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PubMed1995

Expression of EPSP/spike potentiation following low frequency and tetanic stimulation in the CA1 area of the rat hippocampus.

Low frequency stimulation (LFS, 1 Hz for 15 min) has been shown to produce an NMDA receptor dependent homosynaptic long-term depression (LTD) of synaptic potentials in the CA1 area of the rat hippocampus. Here we describe experiments aimed at characterizing EPSP/spike (E/S) coupling associated with this form of LTD. Our data show that following LFS neurons have a higher probability of synchronous discharge in response to a population EPSP of fixed slope (E/S potentiation). This E/S potentiation was not significantly enhanced by a tetanic stimulation. When the protocol was reversed, that is, starting with a tetanic stimulus, E/S potentiation was observed which was unaffected by a subsequent LFS. Saturating these synaptic responses to either a maximal or a minimal value produced similar effects on E/S coupling. E/S depression was never encountered. Finally, we found that the expression of E/S potentiation did not require the activation of NMDA receptors. These data suggest that at the level of a local neuronal network in the CA1 area, LFS is not a very powerful tool since the synaptic depression is associated with a potentiation of the population response of these neurons. Furthermore, the expression of E/S dissociation seems different from that of homosynaptic long-term potentiation and LTD.

2-Amino-5-phosphonovalerate↗
PubMed1995

Facilitation of hippocampal potentials by suramin.

The influence of suramin, a suggested purino-receptor antagonist, on the evoked synaptic potentials recorded from hippocampal slices was evaluated. The suramin induced a nondecremental, concentration-dependent amplification of the slope of excitatory postsynaptic potential and magnitude of the population spike (long-term potentiation, LTP). The effect of suramin was completely abolished by adenylimidodiphosphate, a non-hydrolyzable analogue of ATP, and markedly reduced by NMDA-receptor antagonists DL-2-amino-5-phosphonovaleric acid and MK-801. These results indicate that, in addition to acting as an antagonist of P2 receptors, suramin is also able to facilitate hippocampal potentials in a way that involves mechanisms participating in induction of LTP.

2-Amino-5-phosphonovalerate↗
PubMed1984

Sites and mechanisms of actions of enkephalin in the feline parasympathetic ganglion.

Intracellular recordings were made in vitro from neurones of the cat parasympathetic ciliary ganglion with a current- or voltage-clamp technique. (Met5)enkephalin and (leu5)enkephalin (10 nM to 10 microM) were applied by superfusion. Both caused a membrane hyperpolarization which persisted in a calcium-free/high-magnesium solution, and both reduced the amplitude of excitatory post-synaptic potentials (e.p.s.p.s). These actions of enkephalin were antagonized by naloxone. The enkephalin-induced hyperpolarization was associated with an increase in membrane conductance, reversed in polarity at -90 mV and was not altered by changing external sodium and chloride concentrations. This indicates that the enkephalin hyperpolarization is due mainly to activation of potassium conductance. Enkephalin decreased the mean quantal content of e.p.s.p.s recorded in low-calcium/high-magnesium solution, without changing quantal size. Furthermore, the increase in the frequency of miniature e.p.s.p.s after tetanic preganglionic stimulations was inhibited by enkephalin. Acetylcholine potentials were not altered by enkephalin. These findings suggest that enkephalin reduces transmitter release. The experiments suggest that enkephalin may inhibit ganglionic transmission by both pre- and post-synaptic actions in a mammalian parasympathetic ganglion.

Acetylcholine↗
PubMed1988

Comparative extracellular current flow at dendrites and soma of dentate granule cells during long-term potentiation.

In the study of long-term potentiation (LTP) in the dentate gyrus, the magnitude of the initial slope of the evoked synaptic potential (ESP) in the region of the granule cell layer, is commonly used as a measure of synaptic efficacy at the site of the perforant path (PP) input. To investigate the viability of this assumption, in rats anesthetized with either chloropent or urethane, LTP was induced by tetanic stimulation of the PP and ESPs were measured simultaneously at both the soma and dendritic site of the PP input. Following LTP, the two responses were decoupled, the somal response being greater than the dendritic in rats anesthetized with chloropent, the opposite being true in urethanized animals. We conclude that in investigating changes in synaptic efficacy following LTP, measurements should be taken at the site of the PP input.

