Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Excitatory Postsynaptic Potentials”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed2006

Multiple mechanisms underlying the neuroprotective effects of antiepileptic drugs against in vitro ischemia.

BACKGROUND AND PURPOSE: The possible neuroprotective effects of classic and new antiepileptic drugs on the electrophysiological changes induced by in vitro ischemia on striatal neurons were investigated. In particular, the aim of the study was to correlate the putative neuroprotective effects with the action of these drugs on fast sodium (Na+) and high-voltage-activated (HVA) calcium (Ca2+) currents. METHODS: Extracellular field potentials were recorded from rat corticostriatal brain-slice preparations. In vitro ischemia was delivered by switching to an artificial cerebrospinal fluid solution in which glucose and oxygen were omitted. Na+ and HVA Ca2+ currents were analyzed by whole-cell patch-clamp recordings from acutely isolated rat striatal neurons. Excitatory postsynaptic potential was measured following synaptic stimulation in corticostriatal slices by sharp intracellular microelectrodes. RESULTS: Neuroprotection against in vitro ischemia was observed in slices treated with carbamazepine (CBZ), valproic acid (VPA), and topiramate (TPM), whereas it was not achieved by using levetiracetam (LEV). Fast Na+ conductances were inhibited by CBZ and TPM, whereas VPA and LEV showed no effect. HVA Ca2+ conductances were reduced by CBZ, TPM, and LEV. VPA had no effect on this current. All antiepileptic drugs induced a small reduction of excitatory postsynaptic potential amplitude at concentrations higher than 100 microm without changes of paired-pulse facilitation. CONCLUSIONS: The concomitant inhibition of fast Na+ and HVA Ca2+ conductances is critically important for the neuroprotection, whereas the presynaptic inhibition on glutamate transmission does not seem to play a major role.

Animals↗
PubMed1992

Excitatory synaptic transmission mediated by NMDA and non-NMDA receptors in the superficial/middle layers of the epileptogenic human neocortex maintained in vitro.

Conventional intracellular recordings were made from regular-spiking cells located in layers II-IV to examine the involvement of excitatory amino acid receptors in synaptic transmission in epileptogenic human neocortical slices maintained in vitro. Extracellular stimuli that were below the threshold for generating action potentials evoked an excitatory postsynaptic potential (EPSP) with short latency to onset (0.8-4 ms). When suprathreshold stimuli were delivered, 95% of the neurons fired a single action potential. In 5% of the population, however, an all-or-none bursting discharge was observed. The EPSP and the bursting discharge were tested with the N-methyl-D-aspartate (NMDA) antagonist 3-((+/-)-2-carboxypiperazin-4-yl)propyl-1-phosphonate (CPP, 5 microM) or the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 4 microM). In the presence of CNQX the peak amplitude of the EPSP was reduced by 85% and the bursting discharge was abolished completely. By contrast, CPP reduced the peak amplitude of the EPSP by 52%, attenuated the late phase of the bursting discharge and increased its threshold. These results indicate that excitatory amino acids function as excitatory transmitters in the human brain. While the involvement of non-NMDA receptors in the EPSP is in line with data from normal neocortical slices of other mammals, the participation of NMDA-mediated conductances to the EPSP appears peculiar to the epileptogenic human neocortex. This evidence, together with the contribution of NMDA and non-NMDA receptors to the all-or-none bursting discharge suggests that excitatory amino acid-mediated transmission might be modified in the epileptogenic human neocortex.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1993

Hippocampal pyramidal cells excite inhibitory neurons through a single release site.

Morphologically a synapse consists of a presynaptic release site containing vesicles, a postsynaptic element with membrane specialization, and a synaptic cleft between them. The number of release sites shapes the properties of synaptic transmission between neurons. Although excitatory interactions between cortical neurons have been examined, the number of release sites remains unknown. We have now recorded excitatory postsynaptic potentials evoked by single pyramidal cells in hippocampal interneurons and visualized both cells using biocytin injections. Light and electron microscopy showed that excitatory postsynaptic potentials were mediated by a single synapse. We also reconstructed the entire axon arborization of single pyramidal cells, filled in vivo, in sections counterstained for parvalbumin, which selectively marks basket and axo-axonic cells. Single synaptic contacts between pyramidal cells and parvalbumin-containing neurons were dominant (> 80%), providing evidence for high convergence and divergence in hippocampal networks.

