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PubMed1996

Low ethanol concentrations enhance GABAergic inhibitory postsynaptic potentials in hippocampal pyramidal neurons only after block of GABAB receptors.

Despite considerable evidence that ethanol can enhance chloride flux through the gamma-aminobutyric acid type A (GABA/A/) receptor-channel complex in several central neuron types, the effect of ethanol on hippocampal GABAergic systems is still controversial. Therefore, we have reevaluated this interaction in hippocampal pyramidal neurons subjected to local monosynaptic activation combined with pharmacological isolation of the various components of excitatory and inhibitory synaptic potentials, using intracellular current- and voltage-clamp recording methods in the hippocampal slice. In accord with our previous findings, we found that ethanol had little effect on compound inhibitory postsynaptic potentials/currents (IPSP/Cs) containing both GABA/A/ and GABA/B/ components. However, after selective pharmacological blockade of the GABA/B/ component of the IPSP (GABA/B/-IPSP/C) by CGP-35348, low concentrations of ethanol (22-66 mM) markedly enhanced the peak amplitude, and especially the area, of the GABA/A/ component (GABA/A/-IPSP/C) in most CA1 pyramidal neurons. Ethanol had no significant effect on the peak amplitude or area of the pharmacologically isolated GABA/B/-inhibitory postsynaptic current (IPSC). These results provide new data showing that activation of GABAB receptors can obscure ethanol enhancement of GABA/A/ receptor function in hippocampus and suggest that similar methods of pharmacological isolation might be applied to other brain regions showing negative or mixed ethanol-GABA interactions.

Animals↗
PubMed1994

Waveform parameters of recurrent inhibitory postsynaptic potentials in cat motoneurons during time-varying activation patterns.

A considerable number of theoretical and experimental studies have been undertaken to establish quantitative relationships between the time course of postsynaptic potentials in a neuron and the change in firing probability thereby induced. Depending on background synaptic noise level, the time course of the postsynaptic potential per se as well as its time derivative are both of importance in varying proportion. We have recently begun to study recurrent inhibitory potentials in cat hindlimb motoneurons during rhythmically varying rates of stimulation of motor axons. The amplitude-rate relationship exhibits hysteresis in that amplitudes are usually larger during augmenting than decrementing rates in the cycle. We here report results on the other important variable, that is the slope of recurrent inhibitory potential development, which need not a priori be correlated with amplitude. We found that the slope has a relation to stimulus rate similar to amplitude, so that both parameters are correlated. In pentobarbitone anaesthetized or decerebrate cats, intracellular recordings were obtained from hindlimb skeleto-motoneurons. Various hindlimb muscle nerves were prepared for electrical stimulation to elicit recurrent inhibitory potentials, with dorsal roots cut. Test stimulus patterns consisted of repetitive pulse trains whose rates varied, at modulation frequencies between 0.1 and 1.0 Hz, in one of two waveforms: triangular or sinusoidal. Modulation depths were either "full", with rates varying between a minimum of less than 10 and a maximum of around 50 pulses per s. Or they were about "half" this depth, with mean rates shifted into a "low", "medium" or "high" rate region. Recurrent inhibitory potentials were averaged with respect to stimuli occurring during different phases of the stimulation cycle. Most often when, throughout the cycle, the amplitude changed in a consistent way, so did the slopes of the inhibitory potentials. That is, when the amplitudes rhythmically declined with increasing and recovered with decreasing stimulus rate, the rate of hyperpolarization followed the same pattern. With prominent hysteresis in amplitude, a corresponding hysteresis appeared in slopes. Hence, amplitude and slopes were correlated, occasionally showing a hysteresis among themselves. To a certain extent, these results can be explained by Renshaw cell behaviour, the contribution of the Renshaw cell-motoneuron synapse being unknown and difficult to assess experimentally. For the inhibitory effect of Renshaw cells on motoneurons (and reciprocal Ia inhibitory interneurons), both its magnitude and its time course probably play an important role in determining the efficacy of counteracting local excitatory inputs. The change in slope of inhibitory potentials, and likely its underlying conductance, during cyclic motoneuron activation can be presumed to significantly contribute to the temporal pattern of discharge of motoneurons, in particular in relation to the prevention of synchronization leading to enhanced tremor.

Animals↗
PubMed1996

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

Previous studies using high-resistance sharp electrodes demonstrated that corticosterone (CORT) reduced GABAergic synaptic inhibition in CA1 neurons of the rat hippocampus in vitro. In the present study we used whole-cell gigaseal recordings to investigate the possible role of cytosolic factors in the transduction mechanism underlying this action. The perturbation of the intracellular milieu that occurs under these recording conditions abolished the CORT-induced decrease in inhibitory postsynaptic conductance. CORT actually increased GABAA receptor-mediated conductances in about 50% of the neurons tested when the whole-cell recording mode was employed. As in the high-resistance microelectrode studies, CORT did not change the resting membrane potential, action potential amplitude or input resistance. The results suggest that the reduction of GABAergic synaptic inhibition in hippocampal CA1 pyramidal neurons induced by CORT critically depends on the presence of cytosolic factors, which wash out during whole-cell gigaseal recordings.