Action Potentials↗
PubMedDate not supplied

GluR5 kainate receptor mediated synaptic transmission in rat basolateral amygdala in vitro.

A non-NMDA and non-AMPA receptor mediated excitatory synaptic response was identified in intracellularly recorded basolateral amygdala (BLA) neurons in an in vitro slice preparation. Synaptic potentials were evoked by stimulation of either the external capsule (EC) or basal amygdala (BA). NMDA and GABA(A) receptors were blocked by inclusion of 100 microM (+/-)-2-amino-5-phosphonopentanoic acid and 10 microM bicuculline in the perfusion solution. The AMPA receptor-selective allosteric antagonists GYKI 52466 (50 microM) and GYKI 53655 (50 microM) partially suppressed depolarizing synaptic responses evoked by single shock EC stimulation, but fully blocked synaptic responses evoked by BA stimulation. In recordings carried out in the presence of the AMPA receptor antagonists, EC stimulation with pulse trains (5-8 pulses at 50-100 Hz) evoked a large increase in the amplitude of synaptic responses. The AMPA receptor-independent component of the train-induced synaptic response had a null potential near 0 mV. Such AMPA receptor-independent, train-evoked synaptic responses were largely blocked by the AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (20 microM; 85 +/- 4%). In addition, the responses were blocked by the GluR5-selective kainate receptor antagonist LY293558 (10 microM; 95 +/- 2%). These results indicate that a component of the EC (but not the BA) synaptic response is mediated by kainate receptors containing the GluR5 subunit.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1994

Potentiated transmission and prevention of further LTP by increased CaMKII activity in postsynaptic hippocampal slice neurons.

Calcium-calmodulin-dependent protein kinase II (CaMKII) is a necessary component of the cellular machinery underlying learning and memory. Here, a constitutively active form of this enzyme, CaMKII(1-290), was introduced into neurons of hippocampal slices with a recombinant vaccinia virus to test the hypothesis that increased postsynaptic activity of this enzyme is sufficient to produce long-term synaptic potentiation (LTP), a prominent cellular model of learning and memory. Postsynaptic expression of CaMKII(1-290) increased CaMKII activity, enhanced synaptic transmission, and prevented more potentiation by an LTP-inducing protocol. These results, together with previous studies, suggest that postsynaptic CaMKII activity is necessary and sufficient to generate LTP.

2-Amino-5-phosphonovalerate↗
PubMed2005

Synaptic plasticity and drug addiction.

Recent studies have suggested that the development of addictive behaviours shares common features with traditional learning models. Synaptic plasticity, a possible substrate for learning, has been demonstrated in neural reward circuits and might contribute to the learning of addictive behaviours. Changes in the strength of synaptic connections have been investigated in dopaminergic cells of the ventral tegmental area in response to several addictive drugs. Rapid and persistent forms of synaptic plasticity (specifically, long-lasting synaptic potentiation) have been demonstrated to accompany some of the behavioural effects of addictive drugs. We hypothesize that drug-induced synaptic plasticity might play a role in reward-related learning and addiction by modifying the fine tuning of dopaminergic cell firing.

Brain↗
PubMed1993

Synaptic currents evoked in Purkinje cells by stimulating individual granule cells.

Each cerebellar Purkinje cell receives input from about 160,000 glutamatergic granule cells. In anatomically intact preparations this input has hitherto been studied only as a compound synaptic potential or current. Presented here are simultaneous recordings in cerebellar slices of synaptically connected granule cell-Purkinje cell pairs. The mean amplitude of the excitatory synaptic currents evoked by stimulation of individual granule cells ranged from 2 to 60 pA, whereas the great majority of the spontaneous glutamatergic currents in Purkinje cells in the presence of tetrodotoxin were < 40 pA. In several cases, stimulation of a single granule cell evoked a disynaptic inhibitory current. It is estimated that on the order of 50 simultaneously active granule cells are sufficient to excite a Purkinje cell.

