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At least 1,297 records · Page 72Linked to original sources
PubMed1998

GABAergic input to cholinergic nucleus basalis neurons.

The potential influence of GABAergic input to cholinergic basalis neurons was studied in guinea-pig basal forebrain slices. GABA and its agonists were applied to electrophysiologically-identified cholinergic neurons, of which some were labelled with biocytin and confirmed to be choline acetyltransferase-immunoreactive. Immunohistochemistry for glutamate decarboxylase was also performed in some slices and revealed GABAergic varicosities in the vicinity of the biocytin-filled soma and dendrites of electrophysiologically-identified cholinergic cells. From rest (average - 63 mV), the cholinergic cells were depolarized by GABA. The depolarization was associated with a decrease in membrane resistance and diminution in firing. The effect was mimicked by muscimol, the specific agonist for GABA(A) receptors, and not by baclofen, the specific agonist for GABA(B) receptors, which had no discernible effect. The GABA- and muscimol-evoked depolarization and decrease in resistance were found to be postsynaptic since they persisted in the presence of solutions containing either high Mg2+/low Ca2+ or tetrodotoxin. They were confirmed as being mediated by a GABA(A) receptor, since they were antagonized by bicuculline. The reversal potential for the muscimol effect was estimated to be approximately -45 mV, which was -15 mV above the resting membrane potential. Finally, in some cholinergic cells, spontaneous subthreshold depolarizing synaptic potentials (average 5 mV in amplitude), which were rarely associated with action potentials, were recorded and found to persist in the presence of glutamate receptor antagonists but to be eliminated by bicuculline. These results suggest that GABAergic input may be depolarizing, yet predominantly inhibitory to cholinergic basalis neurons.

2-Amino-5-phosphonovalerate↗
PubMed2003

The alpha-latrotoxin mutant LTXN4C enhances spontaneous and evoked transmitter release in CA3 pyramidal neurons.

Alpha-latrotoxin (LTX) stimulates vesicular exocytosis by at least two mechanisms that include (1) receptor binding-stimulation and (2) membrane pore formation. Here, we use the toxin mutant LTX(N4C) to selectively study the receptor-mediated actions of LTX. LTX(N4C) binds to both LTX receptors (latrophilin and neurexin) and greatly enhances the frequency of spontaneous and miniature EPSCs recorded from CA3 pyramidal neurons in hippocampal slice cultures. The effect of LTX(N4C) is reversible and is not attenuated by La3+ that is known to block LTX pores. On the other hand, LTX(N4C) action, which requires extracellular Ca2+, is inhibited by thapsigargin, a drug depleting intracellular Ca2+ stores, by 2-aminoethoxydiphenyl borate, a blocker of inositol(1,4,5)-trisphosphate-induced Ca2+ release, and by U73122, a phospholipase C inhibitor. Furthermore, measurements using a fluorescent Ca2+ indicator directly demonstrate that LTX(N4C) increases presynaptic, but not dendritic, free Ca2+ concentration; this Ca2+ rise is blocked by thapsigargin, suggesting, together with electrophysiological data, that the receptor-mediated action of LTX(N4C) involves mobilization of Ca2+ from intracellular stores. Finally, in contrast to wild-type LTX, which inhibits evoked synaptic transmission probably attributable to pore formation, LTX(N4C) actually potentiates synaptic currents elicited by electrical stimulation of afferent fibers. We suggest that the mutant LTX(N4C), lacking the ionophore-like activity of wild-type LTX, activates a presynaptic receptor and stimulates Ca2+ release from intracellular stores, leading to the enhancement of synaptic vesicle exocytosis.

Amino Acid Substitution↗
PubMed2003

Endogenous pacemaker potentials develop into paroxysmal depolarization shifts (PDSs) with application of an epileptogenic drug.

