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PubMed1997

Activation and detection of facilitation as studied by presynaptic voltage control at the inhibitor of the crayfish opener muscle.

Facilitation at the crayfish neuromuscular inhibitor synapse was investigated with the use of a presynaptic voltage control method in which 5-ms presynaptic pulses were used to activate and monitor facilitation. A single 5-ms pulse was able to activate facilitation with a decay time constant similar to that of the F2 component of facilitation activated by action potentials. The quality of the control of presynaptic potential during F2 facilitation was evaluated by measuring the amplitude of presynaptic pulses and by analyzing the shape of the depolarization-release coupling plot during facilitation. Both approaches suggested that neither the amplitude of presynaptic depolarizations nor the space clamp of the presynaptic axon was changed during F2 facilitation. The activation of facilitation was examined by changing the amplitude of conditioning pulses systematically and using a test pulse of a constant amplitude to monitor facilitation. We found that a significant amount of facilitation could be activated by conditioning pulses that were subthreshold to the activation of transmitter release. Facilitation plateaued before the inhibitory postsynaptic potentials (IPSPs) activated by conditioning pulses reached their maximum. A double logarithm plot of facilitation magnitude against the conditioning IPSP amplitude yielded a slope of 0.34, which implies that the calcium ion cooperativity of activating facilitation is about one third of the secretion process. These findings enabled us to activate near maximal facilitation, by a burst of subthreshold conditioning pulses, without any conditioning transmitter release, and, therefore, to avoid complications associated with previous transmitter release. The detection of facilitation was examined by changing test pulse amplitude systematically to evaluate the ability of the test pulse to detect a constant level of facilitation. The magnitude of normalized facilitation decreased with increasing test pulse amplitude. The magnitude of absolute facilitation (the amplitude of the facilitated minus the control IPSP) increased with increasing test pulse amplitude. A double logarithm plot between facilitated and control IPSPs gave rise to a slope of 0.77, which suggests that the calcium cooperativity of transmitter release was decreased during facilitation.

Animals↗

PubMed1995

Changes in excitatory neurotransmission in the CA1 region and dentate gyrus in a chronic model of temporal lobe epilepsy.

1. In this report we compare changes of excitatory neurotransmission within the CA1 region and the dentate gyrus (DG) in a model of chronic temporal lobe epilepsy (TLE). Extracellular and intracellular recordings were obtained from in vitro hippocampal-parahippocampal slices > or = 1 mo after a period of self-sustaining limbic status epilepticus (SSLSE) induced by continuous hippocampal stimulation. Pyramidal cells in CA1 were activated by electrodes in the stratum lacunosum/moleculare or stratum radiatum. Granule cells in DG were similarly activated by electrodes positioned in the perforant path. 2. Monosynaptic excitatory postsynaptic potentials (EPSPs) evoked in CA1 pyramidal cells in post-SSLSE tissue were always longer than those evoked in control tissue, irrespective of whether hyperresponsiveness was present or not. EPSPs elicited by stimulus subthreshold for action potentials (APs) in post-SSLSE and in control slices and matched in amplitude had a statistically greater duration in the post-SSLSE slices. Durations of monosynaptic EPSPs elicited by stimuli subthreshold for APs in DG granule cells in post-SSLSE slices were not longer than EPSPs of equal amplitude elicited in control slices. 3. Higher-intensity stimuli produced EPSPs with associated APs and, in certain cases in the post-SSLSE tissue, hyperresponsive events with multiple (> or = 3) APs. Durations of depolarizing profiles with stimuli producing APs were overall longer in both CA1 pyramidal cells and DG granule cells and correlated with the degree of hyperresponsiveness. 4. Neither the amplitudes nor the durations of monosynaptic EPSPs evoked in CA1 pyramidal cells in slices from control animals were affected by the addition of D(-)-2-amino-5-phosphonovaleric acid (APV), a blocker of the N-methyl-D-aspartate (NMDA) receptor, to the artificial cerebrospinal fluid (ACSF) bathing the slices. In contrast to the situation in control tissue, in post-SSLSE tissue APV shortened EPSPs evoked in CA1 pyramidal cells while not changing their amplitudes. After APV, inhibitory postsynaptic potentials (IPSPs) remained greatly diminished or absent in CA1 pyramidal cells. APV did not statistically decrease amplitudes of monosynaptic EPSPs evoked in DG granule cells in either control slices or post-SSLSE slices. APV decreased EPSP durations in both types of slices, more so in the post-SSLSE tissue. 5. In control slices, APV did not change the amplitudes or durations of depolarizing profiles of responses evoked by stimuli producing APs in CA1. Similarly, APV did not change the amplitudes of such responses in DG. However, APV did reduce the durations of such responses in DG in control slices.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1992