Animals↗
PubMed1995

Directionally selective motion detection in the sustaining fibers of the crayfish optic nerve: linear and nonlinear mechanisms.

1. Directional selectivity of crayfish sustaining fibers was examined with drifting sine wave gratings and with intracellular and extracellular recordings. Directionality was measured for variations in stimulus contrast, spatial frequency, and temporal frequency. 2. Sustaining fibers exhibit directional selectivity in the magnitude of the compound postsynaptic potential (PSP), the impulse frequency modulation response, and the mean firing rate. The mean synaptic potential is insensitive to direction. The directionality of the mean impulse rate appears to arise by rectification in the voltage-to-impulse transduction. 3. The preferred directions of three identified sustaining fibers are similar to those of head-down optomotor neurons to which these sustaining fibers project. 4. The modulatory response, elicited by gratings drifting in the preferred direction, increased linearly with contrast until saturation (typically at a contrast of 0.5), where maximum directional selectivity obtains. 5. The magnitude of the directional response is a band-pass function of spatial and temporal frequency and exhibits reversal of directionality (i.e., aliasing) at high spatial and temporal frequencies. The results imply a spatial sampling interval of 4.5 degrees and a temperature-dependent inhibitory delay of 40-90 ms. The PSP modulation response shares several features with that of neighboring tangential (Tan1) neurons. 6. A qualitative model is proposed for the transformation of a phase-sensitive, linear directional response to a phase-insensitive and nonlinear time-averaged response, based on the functional connections from Tan1 neurons to sustaining fibers to optomotor neurons. The model includes a threshold rectification, a synaptic band-pass filter, and differences in temporal phase among converging modulatory signals.

Animals↗
PubMed2002

Up-regulation of glutamate receptors is associated with LTP defects in the early stages of diabetes mellitus.

AIMS/HYPOTHESIS: Recent studies involving electrophysiology and immunolabelling indicate that short-term insulin treatment of hippocampal neurons in culture induces changes in glutamate receptor function, suggesting that this receptor system can be altered on a relatively rapid time scale during diabetic conditions. To investigate this hypothesis, we examined whether brain glutamate receptors and long-term potentiation are altered in the early stages of diabetes mellitus in non-obese diabetic mice, a genetic model of Type I (insulin-dependent) diabetes mellitus. METHODS: In vitro receptor autoradiography and immunoblotting were used to study the impact of diabetes on brain glutamate receptors. From an electrophysiological point of view, field potential recordings were also examined in area CA1 of hippocampal slices to determine the influence of diabetes on long-term potentiation. RESULTS: Quantitative autoradiographic analysis revealed enhanced 3H-glutamate binding to several brain regions of diabetes mice, with maximal increases in the cerebral cortex and hippocampus. Saturation kinetics within the cerebral cortex disclosed that this change of 3H-glutamate was possibly due to an increase in the maximal number of N-methyl- D-aspartate binding sites, an interpretation that was corroborated by Western blot analysis of N-methyl- D-aspartate 2A subunits. Impairment in the expression of hippocampal long-term potentiation was also observed in diabetic mice, while the failure to elicit synaptic potentiation was prevented by insulin treatment. CONCLUSION/INTERPRETATION: Because glutamate receptors are thought to be involved in several degenerative processes, our results suggest that up-regulation of these receptors in the early stages of diabetes could represent an important mechanism underlying neurological complications within the brain of diabetic patients.

Animals↗
PubMed1995

Modulation by adenosine of a neuronal inhibitory interaction in the rat hippocampus.

Adenosine is acknowledged to have a primarily inhibitory function in the central nervous system, but is believed to have little effect on inhibitory neurones themselves. It is, however, difficult to determine the effect of adenosine on inhibitory synaptic potentials since adenosine directly depresses evoked potentials and, in the presence of bicuculline to block GABAA-mediated inhibition, the bicuculline-resistant fraction of paired-pulse inhibition (ppi) is greater between pairs of small potentials than between pairs of larger potentials. Here, adenosine increased bicuculline-resistant ppi when stimulus strength was constant between adenosine and control but ppi of responses in adenosine was markedly less than ppi of control responses of the same size. Adenosine had less effect on the size of 'conditioned' potentials than on control potentials. It is concluded that adenosine can reduce the bicuculline-resistant fraction of paired-pulse inhibition in the hippocampus. Further quantitative comparison of the effects of adenosine on ppi and on single evoked potentials excluded a difference in the potency of adenosine at excitatory and inhibitory terminals as an explanation for this activity. The results suggest that adenosine may diminish bicuculline-resistant paired-pulse inhibition by enhancing a simultaneous facilitatory component of the neuronal responses.

