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PubMed1993

Correlation of physiological subgroupings of nonpyramidal cells with parvalbumin- and calbindinD28k-immunoreactive neurons in layer V of rat frontal cortex.

1. To test the hypothesis that physiologically and morphologically different cortical nonpyramidal cells express different calcium-binding proteins, whole-cell current-clamp recording in vitro was combined with intracellular staining and double immunofluorescence in layer V of frontal cortex of rats 16-20 days old. 2. Nonpyramidal cells were first characterized as fast-spiking (FS) or low-threshold spike (LTS) cells, injected with biocytin, and subsequently stained immunohistochemically for parvalbumin and calbindinD28k. 3. FS cells were identified by input resistances < 350 M omega, spike width at half amplitude < 0.8 ms, and virtually no spike frequency adaptation of spike trains by depolarizing pulses. LTS cells were identified by input resistances > 350 M omega, spike width at half amplitude > 0.8 ms, and the discharge of low-threshold spikes from hyperpolarized potentials. Repetitive firing could be induced by a combination of stimulation-induced excitatory postsynaptic potentials with depolarization in FS cells. Repetitive firing was not observed in LTS cells under these conditions. 4. After biocytin injection of layer V cells characterized in this way, subsequent double immunostaining showed that all biocytin-labeled parvalbumin-immunoreactive cells (n = 18) belonged to the FS cells (FS-PV cells), whereas all biocytin-labeled calbindinD28k-immunoreactive cells (n = 10) belonged to the LTS cells (LTS-Calb cells). 5. FS-PV cells had smooth or sparsely spiny dendrites, whereas LTS-Calb cells had dendrites with a modest number of spines but fewer than pyramidal cells. FS-PV cells showed denser axonal branches near their somata and extended axons in a more horizontal direction. Some of them could be identified as basket cells by the presence of terminal boutons surrounding somata of other cells. LTS-Calb cells extended their main axons more vertically up to layer I. 6. Double immunofluorescent staining revealed that very few cells in layer V showed immunoreactivity for both calcium-binding proteins but that most cells immunoreactive for the calcium-binding proteins in layer V were also immunoreactive for gamma-aminobutyric acid. 7. These results suggest that GABAergic nonpyramidal cells in layer V of neocortex can be divided into two functional groups on the basis of different firing modes, axonal distributions, and calcium-binding protein immunoreactivity: 1) FS-PV cells show repetitive firing by synaptic activation, have axonal arborizations that are more dense near their somata and oriented horizontally, and the cells exhibit parvalbumin immunoreactivity and 2) LTS cells show low-threshold spikes, have more vertical axonal arborizations up to layer I, and exhibit calbindinD28K immunoreactivity.

Animals↗

PubMed1995

Depression of synaptic connections between identified motor neurons in the locust.

1. The fast extensor tibiae motor neuron makes direct excitatory central connections with the posterior group of flexor tibiae motor neurons in the locust metathoracic ganglion. The flexor group has a slow, a fast, and an intermediate motor neuron. The motor neurons are involved in the motor program for kicking and jumping, the defensive and escape behaviors of the locust. An antidromic action potential in fast extensor tibiae motor neuron (FETi) results in a monosynaptic, glutamatergic excitatory postsynaptic potential (EPSP) in each of the flexor motor neurons. 2. A train of 10 antidromic spikes in FETi at frequencies of 1-20 Hz resulted in depression of the amplitude of the EPSP in each of the flexor motor neurons. The depression was not significantly different in the different flexor motor neurons. The depression was greater with higher frequency stimulation and was reduced in low calcium saline. 3. After stimulation at 20 Hz, the EPSP amplitude was depressed by approximately 80%. This did not change when the number of stimuli was increased to 20, when stimulation was done in high calcium saline, or when the frequency of stimulation was increased to 50 or 100 Hz. The recovery from depression was greater after 20-Hz stimulation than at lower frequencies, although the recovery was reduced when the number of stimuli was increased, and also in high calcium saline. 4. In normal saline the depression of the EPSP amplitude was associated with a reduction of the presynaptic spike amplitude at frequencies of > or = 5 Hz. In tetraethylammonium (TEA) saline the width of a TEA-broadened spike was also reduced. The reduction in spike amplitude and spike width correlated with the depression of the EPSP. 5. Certain of these results are consistent with a depletion model of synaptic depression, whereas others are not consistent with this model. The depression may be partly due to an initial depletion of transmitter stores, and partly to modulation of the presynaptic action potential that reduces calcium entry, and therefore transmitter release. The significance of the depression on the motor program for kicking and jumping is discussed.