Nimodipine increases excitability of rabbit CA1 pyramidal neurons in an age- and concentration-dependent manner.

1. Cellular properties were studied before and after bath application of the dihydropyridine L-type calcium channel antagonist nimodipine in aging and young rabbit hippocampal CA1 pyramidal cells in vitro. Various concentrations of nimodipine, ranging from 10 nM to 10 microM, were tested to investigate age- and concentration-dependent effects on cellular excitability. Drug studies were performed on a population of neurons at similar holding potentials to equate voltage-dependent effects. The properties studied under current-clamp conditions included steady-state current-voltage relations (I-V), the amplitude and integrated area of the postburst afterhyperpolarization (AHP), accommodation to a prolonged depolarizing current pulse (spike frequency adaptation), and single action-potential waveform characteristics following synaptic activation. 2. Numerous aging-related differences in cellular properties were noted. Aging hippocampal CA1 neurons exhibited significantly larger postburst AHPs (both the amplitude and the integrated area were enhanced). Aging CA1 neurons also exhibited more hyperpolarized resting membrane potentials with a concomitant decrease in input resistance. When cells were grouped to equate resting potentials, no differences in input resistance were noted, but the AHPs were still significantly larger in aging neurons. Aging CA1 neurons also fired fewer action potentials during a prolonged depolarizing current injection than young CA1 neurons. 3. Nimodipine decreased both the peak amplitude and the integrated area of the AHP in an age- and concentration-dependent manner. At concentrations as low as 100 nM, nimodipine significantly reduced the AHP in aging CA1 neurons. In young CA1 neurons, nimodipine decreased the AHP only at 10 microM. No effects on input resistance or action-potential characteristics were seen. 4. Nimodipine increased excitability in an age- and concentration-dependent manner by decreasing spike frequency accommodation (increasing the number of action potentials during prolonged depolarizing current injection). In aging CA1 neurons, this effect was significant at concentrations as low as 10 nM. In young CA1 neurons, nimodipine decreased accommodation only at higher concentrations (> or = 1.0 microM). 5. We conclude that aging CA1 neurons were less excitable than young neurons. In aging hippocampus, nimodipine restores excitability, as measured by size of the AHP and degree of accommodation, to levels closely resembling those of young adult CA1 neurons. These actions of nimodipine on aging CA1 hippocampal neurons may partly underlie the drug's notable ability to improve associative learning in aging rabbits and other mammals. Reversal of inhibitory postsynaptic potentials (IPSPs) by chloride ion and/or current injections into six motoneurons revealed the presence of inhibition during the period between phrenic bursts during fictive vomiting and also during the final phase of expulsion when phrenic discharge ceased by abdominal discharge continued. 3. Fictive coughing, evoked by repetitive electrical stimulation of superior laryngeal nerve afferents, was characterized by a large phrenic discharge followed immediately by a large abdominal nerve discharge. During fictive coughing, phrenic motoneurons retained their ramplike depolarizations throughout phrenic discharge; however, the amplitude of depolarization was greater than during inspiration. During the subsequent abdominal nerve discharge, the phrenic membrane potential usually underwent an initial rapid, transient hyperpolarization followed by a gradual repolarization associated with increased synaptic noise.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1990

Temporal correlations in sensory-synaptic interactions: example in crayfish stretch receptors.