Well-known invertebrate ganglia (buccal ganglia of Helix pomatia, abdominal ganglia of Aplysia californica) were used to study the contribution of synaptic potentials, central pattern generators, and endogenously generated neuronal potentials to the development of epileptiform activity. Epileptiform activity which was induced with application of pentylenetetrazol (1 to 100 mM) or etomidate (0.12 to 1.0 mM) consisted of paroxysmal depolarization shifts (PDSs) recorded simultaneously from several identified neurons with sharp microelectrodes. With application of an epileptogenic drug, endogenous pacemaker potentials develop into PDSs. With increasing concentration of the drug, (i) amplitude of pacemaker-depolarizations and (ii) delay of pacemaker-repolarization increased progressively finally resulting in PDSs. Additionally, the activation characterists of currents shifted from between -50 and -40 mV (pacemaker potentials, control conditions) to between -100 and -40 mV (PDS, epileptic conditions). Only neurons which generated pacemaker potentials under control conditions could generate PDSs under epileptic conditions. Chemical synaptic inputs triggered or blocked pacemaker potentials as well as PDSs. Activities induced from central pattern generators were identified with simultaneous recordings from several identified neurons. The central pattern generators could trigger or block pacemaker potentials as well as PDSs. Results demonstrate that, in the used model nervous systems, pacemaker potentials which are generated by the single neurons are the physiologic basis of epileptic activity.

Animals↗
PubMed1977

[Postsynaptic excitation and inhibition in neurons of the general cortex of turtles during presentation of moving stimuli].

Reactions to moving stimuli were studied in the turtle general cortex. The evoked potentials, synaptic nature of their components and mechanism of their generation were analysed. The evoked potentials was negative-positive. The negative part consisted of fast negative complexes and a slow negative wave. These negative components reflected EPSP generated in the dendrites of the main cortex neurons. A rhythmical oscillation in the evoked potential started after the initial fast negative complex. The negative waves of this oscillation reflected EPSP and the positive waves, IPSP being generated also in the dendrites of the main cortex neurons. They had probably a recurrent generation mechanism. The positive wave of the evoked potential reflected dendritic IPSP in the main neurons.

Animals↗
PubMed1991

Computation of frequency-to-spatial transform by olfactory bulb glomeruli.

A physiological simulation of 2.5% of the input and inhibitory neurons and 25% of the primary mitral/tufted cells in a single mammalian olfactory bulb glomerulus was constructed. This physiological simulation used the integrate-and-fire paradigm with realistic activation curves and synaptic delays. The dendritic integration incorporated non-linear interactive effects of individual cell excitatory and inhibitory post-synaptic potentials (PSPs) from both axodendritic and dendro-dendritic synaptic contacts. Refractory periods for granule-cell inhibition of mitral/tufted cell activity lead to relatively fixed-frequency rhythmic activity in the glomerulus, independent of the input frequency from the olfactory nerve. Though the frequency of mitral/tufted cell firing in bulb was approximately independent of input frequency, the number of cells active in the glomerulus was a roughly-linear function of input frequency to the glomerulus, indicating the mechanism's ability to function as a frequency-to-spatial encoder.

Animals↗
PubMed1987

Ionic and pharmacological properties of reciprocal inhibition in Xenopus embryo motoneurones.

1. Properties of rhythmic, compound mid-cycle inhibitory post-synaptic potentials (i.p.s.p.s), which constitute one of the three main synaptic drives to motoneurones during fictive swimming in Xenopus embryos, have been examined using ionic and pharmacological manipulation. 2. Mid-cycle i.p.s.p.s are Cl- dependent. They are reversed by intracellular Cl- injection and attenuated by lowered extracellular Cl- concentration. 3. In response to bath application of 100 microM-glycine or 100 microM-gamma-aminobutyric acid (GABA), motoneurones show a decrease in cell input resistance of 24 +/- 2.9 M omega (mean +/- S.E. of mean) or 16 +/- 3.7% and 26 +/- 6.0 M omega or 14 +/- 2.0% respectively. This is associated with a weak hyperpolarization or depolarization of 0 +/- 1.5 mV and -3 +/- 1.4 mV respectively. Both responses can be made strongly depolarizing by intracellular Cl- injection. 4. The response to glycine is blocked by 1 microM-strychnine but is largely unaffected by bicuculline below 50 microM. The response to GABA is largely blocked by 10 microM-bicuculline but is unaffected by 1 microM-strychnine. Both strychnine and bicuculline are therefore specific antagonists in the amphibian embryo preparation. Glycine and GABA are both partially antagonized by 10 microM-picrotoxin. 5. Mid-cycle i.p.s.p.s recorded in motoneurones during fictive swimming are reduced in amplitude by 0.5-1 microM-strychnine but are largely unaffected by 40 microM-bicuculline. In embryos immobilized by ventral root transection, 100 microM-tubocurarine, a likely GABA antagonist in the embryo, has no effect on mid-cycle inhibition. Glycine is suggested to be the probable transmitter released by commissural interneurones and mediating mid-cycle inhibition during fictive swimming, acting to increase conductance of Cl-.