Animals↗
PubMed1966

Synaptic activity in motoneurons during natural stimulation of muscle spindles.

Synaptic activity evoked in cat motoneurons during stretch stimulation of muscle spindles in the homonymous muscle has been studied by intracellular recording. A class of miniature excitatory postsynaptic potentials evoked by such physiologic stimulation results from activity in single group la spindle afferent fibers, and the criterion for identification is a predictable pattern of rhythmic occurrence of the synaptic potentials. Statistical examination of the amplitude distributions of this class of miniature synaptic potentials suggests that some group Ia fibers liberate a relatively large number of quantal excitatory postsynaptic potential units per fiber impulse.

Animals↗
PubMed1992

A model of NMDA receptor-mediated activity in dendrites of hippocampal CA1 pyramidal neurons.

1. The role of synaptic activation of NMDA (N-methyl-D-aspartate) receptor-mediated conductances on CA1 hippocampal pyramidal cells in short-term excitability changes was studied with the use of a computational model. Model parameters were based on experimental recordings from dendrites and somata and previous hippocampal simulations. Representation of CA1 neurons included NMDA and non-NMDA excitatory dendritic synapses, dendritic and somatic inhibition, five intrinsic membrane conductances, and provision for activity-dependent intracellular and extracellular ion concentration changes. 2. The model simulated somatic and dendritic potentials recorded experimentally. The characteristic CA1 spike afterdepolarization was a consequence of the longitudinal spread of dendritic charge, reactivation of slow Ca(2+)-dependent K+ conductances, slow synaptic processes (NMDA-dependent depolarizing and gamma-aminobutyric acid-mediated hyperpolarizing currents) and was sensitive to extracellular potassium accumulation. Calcium currents were found to be less important in generating the spike afterdepolarization. 3. Repetitive activity was influenced by the cumulative activation of the NMDA-mediated synaptic conductances, the frequency-dependent depression of inhibitory synaptic responses, and a shift in the potassium reversal potential. NMDA receptor activation produced a transient potentiation of the excitatory postsynaptic potential (EPSP). The frequency dependence of EPSP potentiation was similar to the experimental data, reaching a maximal value near 10 Hz. 4. Although the present model did not have compartments for dendritic spines, Ca2+ accumulation was simulated in a restricted space near the intracellular surface of the dendritic membrane. The simulations demonstrated that the Ca2+ component of the NMDA-operated synaptic current can be a significant factor in increasing the Ca2+ concentration at submembrane regions, even in the absence of Ca2+ spikes. 5. Elevation of the extracellular K+ concentration enhanced the dendritic synaptic response during repetitive activity and led to an increase in intracellular Ca2+ levels. This increase in dendritic excitability was partly mediated by NMDA receptor-mediated conductances. 6. Blockade of Ca(2+)-sensitive K+ conductances in the dendrites increased the size of EPSPs leading to a facilitation of dendritic and somatic spike activity and increased [Ca2+]i. NMDA receptor-mediated conductances appeared as an amplifying component in this mechanism, activated by the relatively depolarized membrane potential. 7. The results suggest that dendritic NMDA receptors, by virtue of their voltage-dependency, can interact with a number of voltage-sensitive conductances to increase the dendritic excitatory response during periods of repetitive synaptic activation. These findings support experimental results that implicate NMDA receptor-mediated conductances in the short-term response plasticity of the CA1 hippocampal pyramidal neuron.

Animals↗
PubMed1967

Opposite synaptic actions mediated by different branches of an identifiable interneuron in Aplysia.