1. The effects of inhibitory postsynaptic potential (IPSP) barrages on coding of sinusoidal length inputs were investigated in slowly and rapidly adapting stretch receptors of crayfish (RM1 and RM2, respectively). To examine the contribution of postsynaptic firings, a description was obtained of the temporal correlations between sensory stimuli, pre- and postsynaptic spikes, plus the relative position of the latter. In this analysis, the times between an IPSP and the closest spike preceding or following it are known, respectively, as phase (phi) and cophase (theta). 2. Interactions were similar in RM1 and RM2. The usual effect was the expected increased postsynaptic interval durations, but special consequences were also evoked. With regular IPSPs there were epochs including inhibitory (S) and postsynaptic (R) spikes and fixed "alternations" at S/R times the IPSP rate. S/R ratios were usually 1:1 and 1:2, more rarely 2:1. There were sudden postsynaptic interval duration changes, or "jumps," between successive alternation ratios where inhibitory effects increased or decreased. With 1:1 and 1:2 ratios there was a gradual "sliding," or phi increase-theta decrease, at the pull and the opposite at the release. The theta and phi roughly paralleled the control postsynaptic intervals and the inhibited-minus-control differences, respectively, when sliding was present. Sliding disappeared, and phi and theta tended to become invariant, with 2:1 ratio. 3. Irregular IPSP increased postsynaptic interval irregularities and eliminated alternations. Phase values were irregularly distributed, but theta and control postsynaptic intervals were similar irrespective of pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Recurrent inhibition of cat phrenic motoneurons.

These experiments were performed to re-examine the presence of a recurrent inhibitory pathway to phrenic motoneurons in cats. Following intracellular staining of 49 phrenic motoneurons with horseradish peroxidase, initial axon collaterals were demonstrated in six axons (12%). Intracellular recording and averaging of the synaptic responses evoked by stimulation of the phrenic roots with an intensity subthreshold for axons of the examined motoneurons revealed (in spinalized cats with dorsal roots cut) inhibitory postsynaptic potentials (i.p.s.p.s) in 11/28 (40%) motoneurons (amplitude, 115 +/- 69 (SD) microV; latency, 3.0 +/- 0.6 msec; duration from 12 to 25 msec). In the vicinity of the phrenic nucleus, Renshaw-like units were extracellularly recorded, which fired high-frequency bursts of action potentials following the stimulation of the phrenic roots (burst duration, 8 to 21 msec). Antidromic activation of the C5 phrenic root reduced the firing probability of fibers in the C6 root. The duration of the reduced firing probability corresponded to the duration of both the i.p.s.p.s and the Renshaw units' firing period. It is concluded that Renshaw inhibition is present in phrenic motoneurons. The inhibitory effects of this recurrent pathway may be greater than judged from the small amplitude of the i.p.s.p.s recorded in individual motoneurons, particularly when the whole phrenic pool is activated and when motoneurons are near threshold. It is suggested that one of the functions of the pathway is to control phrenic motoneurons supplying the dorsal part of the diaphragm through the C6 root when the more ventral part of the diaphragm is strongly activated.

Animals↗

PubMed2006

Same spinal interneurons mediate reflex actions of group Ib and group II afferents and crossed reticulospinal actions.