Action Potentials↗
PubMed1999

Potent depression of stimulus evoked field potential responses in the medial entorhinal cortex by serotonin.

1. The entorhinal cortex (EC), main input structure to the hippocampus, gets innervated by serotonergic terminals from the raphe nuclei and expresses 5-HT-receptors at high density. Using extra- and intracellular recording techniques we here investigated the effects of serotonin on population and cellular responses within the EC. 2. Stimulation in the lateral entorhinal cortex resulted in complex field potential responses in the superficial EC. The potentials are composed of an early antidromic and a late orthodromic component reflecting the efferent and afferent circuitry. 3. Serotonin (5-HT) reduced synaptic potentials of the stimulus evoked extracellular field potential at all concentrations tested (0. 1 - 100 microM; 59%-depression by 10 microM serotonin), while the antidromic response was not significantly changed by up to 50 microM 5-HT. Depression of field potential responses by serotonin was associated with a significant increase in paired-pulse facilitation from 1.15 to 1.88. 4. The effects of serotonin on field potential responses were mimicked by 5-HT1A-receptor agonists (8-OH-DPAT, 5-CT) and partially prevented by the 5-HT1A-receptor antagonist (S-UH-301). Moreover, the 5-HT1A-receptor antagonist WAY100635 reduced the effect of 5-CT. 5. Fenfluramine, a serotonin releaser, mimics the effects of serotonin on stimulus-evoked field potential responses, indicating that synaptically released serotonin can produce the changes in reactivity to afferent stimulation. 6. Depression of isolated AMPA-receptor mediated EPSCs by serotonin as well as fenfluramine was associated with an increase in paired pulse facilitation, indicating a presynaptic locus of action. 7. We conclude that physiological concentrations of serotonin potently suppresses excitatory synaptic transmission in the superficial entorhinal cortex by a presynaptic mechanism.

Animals↗
PubMed1975

Neurons from fetal rat brain in a new cell culture system: a multidisciplinary analysis.

A new culture system for cells from the mammalian brain was developed by a modification of a previously established technique. This modification involved the use of fluorodeoxyuridine and adult horse serum. The cultures contained large, easily visualized neurons both isolated from other neurons and in networks of varying complexity. These cells were large enough to permit reliable intracellular electrophysiologic recording and were often sufficiently dispersed to allow examination of membrane responses to iontophoretically applied neurotransmitter candidates. Many responses characteristic of central neurons in situ were seen, including evoked and spontaneous action potentials, complex patterns of inhibitory and excitatory post-synaptic potentials, and neurotransmitter-induced membrane responses. These preparations were examined by phase contrast microscopy, by light microscopy after silver impregnation and by Nomarski interference optics. Total choline acetyltransferase (CAT) activity was little changed and specific activity was increased in the new culture system as compared with the earilier system. Conditions which gave the highest specific activity of CAT also provided the best cultures from the standpoint of electrophysiologic and morphologic analysis. This new approach will allow, in culture, detailed multidisciplinary analyses of individual neurons and small networks of neurons from the mammalian brain.

Acetylcholine↗
PubMed2000

Gene transfer into hippocampal slice cultures with an adenovirus vector driven by cytomegalovirus promoter: stable co-expression of green fluorescent protein and lacZ genes.