Animals↗

PubMed1989

Adenylate cyclase system is essential for long-term facilitation at the crayfish neuromuscular junction.

Long-term facilitation (LTF), a form of synaptic plasticity demonstrated at the crayfish neuromuscular junction, is induced by tetanic stimulation and persists for hours. LTF can be divided into 2 phases: a tetanic phase, which occurs during stimulation, and a long-lasting phase, which persists after stimulation. Activators and potentiators of cAMP (forskolin and 3-isobutyl-methyl-xanthine) produce facilitation of excitatory postsynaptic potentials, which attain approximately the amplitude of the long-lasting phase of LTF but last for a shorter time. Localized presynaptic injection of a protein inhibitor ("Walsh inhibitor") specific for the cAMP-dependent protein kinase blocks the long-lasting phase of LTF at synapses near the injection site with no apparent effect on the tetanic phase. Normal LTF develops and persists at synapses of the same axon distant from the injection site. Localization of the injected inhibitor was confirmed by fluorescent tagging. Localized injection of SQ22,536, an adenylate cyclase inhibitor, also blocks the second phase of LTF near the injection site, but not at distant synapses. These experiments establish a role for adenylate cyclase activation in the long-lasting phase of LTF. The phosphatidylinositol second-messenger system is not important in LTF as inhibition of phospholipase C by injection of RA233, which blocks facilitatory effects of serotonin, does not affect any aspect of LTF.

1-Methyl-3-isobutylxanthine↗

PubMed1985

The effects of buspirone, BMY-13805 and 1-(2-pyrimidinyl)-piperazine on cat spinal reflexes.

Buspirone and its analog BMY-13805, clinically effective anxiolytics and their metabolite, 1-PP, were tested on cat spinal reflexes. In the spinal preparation, the monosynaptic reflex and the dorsal root potential were not changed by buspirone, BMY-13805 or 1-PP. Significant changes in the dorsal root potential and monosynaptic reflex were seen after buspirone administration in the intact neuraxis preparation. Generally, these changes had a bimodal pattern, a significant change within 1 hr after buspirone administration, then a period of remittance, followed by a second significant change 3 or more hr later. They included increases in the dorsal root potential and the following changes in the conditioned monosynaptic reflex: an increase in excitatory postsynaptic potential, an increase in postsynaptic inhibition, and decreases in presynaptic inhibition. These data indicate that buspirone does not affect these reflexes directly, but alters supraspinal mechanisms that regulate spinal reflexes.

Animals↗

PubMed2003

Optical detection of developmental origin of synaptic function in the embryonic chick vestibulocochlear nuclei.

Functional organization of the brain stem vestibulocochlear nuclei during embryogenesis was investigated using a multiple-site optical recording technique with a fast voltage-sensitive dye. Brain stem slices with the cochlear and/or vestibular nerves attached were dissected from 6- to 8-day-old (E6-E8) chick embryos. Electrical responses evoked by cochlear or vestibular nerve stimulation were optically recorded simultaneously from many loci of the preparations. In E7 and E8 preparations, we identified two components of the optical response with cochlear or vestibular nerve stimulation; one was a fast spike-like signal related to the action potential, and the other was a slow signal related to the glutamate-mediated excitatory postsynaptic potential. The location of the cochlear nerve response area was mainly located on the dorsolateral region, while that of the vestibular nerve was deviated ventromedially. At E6, cochlear nerve stimulation evoked only the fast spike-like signals in normal Ringer solution. However, when we removed Mg2+ from the extracellular solution, significant slow signals were elicited in the E6 preparation. The present results demonstrated that in the chick vestibulocochlear nuclei, functional synapses are already generated by the E7 embryonic stage and that postsynaptic activity related to N-methyl-d-aspartate receptors emerges latently, at least in the cochlear nerve-related nucleus, at the E6 embryonic stage. This chronological sequence of the emergence of postsynaptic function is different from that reported previously (E10-E11), suggesting that the developmental origin of sensory information transfer in the auditory pathway is much earlier than has been anticipated.