Adenosine↗
PubMed1991

Effects of adrenal steroids and their reduced metabolites on hippocampal long-term potentiation.

We studied the effects of steroid hormones on the hippocampal long-term potentiation (LTP), a putative mechanism of neuronal plasticity and memory storage in the CNS. In vivo experiments were performed in rats under chloral hydrate anesthesia (0.4 mg/kg i.p.). All animals were adrenalectomized 48 h before recording. LTP was induced after priming tetanic stimulation at the perforant pathway (PP) and single pulse field potentials were obtained from the dentate gyrus (DG). The excitatory post-synaptic potential (EPSP) slope and population spike (PS) amplitude were analyzed before and after the i.v. injection of the steroids and after the induction of LTP, and followed up to 1 h. Results obtained with the hormones were compared with matched control animals injected with vehicle alone, Nutralipid 10%. Previous results from our laboratory showed that deoxycorticosterone (DOC) decreased the magnitude of the EPSP at all times after priming stimulation and the PS decreased during the first 30 min of the LTP. Corticosterone decreased the EPSP in the first 15 min and the PS during the first 30 min after priming stimuli. In these experiments the mineralocorticoids aldosterone and 18-OH-DOC elicited a decrease of the EPSP at all times post-train; and no significant difference against vehicle was observed in the PS. Post-injection values were not changed except for 18-OH-DOC at a dose of 1 mg, where a decrease of both the EPSP (P less than 0.01) and the PS (P less than 0.02) was observed against vehicle. ATH-progesterone at 0.1 mg/rat also decreased the EPSP values significantly after priming stimulation and no significant changes against vehicle were observed in the PS. These results show that adrenal steroids can modulate hippocampal LTP, that they can act at different neuronal loci and with different time courses in the development of the phenomena.

Adrenal Glands↗
PubMed1999

Cellular mechanisms underlying spontaneous interictal spikes in an acute model of focal cortical epileptogenesis.

The cellular mechanisms involved in the generation of spontaneous epileptiform potentials were investigated in the pirifom cortex of the in vitro isolated guinea-pig brain. A single, unilateral injection of bicuculline (150-200 nmol) in the anterior piriform cortex induced locally spontaneous interictal spikes that recurred with a period of 8.81+/-4.47 s and propagated caudally to the ipsi- and contralateral hemispheres. Simultaneous extra- and intracellular recordings from layer II and III principal cells showed that the spontaneous interictal spike correlates to a burst of action potentials followed by a large afterdepolarization. Intracellular application of the sodium conductance blocker, QX-314 (80 mM), abolished bursting activity and unmasked a high-threshold slow spike enhanced by the calcium chelator EGTA (50 mM). The slow spike was abolished by membrane hyperpolarization and by local perfusion with 2 mM cadmium. The depolarizing potential that followed the primary burst was reduced by arterial perfusion with the N-methyl-D-aspartate receptor antagonist, DL-2-amino-5-phosphonopentanoic acid (100-200 microM). The non-N-methyl-D-aspartate glutamate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (20 microM), completely and reversibly blocked the spontaneous spikes. The interictal spikes were terminated by a large afterpotential blocked either by intracellular QX-314 (80 mM) or by extracellular application of phaclofen and 2-hydroxysaclofen (10 and 4 mM, respectively). The present study demonstrates that, in an acute model of epileptogenesis, spontaneous interictal spikes are fostered by a primary burst of fast action potentials that ride on a regenerative high-threshold, possibly calcium-mediated spike, which activates a recurrent, glutamate-mediated potential responsible for the entrainment of adjacent and remote cortical regions. The bursting activity is controlled by a GABA(B) receptor-mediated inhibitory synaptic potential.