Among the identifiable cells in the abdominal ganglion of Aplysia californica are five that generate bursting rhythms endogenous to the cells. In the four bursting cells of the left upper quadrant the rhythm is modulated by a unitary inhibitory postsynaptic potential; in the bursting cell of the right lower quadrant the rhythm is modulated by a unitary excitatory postsynaptic potential. Both the excitatory and inhibitory postsynaptic potentials are mediated by separate branches of a single interneuron. The pharmacological properties of the double action interneuron as well as those of the follower cells suggest that a single transmitter (acetylcholine) is involved in both the excitatory and the in-hibitory action of the interneuron.

Acetylcholine↗
PubMed1987

A synaptically evoked late hyperpolarization in the rat dorsolateral geniculate neurons in vitro.

Intracellular potentials were recorded from presumed relay neurons in the rat dorsolateral geniculate nucleus maintained in vitro preparations. In this material, the neuronal circuit includes the excitatory optic tract which innervates monosynaptically both relay and intrinsic neurons, the latter providing a feed-forward GABAergic inhibition on the former. Electrical stimulation of the optic tract evokes in the dorsolateral geniculate neurons an early excitatory postsynaptic potential followed by an inhibitory postsynaptic potential which precedes a so far unreported long-lasting late hyperpolarization. The properties of the inhibitory postsynaptic potential are consistent with the notion that they are of disynaptic (feed-forward) origin and that they are the consequence of GABAA receptor activation. In contrast, the late hyperpolarization, which was found in almost every neuron, was enhanced by GABAA blockers, without accompanying changes in the resting membrane potential or the input resistance of the recorded cells. The late hyperpolarization had a lower threshold than the excitatory postsynaptic potential, a long latency (m = 38 +/- 4 ms, n = 10) and was of long duration (m = 308 +/- 57 ms, n = 10). The occurrence and threshold for producing these two potentials were uncorrelated, and paired stimulations of the optic tract showed a marked difference of their recovery time-courses. The late hyperpolarization could be elicited only by afferent stimulations; it never followed intracellularly induced depolarizations and/or anodal break calcium spikes. It was associated with a small conductance increase, sufficient, however, to inhibit high-frequency discharges induced by intracellular injection of depolarizing currents. The late hyperpolarization decreased in amplitude with membrane hyperpolarization and ultimately reversed polarity. The apparent reversal potential followed shifts in extracellular potassium concentration in an almost Nernstian relation (47 mV for a tenfold increase in [K]0). Involvement of GABAB receptors in the generation of this potential may be postulated since baclofen readily hyperpolarized the neurons and decreased their input resistance in the presence of GABAA blockers. We conclude that the late hyperpolarization is a postsynaptic potential mediated by an increased conductance to K ions. Our results further suggest that a minimal disynaptic feed-forward circuit impinging on the relay neurons of the dorsolateral geniculate nucleus is sufficient to subserve this late hyperpolarization.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2000

ATP inhibits glutamate synaptic release by acting at P2Y receptors in pyramidal neurons of hippocampal slices.

It has been proposed that extracellular ATP inhibits synaptic release of glutamate from hippocampal CA1 synapses after its catabolism to adenosine. We investigated the possibility that at least part of this effect is mediated by ATP itself acting on P2Y receptors. ATP and various analogs decreased the amplitude and duration of glutamate-mediated excitatory postsynaptic potentials in all tested neurons. This effect was reversible and concentration-dependent and had the following rank order of agonist potency: AMP = ATP = adenosine-5'-O-(3-thio)triphosphate > adenosine = ADP. alpha,beta-Methylene ATP, beta,gamma-methylene ATP, 2-methylthioadenosine 5'-triphosphate, GTP, and UTP induced only a partial response. The depolarization induced by exogenous glutamate was not affected by ATP, indicating that this nucleotide acts presynaptically to inhibit glutamate-mediated excitatory postsynaptic potentials. Neither inhibition of ectonucleotidase activity with alpha,beta-methylene ADP, suramin, or pyridaxalphosphate-6-azophenyl-2',4'-disulfonic acid 4-sodium nor removal of extracellular adenosine (with adenosine deaminase) altered ATP effects. 8-Cyclopentyltheophylline competitively inhibited ATP effects, whereas P2 receptor antagonists (pyridaxalphosphate-6-azophenyl-2',4'-disulfonic acid 4-sodium, suramin, and reactive blue 2) were ineffective. ATP effects were by far more sensitive to pertussis toxin (PTX) than those of adenosine. After PTX, adenosine-5'-O-(3-thio)triphosphate induced only a partial response, and ATP concentration-response curve was biphasic. The second phase of this curve was blocked by adenosine deaminase, implying that it is mediated by adenosine as a result of ATP catabolism. Under control conditions, however, catabolism of ATP is not required to explain its actions. In conclusion, ATP inhibits synaptic release of glutamate by direct activation of P2Y receptors that are PTX- and 8-cyclopentyltheophylline-sensitive.