Animals↗
PubMed1975

[Monosynaptic inhibitory postsynaptic potentials of cerebral cortex neurons].

The auditory cortes of cats immobilized with d-tubocurarine was stimulated by monopolar macroelectrodes (tip diameter 100 mu) or micloelectrodes (tip diameter 100--15 mu). In both cases in cortical neurons located closely to the stimulation point IPSPs were recorded with latencies ranging between 0.4--1.2 and 1.4 6.0 ms. It is suggested that IPSPs of the first group are generated in response to direct stimulation of the bodies and axons of the inhibitory cortical neurons (monosynaptically). The amplitude of such IPSPs ranged in different neurons from 3 to 15 mV and their duration was between 4 and 15 ms. Many of them were complicated by later additional inhibitory volleys. 1.5% of all IPSPs generated in response to geniculocortical fibres stimulation had latencies between 0.8--1.3 ms. It is suggested that these IPSPs were also evoked monosynaptically.

Animals↗
PubMed1995

The serotonergic inhibitory postsynaptic potential in prepositus hypoglossi is mediated by two potassium currents.

Synaptic inhibition mediated by the activation of potassium channels has been reported from several types of neurons. In each case, despite mediation by different neurotransmitters, the K+ conductance underlying the synaptic potential is activated by a G protein and inwardly rectifies. We report here a second K+ current that contributes to synaptic inhibition. Intracellular recordings were made from guinea pig nucleus prepositus hypoglossi in vitro, where we have described a 5-HT-mediated IPSP. Voltage-clamp analysis of the current induced by applied 5-HT revealed two separate conductances: an inwardly rectifying, rapidly activating K+ current (IIR) and an outwardly rectifying, slowly activating K+ current (IOR). IIR was blocked by extracellular Ba2+ (200 microM) and TEA+ (126 mM). IOR was insensitive to this concentration of Ba2+ and TEA+, but was inhibited by Cd2+ and intracellular BAPTA, indicating Ca dependence. Single focal electrical stimuli evoked a 5-HT-mediated IPSP, or under voltage clamp, an inhibitory postsynaptic current (IPSC). Ba2+ blocked only a component of this IPSC, which corresponded to the current caused by IIR. When multiple stimuli were applied (to prolong the release of transmitter), the time-dependent current IOR was more fully activated, resulting in an augmentation of the IPSC. We conclude that the IPSC is caused by both currents and that its amplitude can be modulated by the degree to which IOR is activated. This represents a mechanism by which synaptic responses can be potentiated.

Animals↗
PubMed2002

L-type calcium channel-mediated plateau potentials in barrelette cells during structural plasticity.

Development and maintenance of whisker-specific patterns along the rodent trigeminal pathway depends on an intact sensory periphery during the sensitive/critical period in development. Barrelette cells of the brain stem trigeminal nuclei are the first set of neurons to develop whisker-specific patterns. Those in the principal sensory nucleus (PrV) relay these patterns to the ventrobasal thalamus, and consequently, to the somatosensory cortex. Thus PrV barrelette cells are among the first group of central neurons susceptible to the effects of peripheral damage. Previously we showed that membrane properties of barrelette cells are distinct as early as postnatal day 1 (PND 1) and remain unchanged following peripheral denervation in newborn rat pups (Lo and Erzurumlu 2001). In the present study, we investigated the changes in synaptic transmission. In barrelette cells of normal PND 1 rats, weak stimulation of the trigeminal tract (TrV) that was subthreshold for inducing Na(+) spikes evoked an excitatory postsynaptic potential-inhibitory postsynaptic potential (EPSP-IPSP) sequence that was similar to the responses seen in older rats (Lo et al. 1999). Infraorbital nerve transection at birth did not alter excitatory and inhibitory synaptic connections of the barrelette cells. These observations suggested that local neuronal circuits are already established in PrV at birth and remain intact after deafferentation. Strong stimulation of the TrV induced a sustained depolarization (plateau potential) in denervated but not in normal barrelette neurons. The plateau potential was distinct from the EPSP-IPSP sequence by 1) a sustained (>80 ms) depolarization above -40 mV; 2) a slow decline slope (<0.1 mV/ms); 3) partially or totally inactivated Na(+) spikes on the plateau; and 4) a termination by a steep decay (>1 mV/ms) to a hyperpolarizing membrane level. The plateau potential was mediated by L-type Ca(2+) channels and triggered by a N-methyl-D-aspartate (NMDA) receptor-mediated EPSP. gamma-aminobutyric acid-A (GABA(A)) receptor-mediated IPSP dynamically regulated the latency and duration of the plateau potential. These results indicate that after neonatal peripheral damage, central trigeminal inputs cause a large and long-lasting Ca(2+) influx through L-type Ca(2+) channels in barrelette neurons. Increased Ca(2+) entry may play a key role in injury-induced structural remodeling, and/or transsynaptic cell death.