2-Amino-5-phosphonovalerate↗
PubMed1982

Anoxia increases potassium conductance in hippocampal nerve cells.

The effect of anoxia on nerve cell function was studied by intra- and extracellular microelectrode recordings from the CA1 and CA3 region in guinea pig hippocampal slices. Hyperpolarization and concomitant reduction of the nerve cell input resistance was observed early during anoxia. During this period the spontaneous activity first disappeared, then the evoked activity gradually disappeared. The hyperpolarization was followed by depolarization and an absence of a measurable input resistance. All the induced changes were reversed when the slice was reoxygenated. Reversal of the electro-chemical gradient for Cl- across the nerve cell membrane did not affect the course of events during anoxia. Aminopyridines blocked the anoxic hyperpolarization and attenuated the decrease of membrane resistance, but had no effect on the later depolarization. Blockers of synaptic transmission. Mn++, Mg++ and of Na+-channels (TTX) were without effect on the nerve cell changes during anoxia. It is suggested that the reduction of nerve cell excitability in anoxia is primarily due to increased K+-conductance. Thus, the nerve cells are hyperpolarized and the input resistance reduced, causing higher threshold and reduction of synaptic potentials. The mechanism of the K+-conductance activation is unknown at present.

Animals↗
PubMed1982

The action of serotonin on excitatory nerve terminals in lobster nerve-muscle preparations.

1. The action of serotonin on excitatory transmission in the opener muscle of the dactyl of the lobster walking leg was examined by intracellular recording techniques. 2. Serotonin, at concentrations as low as 5 x 10(-9) M, caused a sustained increase in the size of the excitatory junctional (synaptic) potential (e.j.p.). When serotonin was washed out of the bath the e.j.p. declined in two steps (T 1/2 approximately equal to 1-2 min; T 1/2 approximately equal to 30 min) to the control size. The increased e.j.p. size was predominantly due to a serotonin-induced increase in the release of quanta of excitatory transmitter with nerve stimulation. 3. The increase in transmitter release did not require nerve stimulation or the presence of Na+ or Ca2+ ions in the bathing medium during the period of serotonin treatment. 4. Three types of experiments suggested that a part of the action of serotonin on excitatory nerve terminals might involve a long-term metabolic change within terminals, possibly involving the buffering or storage of Ca2+ ions. First, serotonin increased the frequency of spontaneous release of transmitter in both normal saline (26 mM-Ca2+) and saline with very low levels of Ca2+ (less than 10(-8) M). Secondly, serotonin greatly potentiated increases in miniature excitatory junctional potential frequency induced by the loading of the nerve terminal with Na+ either by veratridine or by inhibition of the Na+ pump or by the addition of the Na-ionophore monensin in low-Ca2+ salines. Thirdly, in some experiments, serotonin treatment produced a partial restoration of the nerve-evoked release of transmitter in the low-Ca2+ medium (less than 10(-8) M).

Animals↗
PubMed1993

Early anoxia-induced vesicular glutamate release results from mobilization of calcium from intracellular stores.

1. The cause of the increased frequency of glutamatergic miniature excitatory postsynaptic currents (mEPSCs) resulting from anoxia was investigated in CA1 neurons of the in vitro rat hippocampal slice. These neurons were examined by whole-cell patch-clamp recording, and hypoxia was induced by switching the perfusion of the slice from oxygenated artificial cerebral spinal fluid (ACSF) to ACSF saturated with 95% N2-5% O2. Except where noted, experiments were carried out in ACSF containing 1 microM tetrodotoxin (TTX). 2. Although anoxia resulted in a significant increase in the frequency of mEPSCs, the amplitude, rise time, and half-decay time of the mEPSCs were unchanged. This increase in frequency indicates that there is a change in presynaptic neurotransmitter release mechanisms, probably an increase in calcium concentration, soon after the onset of anoxia. The unchanged kinetics and amplitude of the mEPSCs indicate that anoxic-induced synaptic changes are not a result of changes in the postsynaptic glutamate receptor. 3. When hippocampal slices were exposed to anoxic conditions in ACSF with calcium excluded, an increase in mEPSC frequency equal to that in normal ACSF was observed. When 0.2 mM of CdCl2 was added to the zero-calcium ACSF, anoxia still resulted in increases in mEPSC frequency equal to those of normal ACSF. It is therefore concluded that the anoxia-induced increase in mEPSC frequency does not result from an increase in a transmembrane calcium influx. The zero-calcium plus 0.2 mM CdCl2 ACSF solution completely abolished orthodromically elicited synaptic potential (in the absence of TTX), indicating that calcium currents that mediate normal orthodromic transmitter release were completely abolished in the latter experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Input patterns and pathways from the six semicircular canals to motoneurons of neck muscles. I. The multifidus muscle group.