The aim of the study was to analyze interactions between neuronal networks mediating centrally initiated movements and reflex reactions evoked by peripheral afferents; specifically whether interneurons in pathways from group Ib afferents and from group II muscle afferents mediate actions of reticulospinal neurons on spinal motoneurons by contralaterally located commissural interneurons. To this end reticulospinal tract fibers were stimulated in the contralateral medial longitudinal fascicle (MLF) in chloralose-anesthetized cats in which the ipsilateral half of the spinal cord was transected rostral to the lumbosacral enlargement. In the majority of interneurons mediating reflex actions of group Ib and group II afferents, MLF stimuli evoked either excitatory or inhibitory postsynaptic potentials (EPSPs and IPSPs, respectively) or both EPSPs and IPSPs attributable to disynaptic actions by commissural interneurons. In addition, in some interneurons EPSPs were evoked at latencies compatible with monosynaptic actions of crossed axon collaterals of MLF fibers. Intracellular records from motoneurons demonstrated that both excitation and inhibition from group Ib and group II afferents are modulated by contralaterally descending reticulospinal neurons. The results lead to the conclusion that commissural interneurons activated by reticulospinal neurons affect motoneurons not only directly, but also by enhancing or weakening activation of premotor interneurons in pathways from group Ib and group II afferents. The results also show that both excitatory and inhibitory premotor interneurons are affected in this way and that commissural interneurons may assist in the selection of reflex actions of group Ib and group II afferents during centrally initiated movements.

Afferent Pathways↗

PubMed1998

Critical role of axonal A-type K+ channels and axonal geometry in the gating of action potential propagation along CA3 pyramidal cell axons: a simulation study.

A model of CA3 pyramidal cell axons was used to study a new mode of gating of action potential (AP) propagation along the axon that depends on the activation of A-type K+ current (Debanne et al., 1997). The axonal membrane contained voltage-dependent Na+ channels, K+ channels, and A-type K+ channels. The density of axonal A-channels was first determined so that (1) at the resting membrane potential an AP elicited by a somatic depolarization was propagated into all axon collaterals and (2) propagation failures occurred when a brief somatic hyperpolarization preceded the AP induction. Both conditions were fulfilled only when A-channels were distributed in clusters but not when they were homogeneously distributed along the axon. Failure occurs in the proximal part of the axon. Conduction failure could be determined by a single cluster of A-channels, local decrease of axon diameter, or axonal elongation. We estimated the amplitude and temporal parameters of the hyperpolarization required for induction of a conduction block. Transient and small somatic hyperpolarizations, such as simulated GABAA inhibitory postsynaptic potentials, were able to block the AP propagation. It was shown that AP induction had to occur with a short delay (<30 msec) after the hyperpolarization. We discuss the possible conditions in which such local variations of the axon geometry and A-channel density may occur and the incidence of AP propagation failures on hippocampal network properties.

Action Potentials↗

PubMed1995

Cholinergic modulation of synaptic transmission in the rat visual cortex in vitro.

Cholinergic synaptic modulation in the rat visual cortex was studied using intracellular recordings from slice preparations. A cholinergic agonist, carbachol (CCh), reduced fast excitatory as well as fast and slow inhibitory postsynaptic potentials evoked by white matter stimulation. This effect was antagonized by atropine. CCh perfusion did not reduce glutamate- or gamma-aminobutyric acid-induced depolarizations, suggesting the presynaptic mechanism of the suppression. CCh augmented firing over a long period after transsynaptic stimulation combined with a long depolarizing current pulse, not only due to a decrease in firing accommodation but also due to disinhibition. CCh also induced a large sustained depolarization and bursting of action potentials triggered by tetanic stimulation. These results suggest that cholinergic modulation results in a prolonged increase in neuronal excitability during the late phase of synaptic transmissions at least partly by the mechanism of decreasing inhibitory transmissions, particularly when the synaptic inputs are strongly activated.

Animals↗

PubMed1995

Periodically modulated inhibition and its postsynaptic consequences--I. General features. Influence of modulation frequency.