Adenosine Triphosphate↗
PubMed2003

Long-term potentiation of nicotinic synaptic transmission in rat superior cervical ganglia produced by phorbol ester and tetanic stimulation.

The long-term potentiation of nicotinic synaptic transmission induced by both active phorbol ester (4beta-phorbol-12,13-dibutyrate, PdBu) and tetanic trains of preganglionic stimulation was studied in single neurons of the superior cervical ganglion (SCG) of the rat using intracellular recording techniques. PdBu significantly increased the mean amplitude of both the unitary evoked fast excitatory postsynaptic potentials (EPSPs) and the fast excitatory postsynaptic currents (EPSCs) to 17.0+/-3.3 mV (control 8.4+/-1.9 mV, n=5) and 2.8+/-0.4 nA (control 0.8+/-0.1 nA, n=10), respectively. There was no significant change in either the resting membrane potential, input resistance, or the threshold for the initiation of an action potential. The response to exogenously applied acetylcholine (ACh) was also not changed following exposure to PdBu. In low-calcium, high-magnesium solutions, PdBu significantly increased the quantal content of EPSPs approximately threefold from a control of 0.9+/-0.2 (n=5) to 2.6+/-0.6 (n=5). The quantal content of EPSCs was also increased to 1.3+/-0.2 (control 0.5+/-0.1, n=10). PdBu increased the frequency of miniature EPSPs (mEPSPs) to 196+/-47% (n=6) of control, while the amplitude, rise time, rate of rise, and decay of mEPSPs were not significantly changed. Tetanic stimulation significantly increased the amplitude of the unitary synaptic EPSPs and EPSCs without significantly changing the resting membrane potential, input resistance, threshold for initiation of an action potential, or the response to exogenously applied ACh. Tetanic stimulation significantly increased quantal content of EPSPs and EPSCs threefold. The results obtained with tetanically induced LTP are similar to the results obtained with phorbol ester-induced LTP in these ganglion neurons. These results suggest that both tetanically induced and phorbol ester-induced LTP, in the rat, share similar mechanisms which involve, at least in part, activation of PKC-dependent mechanisms to increase quantal release from sympathetic preganglionic axon terminals.

Animals↗
PubMed1999

Synaptic response patterns of neurons in the cortex of rat inferior colliculus.

The present study examined synaptic potentials of neurons in inferior colliculus (IC) cortex slice and the roles of GABA and glutamate receptors in generating these potentials. Multipolar (82%) and elongated (18%) cells were observed with intracellular biocytin staining. Electrical stimulation of the IC commissure (CoIC) elicited only inhibitory postsynaptic potentials (IPSPs) (10% of cells), only excitatory postsynaptic potentials (EPSPs) (51%), or both (38%). IPSPs were elicited at lower thresholds and shorter latencies than EPSPs (mean: 1.6+/-1.2 ms) and IPSPs were observed in all neurons following membrane depolarization. Short-latency EPSPs were blocked by non-NMDA receptor antagonists, and longer-latency EPSPs were blocked by NMDA antagonists. CoIC stimulation evoked short-latency IPSPs (mean: 0.55+/-0.33 ms) in 48% of neurons, and the IPSPs persisted despite glutamate receptor blockade, which implies monosynaptic inhibitory input. A GABA(A) antagonist blocked IPSPs and paired pulse inhibition of EPSPs, suggesting GABA(A) receptor mediation. A GABA(B) antagonist reduced paired pulse inhibition of IPSPs, suggesting GABA(B) receptor modulation. Thus, GABA-mediated inhibition plays a critical role in shaping synaptic responses of IC cortex neurons. Normal GABAergic function in IC has been shown to be important in acoustic coding, and reduced efficacy of GABA function in IC neurons is critical in IC pathophysiology in presbycusis, tinnitus and audiogenic seizures.

