSCs in hippocampal CA1 pyramidal cells via multiple presynaptic mechanisms.

Animals↗