Virus-mediated gene transfer into identified neurons of organotypic hippocampal slice cultures offers a great potential for studying the cellular and molecular mechanisms of synaptic plasticity. We describe here a new adenovirus vector Ad-GFP-lacZ carrying an early cytomegalovirus (CMV) gene promoter that efficiently co-transferred the beta-galactosidase (lacZ) and green fluorescent protein (GFP) genes in rat organotypic hippocampal slice cultures. Monitoring of GFP fluorescence and immuno-histochemical staining for beta-galactosidase showed that the expression of the transferred genes was widespread in the glial cells and neurons of CA1, CA3/4, and dentate gyrus regions. Immunoblot analyses showed that the expression of gamma-galactosidase and GFP was maximal about 48 h after infection of hippocampal slices with the adenovirus vector and the expression levels were maintained for several weeks. Also, immunoblot analyses showed no significant differences in the MAP-2 and glial fibrillary acidic protein levels in the adenovirus vector infected and uninfected hippocampal slices. In addition, we found that the infection of hippocampal slices with the adenovirus vector caused no significant increase in the induction of heat shock protein (HSP)-70 and showed no change in their electrophysiological properties as measured by stable field synaptic potentials in CA1 region and its reactivity to high frequency stimulation. Our data suggest that this adenovirus vector can be exploited to transfer multiple genes into neurons and may have implications for developing strategies for gene therapy.

Adenoviridae↗
PubMed1987

Reversibility of alcohol-related brain damage: clinical and experimental observations.

Chronic alcoholics who maintain abstinence often demonstrate remarkable improvement of neurological and mental dysfunction. This paper presents an overview of the clinical and laboratory work of our group. Reversible clinical manifestations include psychometric scores, ataxia, tremor, Parkinsonism, dyskinesia, cerebral atrophy, EEG parameters, and a CSF acidosis. Electrophysiological investigations showed that in the in vitro hippocampus of rats fed ethanol for several months there was evidence for diminished long-term potentiation, impaired neuronal inhibitory mechanisms (diminished inhibitory post-synaptic potentials and post-spike after hyperpolarisations), decreased neuronal specific membrane capacitance and increased specific membrane resistance. Golgi stains showed attenuation of hippocampal CA1 neuronal dendrites in rats fed ethanol for five months, which reverted to control size in rats permitted two months of alcohol withdrawal.

Action Potentials↗
PubMed1986

Correlation between long-term potentiation and release of endogenous amino acids from dentate gyrus of anaesthetized rats.

The relationship between long-term potentiation (l.t.p.) and the release of endogenous amino acid transmitters has been investigated in the dentate gyrus of rats anaesthetized with urethane. The molecular layer was perfused with artificial cerebrospinal fluid using a push-pull cannula. The perfusate was collected and analysed for glutamate, aspartate, glycine, glutamine and gamma-aminobutyric acid (GABA) using high-performance liquid chromatography (h.p.l.c.) with fluorometric detection. Recording electrodes were attached to the cannula to enable responses evoked by test stimuli to the perforant path to be monitored in the molecular and cell body layers. Perfusion was continued for 3 h while test stimuli were delivered to the perforant path at 30 s intervals. In the control group (n = 8), no further stimulation was given. In a second group (n = 8), a single high-frequency train (250 Hz for 200 ms) was delivered at the end of the first hour to induce l.t.p. The average potentiation of the slope of the excitatory post-synaptic potential (e.p.s.p.) 2 h later was 15%. In a third group (n = 8), the train to the perforant path was paired with a train to the commissural input to the dentate gyrus, a procedure which blocks the induction of l.t.p. In the potentiated group, there was an increase in the concentrations of glutamate and aspartate following the induction of l.t.p., relative to the decline seen in corresponding periods of the control group. This increase remained statistically significant for 1.5 h in the case of glutamate and for 45 min in the case of aspartate. There were no l.t.p.-associated changes in the release of glutamine or glycine; there was an indication that l.t.p. may be associated with a decrease in the release of GABA. Increasing the frequency and intensity of perforant path activation resulted in enhanced concentrations of glutamate and aspartate in the perfusate; no such changes occurred when granule cells were activated antidromically. We discuss the origin of the relative increases in the concentration of glutamate and aspartate which are found in the perfusate following the induction of l.t.p. and conclude that the most likely source is a sustained increase in activity-dependent release of these amino acids from perforant path terminals.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1987

Thresholds of action potentials evoked by synapses on the dendrites of pyramidal cells in the rat hippocampus in vitro.