Animals↗

PubMed1996

Spindle oscillation in cats: the role of corticothalamic feedback in a thalamically generated rhythm.

1. Spindles represent an oscillatory activity (7-14 Hz) of the electroencephalogram (EEG) originating in the thalamus and appearing during early stages of sleep. We investigated: (i) the phase relations between thalamic and cortical neurons during this rhythm; (ii) the patterns of spindles under different anaesthetics and their modifications at various levels of the membrane potential (Vm); and (iii) the potentiating role of the corticothalamic feedback in the genesis of spindles. Intra- and extracellular recordings were performed in cats from reticular and dorsal thalamic nuclei, as well as from various cortical areas. 2. In thalamic reticular neurons, spindles were sequences of waves at 7-14 Hz, riding on a prolonged depolarizing plateau and occurring in phase with depth-negative cortical EEG waves. In thalamocortical cells, spindles consisted of inhibitory postsynaptic potentials (IPSPs) in phase with depth-positive cortical EEG waves and occasionally leading to rebound spike bursts. In cortical cells, spindle waves were rhythmic (7-14 Hz) excitatory postsynaptic potentials (EPSPs) that sometimes gave rise to action potentials. Spindles occurred in phase among thalamic reticular, thalamocortical and neocortical neurons. 3. In thalamic reticular neurons, spindle waves and their depolarizing plateaux increased in amplitude with slight cellular hyperpolarization, but at a Vm more negative than -80 or -85 mV they decreased in amplitude. No frequency alterations were observed with these Vm changes. 4. The waxing-and-waning pattern of spontaneous spindles under barbiturate anaesthesia was distinct from the waning pattern under ketamine-xylazine anaesthesia. Under all anaesthetics, spindles had a waning pattern when elicited by cortical stimuli. The amplitude of cortical-evoked spindle waves diminished with the decrease in stimulation intensity. 5. Under urethane or ketamine-xylazine anaesthesia, spindle sequences were grouped by a cortically generated slow oscillation (< 1 Hz) and were preceded by a depth-positive EEG wave that corresponded to a prolonged hyperpolarization in all three investigated (cortical, thalamic reticular, and thalamocortical) cellular types. 6. We propose that the waxing pattern of spindle oscillation is due to a progressive entrainment of units into the oscillation until a maximum number is reached, depending on the background activity in the network. The phase relations between cortical, thalamic reticular and thalamocortical neurons are ascribed to distributed excitatory signals from thalamocortical neurons to both cortical and reticular neurons at each cycle of the oscillation. In turn, cortical neurons provide a powerful drive to potentiate the genesis of thalamic spindles.

Animals↗

PubMed1993

Effects of trifluoperazine on synaptically evoked potentials and membrane properties of CA1 pyramidal neurons of rat hippocampus in situ and in vitro.

The effects of trifluoperazine (TFP), a phenothiazine antipsychotic, on hippocampal activity were studied in the CA1 subfield, both in situ and in slices. In the extracellular studies in situ and in vitro, both somatic population spikes and dendritic excitatory postsynaptic potentials (EPSP) fields were depressed reversibly by TFP, applied by microiontophoresis or in the bath (50-100 microM). Similar effects were also seen during iontophoretic applications of sphingosine in situ. Like TFP (at micromolar concentrations) sphingosine is a dual Ca2+/calmodulin-dependent kinase and protein kinase C (PKC) inhibitor. In intracellular recordings from slices, 50-100 microM TFP induced a slow depolarization and a decrease in input resistance (RN), probably through a gamma-aminobutyric acid (GABA)-mediated increase in Cl- conductance (GCl). TFP also reduced the slow afterhyperpolarization (AHP) as well as electrically evoked inhibitory postsynaptic potentials (IPSPs), but EPSPs were augmented in both amplitude and duration. When CA1 neurons were voltage clamped, TFP elicited a corresponding inward current (consistent with depolarization), increased the leak conductance, and enhanced excitatory synaptic currents; whereas inhibitory synaptic currents and high-threshold Ca2+ currents were reduced. In conclusion, these effects of TFP--which cannot be readily explained by its potent antidopamine action--are in keeping with other evidence that both Ca2+/calmodulin-dependent kinase and PKC can modulate GCl-conductance and high-threshold Ca(2+)-conductance, as well as inhibitory and excitatory postsynaptic currents.