Our aim was to examine the relation, or "synaptic coding", between spike trains across a synapse with inhibitory postsynaptic potentials when the presynaptic rate is modulated periodically and the postsynaptic cell is a pacemaker. Experiments were on the synapse in crayfish stretch receptor organs. Spike trains were considered point processes along time; the time series of corresponding pre- and postsynaptic intervals were extracted. Analyses used displays of intervals along time and order ("basic graphs", and "rasters", respectively), displays of differences between intervals along order ("recurrence plots"), cycle histograms (as such and as Lissajous diagrams with presynaptic and postsynaptic on the abscissae and ordinate, respectively), and correlation histograms. Cycle histograms and correlation histograms demonstrated that all presynaptic modulation frequencies (1/60-10 Hz) are reflected postsynaptically; novel frequencies may arise, not always relating simply to the pre- or postsynaptic ones. The transferred frequency domain is broad and physiologically meaningful. Indeed, vitally important functions have strong periodicities in all portions of the explored domain, and so do the discharges of participating neurons. Overall, pre- and postsynaptic discharges change oppositely, one accelerating while the other slows. Locally, however, pre- and postsynaptic discharges contrast clearly in other ways. The presynaptic evolution is everywhere smooth and orderly, half-cycles usually are symmetric, and there is a single kind of discharge, as expected because the presynaptic axon follows well the controlling stimuli. The postsynaptic cycle shows marked local distortions. These involve presynaptic domains called "congruent portions" where changes are in the same sense (e.g., joint accelerations), "saturated" domains where postsynaptic discharges are arrested, and asymmetric sensitivities to presynaptic change with hysteretic loops in the Lissajous diagrams; the postsynaptic discharge is heterogeneous showing dissimilar forms in succession. Congruent portions are either "positive segments" with pre- to postsynaptic rate ratios practically 1:1, 2:1, 1:1, or parts of Lissajous loops. Different modulation frequencies have different postsynaptic consequences. Differences involve the width and number of positive segments, the proportion of the cycle with saturation, the sense, magnitude and lead-lag characteristics of the hysteretic loops, etc. Because their consequences are separable, frequencies are classified within categories labelled "low" (under 0.5 Hz), "high" (between 0.5 and 5.0 Hz) and "very high" (over 5.0 Hz). Categories arise widely but each prevails in different biological functions (e.g., low or high in, respectively, respiration or vibratory sensitivity). The refactoriness of the inhibitory fibre affects how it can be modulated: consequently, the very high category resembles pacemaker discharges and was not analysed.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed2000

Linking 600-Hz "spikelike" EEG/MEG wavelets ("sigma-bursts") to cellular substrates: concepts and caveats.

Somatosensory evoked human EEG and magnetoencephalographic (MEG) responses comprise a brief burst of low-amplitude, high-frequency (approximately 600 Hz) spikelike wavelets ("sigma-bursts") superimposed on the primary cortical response (e.g., the N20 to electrical median nerve stimulation). The recent surge of interest in these macroscopic sigma-burst responses is energized by the prospect of monitoring noninvasively, highly synchronized and rapidly repeating population spikes generated in the human thalamic and cortical somatosensory system. Thus, analyses of spike-related sigma-bursts could uniquely complement conventional low-frequency EEG/MEG, reflecting mass excitatory and inhibitory postsynaptic potentials that potentially also incorporate subthreshold activities of undetermined functional relevance. Recent studies using spatiotemporal source analysis of multichannel recordings identified regional burst sources subcortically (near-thalamic) as well as cortically. At the primary somatosensory cortex, sigma-burst generators showed the well-established homuncular somatotopic ordering. Functionally, the 600-Hz burst appears to comprise multiple subcomponents with differential sensitivity to stimulus rate, intensity, sleep-wake cycle, tactile interference, subject age, and certain movement disorders. A plenitude of cellular candidates contributing to burst generation at different levels can already now be envisaged, including cuneothalamic and thalamocortical relay cells, as well as cortical bursting pyramidal cells and fast-spiking inhibitory interneurons. Although cellular burst coding might serve to relay information with high efficiency, concepts to link macroscopic sigma-bursts and cellular substrates call for additional study.

Brain Stem↗

PubMed1999

Coefficient of variation of interspike intervals greater than 0.5. How and when?