1. In this study we have measured the thresholds of action potentials and some properties of e.p.s.p.s (excitatory post-synaptic potentials) produced by activation of distal and proximal dendritic synapses in CA1 pyramidal cells in rat hippocampal slices. 2. Simultaneous intracellular and extracellular electrophysiological recordings were made from pyramidal cells. The two recording electrodes were positioned very close together to provide an accurate measurement of the transmembrane potential by subtraction of the extracellular field from the intracellular potential. 3. Two pairs of stimulating electrodes were placed in the stratum radiatum of area CA1. The proximal and distal afferents were stimulated alternately within a 15 s cycle and at an intensity to produce action potentials in about 50% of the trials. 4. At this stimulus intensity there was a slight difference in the mean 10-90% rise times of the e.p.s.p.s produced by stimulation of proximal and distal afferents. The ratio of the distal: proximal rise time was 1.27. 5. In those trials where the action potential failed there was also a significant difference in the time-to-peak of the e.p.s.p.s evoked from proximal or distal sites. The times-to-peak of the e.p.s.p.s from proximal stimulation were between 1.5 and 3.8 ms, whilst the times-to-peak from distal stimulation were longer (2.1-7.2 ms). 6. In 16/18 cells included in this study the thresholds for action potentials evoked by distal stimulation were significantly lower than those following proximal activation. The mean threshold for distal activation was 12 mV compared with 16 mV for proximal activation. 7. The threshold of action potentials activated by depolarizing current pulses appeared to be close to that for action potentials evoked from proximal synapses. 8. Whilst the shape indices of the e.p.s.p.s were slightly different when comparing transmembrane with conventional intracellular recordings, the thresholds of the action potentials were not affected by this procedure. 9. Possible explanations for the low threshold for action potentials evoked from distal synapses are discussed, including an active dendritic membrane and differences in inhibition.

Action Potentials↗
PubMed1998

From biophysics to models of network function.

Neurons and synapses display a rich range of time-dependent processes. Which of these are critical to understanding specific integrative functions in the brain? Computational methods of various kinds are used to understand how systems of neurons interact to produce behavior. However, these models often assume that neuronal dynamics and synaptic strengths are fixed. This review presents some recent models that illustrate that short-term synaptic plasticity mechanisms such as facilitation and depression can have important implications for network function. Other features of synaptic transmission such as multi-component synaptic potentials, cotransmission, and neuromodulation with obvious potential computational implications are presented. These examples illustrate that synaptic strength and intrinsic properties in networks are continuously varying on numerous time scales as a function of the temporal patterns of activity in the network. Thus, both firing frequency of the neurons in a circuit, and the modulatory environment determine the intrinsic and synaptic properties that produce behavior.

Animals↗
PubMed1987

GABA-mediated synaptic inhibition of projection neurons in the antennal lobes of the sphinx moth, Manduca sexta.

Responses of neurons in the antennal lobe (AL) of the moth Manduca sexta to stimulation of the ipsilateral antenna by odors consist of excitatory and inhibitory synaptic potentials. Stimulation of primary afferent fibers by electrical shock of the antennal nerve causes a characteristic IPSP-EPSP synaptic response in AL projection neurons. The IPSP in projection neurons reverses below the resting potential, is sensitive to changes in external and internal chloride concentration, and thus is apparently mediated by an increase in chloride conductance. The IPSP is reversibly blocked by 100 microM picrotoxin or bicuculline. Many AL neurons respond to application of GABA with a strong hyperpolarization and an inhibition of spontaneous spiking activity. GABA responses are associated with an increase in neuronal input conductance and a reversal potential below the resting potential. Application of GABA blocks inhibitory synaptic inputs and reduces or blocks excitatory inputs. EPSPs can be protected from depression by application of GABA. Muscimol, a GABA analog that mimics GABA responses at GABAA receptors but not at GABAB receptors in the vertebrate CNS, inhibits many AL neurons in the moth.

Animals↗
PubMed1984

Synaptic and antidromic potentials of visceral neurones in ganglia of the lumbar sympathetic chain of the cat.