Animals↗

PubMed1988

Electrophysiological analysis of the dorsal hippocampal commissure projections to the entorhinal area.

Synaptic effects evoked in the entorhinal area by dorsal hippocampal commissure (dorsal psalterium) projections were analysed in anesthetized adult guinea-pigs by means of a field potential analysis. Stimuli applied to the caudal part of the dorsal psalterium evoked a complex response in the dorsal third of the entorhinal area. The early part of the entorhinal response consisted of a slow wave interrupted by a spike potential. The electrophysiological characteristics and the laminar distribution of the slow wave and of the spike potential, together with the presence of time-locked unit activity, suggested that dorsal psalterium projections evoke monosynaptic excitatory postsynaptic potentials leading to cellular discharge in radially oriented neurons of layers II and III. The commissural fibers responsible for these effects originate in the contralateral presubiculum. The early part of the entorhinal response was followed by three waves in close temporal sequence. These waves were polysynaptically generated and associated with excitatory and inhibitory synaptic effects. Inhibition was demonstrated for the monosynaptically generated spike potential. Whether these effects were mediated by intracortical circuits and/or extrinsic projections cannot be stated from the present results. Causal relations were observed between the entorhinal monosynaptic response and that evoked by dorsal psalterium stimulation in the ipsilateral dentate gyrus, previously shown to be relayed by perforant path fibers. The results indicate that presubicular commissural projections to the entorhinal area monosynaptically activate neurons of the perforant pathway, whose discharge brings about activation of the ipsilateral dentate gyrus.

Action Potentials↗

PubMed1991

Adenosine A1 and A2 receptors mediate presynaptic inhibition and postsynaptic excitation in guinea pig submucosal neurons.

Intracellular recordings were made from guinea pig submucosal neurons in vitro. Adenosine, 2-[p-(carboxyethyl)phenylethylamino]-5'-N- ethylcarboxamidoadenosine (CGS21680), 2-chloroadenosine (CADO), 5'-N-ethylcarboxamidoadenosine (NECA), R(-)-N6-(2-phenylisopropyl)adenosine (R-PIA), N6-cyclohexyladenosine (CHA) and 1-deaza-2-chloro-N6-cyclopentyladenosine (DCCPA) were applied by adding them to the superfusion solution. Adenosine (30 nM to 30 microM) depolarized S-type neurons neurons and this was mimicked by analogs with potency order: CGS21680 = NECA greater than R-PIA greater than CADO greater than adenosine greater than CHA much greater than DCCPA. 8-Cyclopentyltheophylline (CPT) blocked the depolarizing action of CADO or R-PIA; this antagonism was surmountable and the dissociation equilibrium constant (KD) estimated by the Schild method was 295 nM. Synaptic potentials were evoked by focal stimulation of nerve strands running between submucosal ganglia. The nicotinic excitatory postsynaptic potential was reduced by adenosine and analogs with potency order CHA = R-PIA greater than DCCPA = NECA = CADO greater than adenosine much greater than CGS21680; CPT competitively antagonized this effect of CADO or CHA with a KD of 13 nM. The noradrenergic inhibitory postsynaptic potential was also reduced; the potency order was R-PIA greater than CHA = CADO = NECA = DCCPA greater than adenosine much greater than CGS21680; the KD of CPT as an antagonist was 7 nM. It is concluded that adenosine directly depolarizes submucosal neurons by acting at an A2 receptor, and that it inhibits the release of acetylcholine (from intramural nerves) and noradrenaline (from sympathetic nerves) by acting at a presynaptic A1 receptor.

Acetylcholine↗

PubMed1990

Synaptic excitation of inhibitory cells by single CA3 hippocampal pyramidal cells of the guinea-pig in vitro.