Using Stein's model with and without reversal potentials, we investigated the mechanism of production of spike trains with a CV (ISI)(standard deviation/mean interspike interval) greater than 0.5, as observed in the visual cortex. When the attractor of the deterministic part of the dynamics is below the firing threshold, spike generation results primarily from random fluctuations. Using computer simulation for a range of membrane decay times and with other model parameters set to values appropriate for the visual cortex, we demonstrate that CV (ISI) is then usually greater than 0.5; if the attractor is above the threshold, spike generation is mainly due to deterministic forces, and CV (ISI) is then usually lower than 0.5. The critical value of the inhibitory postsynaptic potential (IPSP) rate at which CV (ISI) becomes greater than 0.5 is determined, resulting in specifications of how neurones might adjust their synaptic inputs to elicit irregular spike trains.

Analysis of Variance↗

PubMed1990

Dynamic analysis of sensory-inhibitory interactions in crayfish stretch receptor neurons.

1. The effects of regular and random inhibition at moderate rates on the sensory response evoked by sinusoidal stretches were investigated in slowly and rapidly adapting stretch receptors of crayfish (RM1 and RM2, respectively). 2. Although the RM1 has pacemaker properties and the RM2 is spontaneously silent, inhibitory postsynaptic potential (IPSP) effects were similar in both mechanosensory neurons. The most common consequence was the expected reduction of the sensory response and the increase of the elongation needed to reach firing threshold. With regular IPSPs there were regions where pre- and postsynaptic spikes alternated at fixed integer ratios, usually 1:1, more rarely 1:2 and 1:3. Increases or decreases of the sensory excitation caused sudden postsynaptic accelerations or decelerations when specific length bounds were crossed and where pre- and postsynaptic alternations changed to lower (e.g., from 1:1 to 1:2) or higher ratios (e.g., from 1:2 to 1:1), respectively. 3. Paradoxical effects were also observed because increasing or decreasing the inhibitory rate for a given alternation ratio (e.g., 1:1) accelerated or decelerated the output rate, respectively. Alternations and paradoxical behaviors disappeared with IPSP pattern irregularization. Random IPSPs strongly irregularized the receptor's output. Inhibition, especially if the pattern was irregular, could excite under special conditions. 4. With regular IPSPs, mechanical sensitivity became zero at the lengths at which receptors were silenced, low during alternations, and maximum at transitions between successive alternation ratios. Irregular IPSPs did not have this delinearizing consequence. 5. In conclusion, inhibition introduced important complex modifications in the coding of mechanosensory information. Effects were similar in both receptor types, indicating that self-sustained oscillations are not fundamental. The observed changes were critically dependent on pre- and postsynaptic rate and pattern. They cannot be explained by simple summation of converging sensory and inhibitory inputs and represent another observation of the complex dynamic behavior of periodically driven nonlinear systems.

Animals↗

PubMed2005

Localization and properties of respiratory neurons in the rostral pons of the newborn rat.

The distribution and discharge pattern of respiratory neurons in the 'pneumotaxic center' of the rostral pons in the rat has remained unknown. We performed optical recordings and whole-cell patch clamp recordings to clarify respiratory neuron activity in the rostral pons of a brainstem-spinal cord preparation from a newborn rat. Inspiratory nerve activity was recorded in the 4th cervical nerve and used as a trigger signal for optical recordings. Respiratory neuron activity was detected in the limited region of the rostral-lateral pons. The main active region was presumed to be primarily the Kölliker-Fuse nucleus. The location of respiratory neurons was further confirmed by Lucifer Yellow staining after conducting whole-cell recordings. From a membrane potential analysis of the respiratory neurons in the rostral pons, the respiratory neurons were divided into four types: inspiratory neuron (71.9%), pre-inspiratory neuron (5.3%), post-inspiratory neuron (19.3%), and expiratory neuron (3.5%). A noticeable difference between pontine and medullary respiratory neurons was that post-inspiratory neurons were more frequently encountered in the pons. Application of a mu-opioid agonist, [d-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin, transformed the burst pattern of post-inspiratory neurons into that of pre-inspiratory neurons. The electrical stimulation of the sensory root of the trigeminal nerve induced three types of responses in 85% of pontine respiratory neurons: inhibitory postsynaptic potentials (42.7%), excitatory postsynaptic potentials (37.7%) and no response (15.1%). Our findings provide the first evidence in the rat for the presence of respiratory neurons in the rostral pons, with localization in the lateral region approximately overlapping with the Kölliker-Fuse nucleus.