Action Potentials↗
PubMed1997

Depression of early and late monosynaptic inhibitory postsynaptic potentials in hippocampal CA1 neurons following prolonged benzodiazepine administration: role of a reduction in Cl- driving force.

GABAergic synaptic responses were studied by direct, monosynaptic activation of GABAergic interneurons in the CA1 region of in vitro hippocampal slices from rats made tolerant to the benzodiazepine, flurazepam. Monosynaptic IPSPs were elicited in CA1 pyramidal neurons, following 1 week oral flurazepam administration, by electrical stimulation at the stratum oriens/stratum pyramidale or stratum radiatum/ stratum-lacanosum border < or = 0.5 mm from the recording electrode plane. Excitatory input to pyramidal cells and interneurons was eliminated by prior superfusion of the glutamate receptor antagonists, APV (50 microM) and DNQX (10 microM). GABAA receptor-mediated early IPSPs were further isolated by perfusion of the GABAB antagonist, CGP 35348 (25 microM) or by diffusion of Cs- from the recording electrode. GABAB receptor-mediated late IPSPs were pharmacologically isolated by perfusion of the GABAA antagonist, picrotoxin (50 microM). There was a significant decrease in the amplitude of pharmacologically isolated early and late IPSPs in FZP-treated neurons without a change in passive membrane properties. A shift of the early IPSP, but not the late IPSP, reversal potential in FZP-treated neurons suggested that a change in the driving force for anions, presumably Cl, in CA1 neurons was one important factor related to the decreased early IPSP amplitude after prolonged activation of GABAA receptors by flurazepam. A decreased early IPSP amplitude accompanied by a decreased late IPSP amplitude suggested that presynaptic GABA release onto FZP-treated pyramidal cells may also be reduced. We conclude from these data that an impairment of GABAergic transmission in CA1 pyramidal neurons associated with the development of tolerance during chronic benzodiazepine treatment may be related to the regulation of both pre- and postsynaptic mechanisms at the GABA synapse.

Animals↗
PubMed1992

Depression by neuropeptide Y of noradrenergic inhibitory postsynaptic potentials of locus coeruleus neurones.

Intracellular recordings were performed in a pontine slice preparation of the rat brain containing the locus coeruleus (LC). The spontaneous firing of action potentials was prevented by passing continuous hyperpolarizing current via the recording electrode. Focal electrical stimulation evoked a synaptic depolarization (PSP) followed by a hyperpolarization (IPSP). Neuropeptide Y (NPY; 0.1 mumol/l) inhibited the IPSP only. Pressure ejection of noradrenaline produced hyperpolarization which was potentiated in the presence of NPY (0.1 mumol/l). Hence, NPY appears to inhibit the release of noradrenaline from dendrites or recurrent axon collaterals of LC neurones.

Action Potentials↗
PubMed1985

Selective depression of hippocampal inhibitory postsynaptic potentials and spontaneous firing by volatile anesthetics.

The effects of halothane, isoflurane and enflurane on the rat hippocampal CA1 neurons in in vitro preparations were studied by intracellular recordings. All volatile anesthetics, at the concentrations which are likely to be in the range of clinical doses, depressed the IPSPs and the spontaneous firing without affecting the resting membrane properties and the EPSPs. The results suggest that the simultaneous blocking effects of the anesthetics on both the spontaneous firing and IPSPs are responsible for production of general anesthesia rather than their blocking actions on the EPSPs in terms of behavior of hippocampal neurons.

Anesthetics↗
PubMed1990

A subset of local interneurons generate slow inhibitory postsynaptic potentials in hippocampal neurons.

Topical application of 4-aminopyridine (4-AP) onto hippocampal slices produced spontaneous repetitive large hyperpolarizing potentials in CA1 neurons. This effect of 4-AP was blocked by a new GABAB receptor antagonist, 2-hydroxy-saclofen. 2-Hydroxy-saclofen also blocked slow IPSPs evoked by stimulation of stratum radiatum. It is suggested that 4-AP-evoked slow hyperpolarizing potentials are in fact slow IPSPs evoked by activation of a selective subset of interneurons which do not produce fast IPSPs.

4-Aminopyridine↗