1. In simultaneous recordings from pairs of neurones in hippocampal slices from guinea-pigs, single action potentials fired by CA3 pyramidal cells could initiate inhibitory postsynaptic potentials (IPSPs) in nearby pyramidal cells. 2. The latencies of these IPSPs could be as short as 3 ms. However, they were mediated disynaptically via chemical, excitatory synapses, since inhibitory coupling was suppressed by an excitatory amino acid antagonist. 3. The properties of excitatory synapses made onto inhibitory cells were examined to assess the basis for this strong coupling. Inhibitory cells were identified either by showing that they inhibited another cell or by their characteristic firing pattern. 4. Excitatory postsynaptic potentials (EPSPs) elicited by single pyramidal cell action potentials had a mean amplitude of 1-4 mV and a time to peak of 1.5-4 ms. In most cases they decayed with a time constant similar to that of the inhibitory cell membrane. 5. EPSP amplitude increased with hyperpolarization of the postsynaptic membrane. Membrane polarization had little effect on EPSP shape. 6. EPSPs fluctuated in amplitude and transmission sometimes failed, suggesting transmission was quantal and that few quanta were released. 7. When presynaptic cells were made to fire bursts of action potentials, EPSPs in inhibitory cells were initially potentiated. 8. EPSPs could cause inhibitory cells to fire. The interval between pre- and postsynaptic spikes could be as short as 2.5 ms and the probability of spike transmission could be as high as 0.6. Some inhibitory cells which received feedback excitation were also excited in feedforward fashion by mossy fibre stimuli. 9. One pyramidal cell could activate several disynaptic inhibitory pathways terminating on another pyramidal cell. This suggests that excitatory synapses made by pyramidal cell axon collaterals onto inhibitory cells are divergent. 10. This strong, divergent excitation of inhibitory cells ensures recurrent inhibition is sufficiently widespread, rapid and potent to control the spread of activity by recurrent excitatory connections between CA3 pyramidal cells.

Action Potentials↗

PubMed1996

Regulation of EPSPs by the synaptic activation of GABAB autoreceptors in rat hippocampus.

1. Intracellular recording was used to study the influence of GABAB autoreceptor-mediated regulation of monosynaptic GABAA and GABAB receptor-mediated hyperpolarizing inhibitory postsynaptic potentials (IPSPAs and IPSPBs, respectively) on alpha-amino-3-hydroxy-5-methyl -4-isoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated excitatory postsynaptic potentials (EPSPAs and EPSPNs, respectively) in the CA1 region of rat hippocampal slices. To achieve this, synaptic potential were evoked monosynaptically by near stimulation following blockade of either EPSPNs, by the NMDA receptor antagonist (R)-2-amino-5-phosphonopentanoate (AP5; 0.05 mM), or EPSPAs, by the AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 0.01 mM). 2. Paired-pulse stimulation at 3-50 Hz caused an increase in the duration (paired-pulse widening) of EPSPAs, which paralleled the time course of paired-pulse depression of monosynaptic IPSCs, and a potentiation of the amplitude (paired-pulse potentiation) of EPSPAs, which did not. Paired-pulse stimulation also caused frequency-dependent changes in EPSPNs. At frequencies > 40 Hz it produced paired-pulse depression of EPSPNs, along with marked summation of IPSPS, and at frequencies < 40 Hz it caused paired-pulsed enlargement of EPSPNs, concomitant with a reduction in IPSPS. 3. Paired-pulse potentiation of EPSPAs at 50 Hz was enhanced by picrotoxin (0.1 mM) but was not significantly affected by 3-amino-propyl(diethoxymethyl)phosphinic acid (CGP 35348; 1 mM). Paired-pulse depression of EPSPNs at 50 Hz was converted to paired-pulse enlargement by picrotoxin but was unaffected by CGP 35348. These effects can be explained by block of IPSPAs by picrotoxin. 4. Paired-pulsed widening of EPSPAs at 5 Hz was occluded by picrotoxin and abolished by CGP 35348. Similarly, paired-pulsed enlargement of EPSPNs at 5 Hz was occluded, and in some cases converted to paired-pulse depression, by picrotoxin. The effects of CGP 35348 were more complex in that this antagonist reduced paired-pulse enlargement of EPSPNs in control medium whereas it eliminated paired-pulsed depression of EPSPNs in the presence of picrotoxin, effects consistent with its block of GABAB autoreceptors and IPSPBS, respectively. 5. 'Priming' using a 'priming stimulation protocol' (a single 'priming stimulus' followed at 1-50 Hz ('priming frequency') by a 'primed burst' of four shocks at 20-100 Hz ('burst frequency')) caused an increase in both 'primed' EPSPAs and EPSPNs compared with 'unprimed' EPSPAs and EPSPNs. This effect was optimal when the respective priming and burst frequencies were 5 and 100 Hz. 6. In the presence of either picrotoxin or CGP 35348 the primed EPSPAs and EPSPNs resembled unprimed EPSPAs and EPSPNs, respectively. This was because picrotoxin occluded whereas CGP 35348 blocked the effect of priming on EPSPS. 7. CGP 35348 had only modest effects on EPSPAs but enhanced EPSPNs evoked by a tetanus (20 stimuli at 100 Hz), in either the presence or absence of picrotoxin. In the absence of picrotoxin, CGP 35348 also promoted depolarization by enhancing a depolarizing GABAA receptor-mediated component (IPSPD). These effects can all be attributed to block of IPSPBS by CGP 35348. 8. CGP 35348 blocked the induction of long-term potentiation (LTP) of extracellularly recorded field EPSPs elicited by a priming stimulation protocol in control medium but was ineffective in the presence of picrotoxin. CGP 35348 was also ineffective at preventing tetanus-induced LTP (100 Hz, 1 s) in both the absence and presence of picrotoxin. 9. These data demonstrate the complex regulation of AMPA and NMDA receptor-mediated EPSPs during various patterns of synaptic activation caused by the dynamic changes in GABA-mediated synaptic inhibition, which are orchestrated by GABAA autoreceptors in a frequency-dependent