Intracellular recordings were obtained in vitro from two hundred and twenty post-ganglionic neurones of the fourth and fifth lumbar paravertebral ganglia of cats. Thirty-seven percent of neurones tested evoked antidromic responses during electrical stimulation of post-ganglionic fibres in the inferior lumbar splanchnic nerves. Twenty-seven percent of neurones tested evoked antidromic responses during electrical stimulation of post-ganglionic fibres in the lumbar sympathetic chain. Twenty-four percent of neurones tested evoked convergent antidromic responses during electrical stimulation of post-ganglionic fibres in separate inferior lumbar splanchnic nerves or lumbar sympathetic chain, and by inferior lumbar splanchnic nerves and lumbar sympathetic chain. Eighty-six percent of paravertebral post-ganglionic fibres which project to the inferior lumbar splanchnic nerves or lumbar sympathetic chain were composed of B fibres with maximal conduction velocities ranging from above 2.0 to 16.0 m/s. Fourteen percent of post-ganglionic fibres were composed of C fibres with maximal conduction velocities ranging from 0.2 to 2.0 m/s. Synaptic responses of neurones were recorded intracellularly during electrical stimulation of preganglionic fibres in inferior lumbar splanchnic nerves, lumbar white rami communicantes and lumbar sympathetic chain located one to three segments above the fourth and fifth lumbar ganglia and one to two segments below. Synaptic responses consisting of excitatory post-synaptic potentials and action potentials were mediated via nicotinic receptors. Twenty-seven percent of neurones tested received synaptic input from only one or two segments of the lumbar sympathetic chain. Seventy-three percent of neurones tested received convergent synaptic input from one or two segments of the lumbar sympathetic chain, lumbar white rami communicantes and inferior lumbar splanchnic nerves. It is concluded that central preganglionic fibres which project to inferior lumbar splanchnic nerves also project to the lumbar sympathetic chain to innervate neurones in the L4 and L5 ganglia. Synaptic responses of neurones during electrical stimulation of preganglionic fibres in the lumbar sympathetic chain and in the inferior lumbar splanchnic nerves were reduced in a chronic isolated segment of the sympathetic chain devoid of central preganglionic inputs. It is concluded that synaptic responses elicited in neurones during electrical stimulation of inferior lumbar splanchnic nerves and lumbar sympathetic chain were mediated in part via collaterals of central preganglionic axons and in part via axons whose cell bodies were located in the periphery.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1986

Is synaptic transmission modulated by progesterone?

The influence of the gonadosteroid hormone progesterone on synaptic transmission was studied using the frog neuromuscular preparation. Intracellular recording of synaptic potentials revealed enhanced release of acetylcholine from motor nerve terminals exposed to progesterone (3 nM-3 mM). The following effects were observed. An augmented quantal content of evoked release of transmitter; an elevation in synaptic facilitation; and a substantial increase in the rate of spontaneously occurring miniature endplate potentials. It is suggested that synaptic transmission at the neuromuscular junction may be naturally modulated by the physiologically oscillating level of progesterone.

Acetylcholine↗
PubMed2005

Nicotinic modulation of glutamatergic synaptic transmission in region CA3 of the hippocampus.

Cholinergic modulation of synaptic transmission in the hippocampus appears to be involved in learning, memory and attentional processes. In brain slice preparations of hippocampal region CA3, we have explored the effect of nicotine on the afferent connections of stratum lacunosum moleculare (SLM) vs. the intrinsic connections of stratum radiatum (SR). Nicotine application had a lamina-selective effect, causing changes in synaptic transmission only in SLM. The nicotinic effect in SLM was characterized by a transient decrease in synaptic potential size followed by a longer period of enhancement of synaptic transmission. The effect was blocked by gamma-aminobutyric acid (GABA)ergic antagonists, indicating the role of GABAergic interneurons in the observed nicotinic effect. The biphasic nature of the nicotinic effect could be due to a difference in receptor subtypes, as supported by the effects of the nicotinic antagonists mecamylamine and methyllycaconitine. Nicotinic modulation of glutamatergic synaptic transmission could complement muscarinic suppression of intrinsic connections, amplifying incoming information and providing a physiological mechanism for the memory-enhancing effect of nicotine.

Aconitine↗
PubMed1983

Large long-lasting potentiation in the dentate gyrus in vitro during blockade of inhibition.

The generation of long-lasting synaptic potentiation was studied in the dentate gyrus of hippocampal slices before and after blockade of inhibition by application of GABA antagonists. Field potential analysis showed that inhibition in the dentate gyrus is to a large extent dendritically located. During blockade of inhibition, induction of long-lasting potentiation was facilitated, together with a large increase in the maximal potentiation that could be produced. It is suggested that the enhanced production of long-lasting potentiation in inhibition-free slices is related to an increased postsynaptic depolarization in granule cell dendrites.

Animals↗