Animals↗

PubMed1996

Short-term synaptic enhancement and long-term potentiation in neocortex.

Repetitive stimuli reliably induce long-term potentiation (LTP) of synapses in the upper layers of the granular somatosensory cortex but not the agranular motor cortex of rats. Herein we examine, in these same cortical areas, short-term changes in synaptic strength that occur during the LTP induction period. theta-Burst stimulation produced a strong short-term enhancement of synapses in the granular area but only weak enhancement in the agranular area. The magnitude of enhancement during stimulation was strongly correlated with the magnitude of LTP subsequently expressed. Short-term enhancement was abolished by an antagonist of N-methyl-D-aspartate (NMDA) receptors but remained in the presence of a non-NMDA receptor antagonist. Inhibitory postsynaptic potentials of the granular and agranular areas displayed similar frequency sensitivity, but the frequency sensitivity of NMDA receptor-dependent excitatory postsynaptic potentials differed significantly between areas. We propose that pathway-specific differences in short-term enhancement are due to variations in the frequency dependence of NMDA currents; different capacities for short-term enhancement may explain why repetitive stimulation more readily induces LTP in the somatosensory cortex than in the motor cortex.

2-Amino-5-phosphonovalerate↗

PubMed1991

Cholinergic disinhibition in area CA1 of the rat hippocampus is not mediated by receptors located on inhibitory neurons.

We studied the effects of carbamylcholine (carbachol; CCh) on monosynaptic inhibitory postsynaptic potentials (IPSPs) evoked in the presence of the excitatory amino acid receptor antagonists 6,7-dinitroquinoxaline-2,3-dione (DNQX) and D,L-2-amino-5-phosphonovalerate (APV). CCh (30 microM) blocked late afterhyperpolarizations but did not depress GABAA receptor-mediated fast monosynaptic IPSPs or GABAB receptor-mediated late monosynaptic IPSPs. In the presence of CCh the GABAB receptor agonist (+/- )-baclofen (2 microM) reversibly hyperpolarized pyramidal neurons and depressed monosynaptic IPSPs as under control conditions. Phorbol-12,13-diacetate (PDAc; 10 microM) increased fast and depressed late monosynaptic IPSPs, and prevented depression of IPSPs by baclofen. These results suggest that cholinergic disinhibition in area CA1 of the hippocampus results from decreased synaptic excitation of inhibitory neurons.

2-Amino-5-phosphonovalerate↗

PubMed1990

Whole-cell patch study of GABAergic inhibition in CA1 neurons of immature rat hippocampal slices.

Inhibitory processes mediated by gamma-aminobutyric acid (GABA) were studied in immature rat hippocampal slices using the whole-cell patch clamp technique. Orthodromically evoked hyperpolarizing inhibitory postsynaptic potentials (IPSPs) were observed in CA1 neurons of postnatal 2-5 (P2-5) and 7-13 (P7-13) day old rats under conditions of low internal [Cl-]. In the whole-cell voltage-clamp mode, applications of GABA evoked outwards currents which reversed at -55 mV and -62 mV in P2-5 and P7-13 CA1 neurons, respectively, with comparable reversal potential for the IPSPs for each age. An increase in internal [Cl-] caused a depolarizing shift of the GABA reversal potential which followed the Nernst equation. In both groups of neurons, the IPSPs and GABA currents were blocked with the bath applications of bicuculline (10 microM) and picrotoxin (100 microM). We conclude that the GABAA-mediated inhibitory synaptic process exists in P2-5 CA1 neurons and hypothesize that the absence of such IPSPs noted in previous studies of immature CA1 neurons was likely due to higher internal [Cl-] in the more immature neurons.

Animals↗

PubMed2004

Functional properties of fast spiking interneurons and their synaptic connections with pyramidal cells in primate dorsolateral prefrontal cortex.