Animals↗

PubMed1997

Synaptic and synaptically activated intrinsic conductances underlie inhibitory potentials in cat lateral amygdaloid projection neurons in vivo.

The companion paper demonstrated that the responses of lateral amygdaloid (LAT) projection neurons to the stimulation of major input and output structures are dominated by monophasic hyperpolarizing potentials of large amplitude. To characterize the mechanisms underlying these inhibitory potentials, intracellular recordings of cortically evoked responses were obtained from morphologically and/or physiologically identified LAT projection neurons in barbiturate anesthetized cats. The reversal potential of the cortically evoked hyperpolarization was measured at its peak, and 115 ms later (tail), an interval corresponding to the peak latency of the gamma-aminobuturic acid-B (GABAB) response previously recorded in vitro. When recorded with K-acetate (KAc) pipettes, these reversal potentials were -86.9 +/- 1.6 mV (peak; mean +/- SE) and -90.7 +/- 1.7 mV (tail), suggesting that both Cl- and K+ conductances contribute throughout the cortically evoked hyperpolarization. The small, but consistent, difference between the two reversal potentials suggested that an additional slowly activating K(+)-mediated component contributed to the inhibitory postsynaptic potential (IPSP) tail. To determine whether Cl- conductances contributed to the evoked hyperpolarization, recordings were performed with KCl; the peak (-57.8 +/- 2.2 mV) and tail (-61.3 +/- 2.1 mV) reversal potentials were approximately 15-20 mV more depolarized than those recorded with KAc pipettes. However, the difference between the peak and tail reversals remained. In an attempt to block the Cl- conductance, recordings were obtained with pipettes filled with KAc or KCl and 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS), a Cl- pump blocker that also was reported to block GABAA responses. With KAc and DIDS, the initial depolarization was prolonged and the amplitude of the hyperpolarization decreased relative to that seen with KAc alone. However, with KCl and DIDS, the reversal potential was shifted to an even greater extent than with KCl pipettes with the evoked response consisting entirely of a large depolarization, which produced a spike burst. These results suggest that LAT neurons have a Cl- pump that is blocked by DIDS, but that their Cl- channels are not blocked by DIDS. To assess the contribution of K+ conductances to cortically evoked hyperpolarizing potentials, recordings were obtained with Cs-acetate pipettes. Under these conditions, the response reversed at more depolarized potentials (peak, -71.9 +/- 1.0 mV; tail, -72.0 +/- 0.9 mV) compared with KAc recordings, with no difference between the peak and tail reversal potentials. These cells also had depolarized resting potentials (-66.2 +/- 1.8 mV) compared with those of cells recorded with KAc pipettes (-73.6 +/- 1.8 mV); however, this difference was too small to attribute the shift in reversals to a redistribution of Cl- ions across the membrane. The action potentials generated by LAT neurons under Cs+ had a shoulder that prolonged their falling phase. The increased duration of the spikes was presumably due to a dendritic Ca2+ conductance because LAT amygdaloid neurons are known to possess such conductances and Cs+ blocks the delayed rectifier and some Ca(2+)-dependent K+ currents. The dramatic reduction of this shoulder by spontaneous and evoked IPSPs suggests that the activation of dendritic conductances by back-propagating somatic action potentials is regulated tightly by synaptic events. Intracellular injection of the Ca2+ chelating agent, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (100 mM) caused a depolarization of the peak (-75.3 +/- 1.3 mV) and tail (-77.7 +/- 1.7 mV) reversal potentials during a time course of 15-45 min. Concurrently, the amplitude of the excitatory postsynaptic potential increased whereas that of the hyperpolarization decreased, suggesting that a Ca(2+)-dependent K+ conductance contributes significantly to the evoked hyperpolarization. (ABSTRACT TRUNCATED)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1996