1. The pattern of connections between the six semicircular canals and neck motoneurons of the multifidus muscle group was investigated by recording intracellular potentials from motoneurons in the upper cervical cord of anesthetized cats. 2. Synaptic potentials were recorded in motoneurons of the rectus capitis posterior (RCP) muscle at C1, the obliquus capitis inferior (OCI) muscle at C1 and C2, and the cervical multifidus muscle (Multi) at C4 in response to electrical stimulation of individual ampullary nerves of the six semicircular canals. Excitatory or inhibitory postsynaptic potentials (EPSPs or IPSPs, respectively) were evoked by separate stimulation of individual ampullary nerves in all of the neck motoneurons. Virtually all of the neck motoneurons received convergent inputs from the six ampullary nerves. 3. Motoneurons that supplied a single muscle had a homogeneous pattern of input from the six semicircular canals. There were two patterns of input from the six semicircular canals to motoneurons of the multifidus muscle group. RCP and Multi motoneurons were excited by stimulation of the bilateral anterior canal nerves (ACNs) and the contralateral lateral canal nerve (LCN) and inhibited by stimulation of the bilateral posterior canal nerves (PCNs) and the ipsilateral LCN. This input pattern is similar to that previously observed in other dorsal extensor muscles, whereas the other input pattern observed in OCI motoneurons is entirely new. OCI motoneurons at C1 and C2 were excited by stimulation of the ipsilateral ACN, PCN, and the contralateral LCN and inhibited by stimulation of the contralateral ACN, PCN, and the ipsilateral LCN. 4. Most postsynaptic potentials (PSPs) were disynaptic, but there were trisynaptic inhibitory connections between the contralateral ACN and PCN and OCI motoneurons, and between the contralateral PCN and RCP motoneurons. 5. The pathways for mediating these inputs from different semicircular canals to neck motoneurons were determined by making lesions in the lower medulla. Transection of the ipsilateral medial longitudinal fascicle (MLF) abolished the following potentials: all disynaptic PSPs in RCP motoneurons except the disynaptic EPSPs from the ipsilateral ACN, and in OCI motoneurons, disynaptic PSPs from the bilateral LCNs, and disynaptic IPSPs from the contralateral PCN. Complete bilateral section of the MLF did not affect the disynaptic EPSPs from the ipsilateral ACN in RCP motoneurons, the disynaptic EPSPs from the ipsilateral ACN and PCN in OCI motoneurons, nor the trisynaptic IPSPs from the contralateral ACN and PCN in COI motoneurons and from the contralateral PCN in RCP motoneurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1979

Spinal evoked potential (SEP) obtained by stimulation on the median nerve--experimental and clinical studies.

The present study was done experimentally and clinically to measure the segmental spinal evoked potential (SEP) of the cervical cord, stimulated on the median nerve, to try to determine the location and severity of cord lesion in patients with cervical spondylotic myelopathy. SEP in control subjects consisted of two waves. The primary reactive wave (R wave) consists of both the nerve root potential and the funiculus posterior potential. The secondary reactive wave (N wave) consists of the post-synaptic potential in the spinal cord. With regard to cervical spondylotic myelopathy, in the early stages the N-wave weakens or disappears at the level of lesion, then, as damage progresses, the R-wave also weakens or disappears.

Adult↗