Recent studies suggest that fast-spiking (FS) interneurons of the monkey dorsolateral prefrontal cortex (DLPFC) exhibit task-related firing during working-memory tasks. To gain further understanding of the functional role of FS neurons in monkey DLPFC, we described the in vitro electrophysiological properties of FS interneurons and their synaptic connections with pyramidal cells in layers 2/3 of areas 9 and 46. Extracellular spike duration was found to distinguish FS cells from non-FS interneuron subtypes. However, a substantial overlap in extracellular spike duration between these populations would make classification of individual interneurons difficult. FS neurons could be divided into two main morphological groups, chandelier and basket neurons, with very similar electrophysiological properties but significantly different horizontal spread of the axonal arborization. In paired cell recordings, unitary inhibitory postsynaptic potentials (IPSPs) elicited by FS neurons in pyramidal cells had rapid time course, small amplitude at resting membrane potential, and were mediated by GABA(A) receptors. Repetitive FS neuron stimulation, partially mimicking the sustained firing of interneurons in vivo, produced short-term depression of the unitary IPSPs, present at connections made by both basket and chandelier neurons and due at least in part to presynaptic mechanisms. These results suggest that FS neurons and their synaptic connections with pyramidal cells have homogeneous physiological properties. Thus different functional roles of basket and chandelier neurons in the DLPFC in vivo must arise from the distinct properties of the interneuronal axonal arborization or from a different functional pattern of excitatory and inhibitory connections with other components of the DLPFC neuronal network.

Action Potentials↗

PubMed1988

Unitary conductance changes at teleost Mauthner cell glycinergic synapses: a voltage-clamp and pharmacologic analysis.

1. The magnitude and kinetics of inhibitory postsynaptic currents (IPSCs) evoked in the goldfish Mauthner (M-) cell by intracellular stimulation of identified presynaptic interneurons (unitary responses) and by activation of the recurrent collateral network were determined with single-and double electrode voltage-clamp techniques. 2. The peak magnitude of the inhibitory conductance changes were 5610 +/- 4800 nS (mean +/- SD; n = 13) for the collateral response, and 144 +/- 44 nS (n = 7) for the unitary IPSCs. These synaptic conductances, which are due to the opening of Cl- channels, were independent of the degree of Cl- -loading of the M-cell. 3. The peak amplitude of the collateral inhibitory postsynaptic potential (IPSP) was a constant fraction (0.52 +/- 0.06) of the driving force, which was determined from current-voltage plots for both types of IPSCs and ranged from 10 to 37 mV. These findings confirm indirect measurements from previous current-clamp studies and validate the normalization procedure used to previously calculate synaptic conductances from IPSP amplitudes, a method that therefore may be applicable to other central neurons. 4. At the resting membrane potential, the rise time of the unitary IPSCs was 0.34 +/- 0.07 ms (n = 18), whereas their decay was exponential, with a time constant of 5.7 +/- 1.1 ms (n = 16). 5. Iontophoretic and intramuscular applications of the glycine antagonist strychnine reduced or blocked M-cell inhibitory responses, without altering the excitability of the presynaptic neurons, or the driving force. 6. Amplitude fluctuations of unitary IPSPs recorded during partial blockade by strychnine were analyzed according to a binomial model of quantal transmitter release. In one experimental series, comparison of the binomial parameters before and after applying the antagonist indicated that only quantal size, q, was reduced, whereas n, the number of available release units, and p, the probability of release, were unaffected by strychnine. In a second series, the individual presynaptic cells were injected with horseradish peroxidase (HRP), and it was found that the correlation between n and the number of stained presynaptic boutons and, therefore, of active zones, was maintained in the presence of the drug. No evidence was found for silent synapses in these conditions. 7. The quantal conductance, gq, was estimated from the binomially derived quantal size, in millivolts, and the voltage-clamp measurements of the IPSP driving force and M-cell input conductance. gq averaged 21.5 nS in control conditions and 12.3 nS in the presence of strychnine.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