Involvement of silent synapses in the induction of long-term potentiation and long-term depression in neocortical and hippocampal neurons.

Changes in the latency of small excitatory postsynaptic potentials were observed in association with induction of long-term modifications of synaptic transmission in slices of rat neocortex and guinea-pig hippocampus. After potentiation response latency decreased in 3/10 cases in the neocortex and in 6/24 cases in the hippocampus, and increased after depression in 4/8 cases in the neocortex. These latency changes could not be attributed to changes in presynaptic fibre excitability, monosynaptic inhibition, release kinetics or activation kinetics of postsynaptic ion channels. We conclude therefore that potentiation led to the activation of previously silent synapses of fast-conducting afferents and depression to the inactivation of previously functional synapses. Thus, neocortical and hippocampal synapses can be in a non-functional state, and regimes that induce long-term potentiation and depression not only change the efficacy of synapses but also alter their functional state.

Animals↗

PubMed1989

Synaptic potentials evoked in cat dorsal spinocerebellar tract neurones by impulses in single group I muscle afferents.

1. Excitatory postsynaptic potentials (EPSPs) evoked by impulses in single group I muscle afferents were recorded intracellularly in dorsal spinocerebellar tract (DSCT) neurones in the spinal cords of anaesthetized cats. 2. In the same experiments, electrotonic membrane properties of DSCT neurones were measured using the voltage response of each cell to a brief intracellular current pulse. 3. Single group I fibre EPSPs were found to exhibit a large range of amplitudes, from 210 microV to 3.4 mV. All of these EPSPs exhibited uniformly rapid rise times, in contrast to the wide range of time courses exhibited by group I a EPSPs recorded in motoneurones. 4. Electrotonic analysis of DSCT neurones indicated that the time constants of these cells ranged from 5.9 to 18.2 ms, with an average value of 10.9 ms. 5. Current pulse responses of the majority (approximately three-quarters) of DSCT neurones were well described by a simple cable model. Equivalent dendritic cable lengths were calculated for DSCT neurones and found to have an average value of 1.0 space constants, which is considerably less than that calculated for motoneurones. 6. Application of the simple cable model of DSCT neurones demonstrated that the rapid rise-times of single group I EPSPs can be explained by a substantial somatic input to these cells. However, in addition to this strong somatic component, there may also be a contribution from dendritic synapses which prolong the initial decay phase of these EPSPs. The final decay of single fibre EPSPs in DSCT neurones is explained simply by the passive membrane time constant of these cells.

Action Potentials↗

PubMed1985

Septohippocampal connections to field CA1 of the rat identified with field potential analysis and retrograde labeling by horseradish peroxidase.

Electrical stimulation of the medial septal nucleus produced field potentials in the hippocampal CA1 region of the rat. The laminar field-potential analysis suggested that the electromotive force of the septum-induced responses might be attributable mainly to excitatory postsynaptic potential currents generated in the stratum oriens (layer of distribution of basal dendrites of hippocampal pyramidal cells). Neural cell bodies in the medial septum-diagonal band complex were retrogradely labeled with horseradish peroxidase (HRP) injected into the stratum oriens of CA1, but not with HRP injected into other CA1 strata. Thus the medial septal nucleus was indicated to send excitatory inputs to basal dendrites of CA1 pyramidal cells.

Animals↗

PubMed1989

Modification of evoked hippocampal dentate inhibition by diazepam and three antagonists in urethane-anesthetized rats.

Urethane-anesthetized rats with perforant pathway stimulating electrodes and recording electrodes placed in the hippocampal dentate gyrus were exposed to increasing doses of either the benzodiazepine agonist diazepam or an antagonist (PK-11195, CGS-8216, and RO15-1788). Analysis of the monosynaptic evoked field potentials indicated that none of the four compounds altered the threshold for eliciting the excitatory postsynaptic potential (EPSP). Reductions in field population spike (PS) amplitudes were seen after exposure to RO15-1788, CGS-8216, and diazepam, but not PK-11195. Using a paired-pulse paradigm, diazepam significantly increased early gamma-aminobutyric acid (GA-BAA)-mediated recurrent inhibition. The antagonist RO15-1788, but not CGS-8216 or PK-11195, also significantly increased early GABAA-mediated inhibition. The increase in GABAA-mediated inhibition after diazepam was reversed by the subsequent administration of the central antagonists RO15-1788 or CGS-8216, but not the peripheral antagonist PK-11195. Pretreatment with CGS-8216 or RO15-1788 prevented diazepam-induced inhibition. These data support the important modulatory role of the central benzodiazepine receptor in early GABAA-mediated inhibition at this synapse. They also suggest that basal granule cell excitability is not importantly modulated by this benzodiazepine receptor.

Anesthesia↗

PubMed1987

Amphetamine alteration of amplitude and timing of cortical-neostriatal interactions.

Amphetamine (0.1 to 5.0 mg/kg, IV) altered frontal cortex stimulation evoked neostriatal potentials in rats. The amplitude of wave P1, which corresponds to an initial intracellular excitatory postsynaptic potential, was reduced, as was the latency to wave N3, which corresponds to the late rebound depolarization. Repetitive electric stimulation of the mesencephalic reticular formation at low currents (0.05 to 0.5 mA, 0.2-ms duration, 60 Hz square waves) produced similar effects. The peripherally acting sympathomimetics, norepinephrine (3 and 10 micrograms/kg, IV) and vasopressin (10 mU/kg, IV), increased blood pressure but did not alter the neostriatal evoked response. In rats with medial thalamic lesions induced by kainic acid, wave N3 was eliminated, and the effects of amphetamine and mesencephalic reticular formation stimulation on neostriatal evoked responses were reduced or eliminated. Thus many of the effects of systemic amphetamine on frontal cortex evoked neostriatal potentials may be mediated via extrastriatal sites, including the mesencephalic reticular formation and the medial thalamus.

Amphetamine↗

PubMed1984

Inhibition of calcium spikes and transmitter release by gamma-aminobutyric acid in the guinea-pig myenteric plexus.

The effect of gamma-aminobutyric acid (GABA) (1 microM-1 mM) on synaptic transmission in isolated myenteric ganglia of guinea-pig ileum was investigated with intracellular recording techniques. GABA (up to 1 mM) had no effect on the resting membrane potential and membrane conductance of S neurones. GABA reduced the amplitude of the fast excitatory postsynaptic potential e.p.s.p.) without changing the amplitude of the nicotinic response to ionophoretic application of acetylcholine (ACh). This effect was mimicked by baclofen (10-100 microM) and was not blocked by bicuculline (10 microM). The preparation did not become desensitized during prolonged GABA applications. Cholinergic and non-cholinergic slow e.p.s.ps evoked by single or repetitive presynaptic nerve stimulation were reduced in amplitude by GABA. GABA did not depress muscarinic responses to ionophoretic application of ACh. GABA reduced the duration of the action potential in AH neurones in concentrations that did not affect the membrane potential or conductance. The effect was very marked when electrodes were filled with CsCl, and tetrodotoxin was in the superfusing solution. This effect was also mimicked by baclofen, was insensitive to bicuculline and was not reduced with repeated application or GABA. It is concluded that GABA inhibits release of ACh and the transmitter mediating the slow e.p.s.p. This effect may result from inhibition of an inward calcium current.

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