2-Amino-5-phosphonovalerate↗
PubMed1994

Characterization of a muscarinic current that regulates excitability of an identified insect motoneuron.

1. Application of the muscarinic agonist oxotremorine-M (oxo-M) to isolated abdominal ganglia of larval Manduca sexta excited an identified proleg retractor motoneuron called PPR. This excitation consisted of a persistent depolarization and an increased tendency to generate action potentials. Previous work has established that the action of oxo-M is probably mediated by muscarinic acetylcholine receptors (mAChRs) on PPR and that oxo-M mimics an afferent-induced long-lasting depolarization called the slow excitatory postsynaptic potential (sEPSP). 2. Action potentials in the ganglion could be blocked by applying tetrodotoxin (TTX) in the bath saline. Under these conditions all excitatory postsynaptic potentials in PPR were also blocked, but the depolarizing action of oxo-M was unaffected. In the absence of background activity PPR could be voltage clamped using a single-electrode switching clamp to study the currents underlying the response to oxo-M. 3. At a membrane potential of -50 mV, application of oxo-M to the ganglion in the bath saline (3-6 x 10(-7) M) or by brief (20-40 ms) pulses from a micropipette into the neuropil (1 x 10(-5) M) evoked an apparently inward current called Iox. The mean peak current change in response to pulses was -0.80 +/- 0.04 nA (n = 48 preparations). 4. The voltage dependence of Iox was determined by subtracting the current-voltage relationship for PPR in control saline from that during a response to oxo-M. Iox was maximal near the resting potential of PPR (-45 to -40 mV), decreasing slightly with hyperpolarization and strongly with depolarization. 5. Peak Iox was directly dependent on the bath Na+ concentration. Complete replacement of Na+ with N-methyl-D-glucamine in the saline blocked Iox. Changes in the bath K+ concentration (extracellular K+ concentration, [K+]o) had only a small effect on Iox. Reducing [Cl-]o from 140 to 74.5 mM had no significant effect on Iox during a 15-min exposure. Intracellular injections of Cl- from a KCl-containing electrode also had no measurable effect on Iox. 6. Changes in the bath Ca2+ concentration above or below 2 mM inhibited Iox. Furthermore, the divalent cations Ni2+, Co2+, Mg2+, and Ba2+ at millimolar concentrations and the Ca2+ channel blocking agents nifedipine and Cd2+ at micromolar concentrations inhibited Iox. 7. These results suggest that mAChRs on PPR activate an inward current that is persistent, TTX insensitive, voltage dependent and carried predominantly by Na+. However, the results cannot eliminate the possibility that changes in K+ or Cl- conductances might also be involved.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1991

Opioid-mediated facilitation of long-term potentiation at the lateral perforant path-dentate granule cell synapse.

Opioid effects on the development of long-term potentiation (LTP) were investigated at the lateral perforant path (LPP)-dentate granule cell synapse of the hippocampal slice. High frequency stimuli were delivered to the outer molecular layer of the dentate to tetanize the LPP. Significant LTP was induced in the amplitude of the orthodromic population spike and the slope of the population excitatory postsynaptic potential recorded from the granule cell layer and molecular layer. Bath application of naloxone (0.1-10 microM), an opioid antagonist, induced a dose-dependent reduction in the potentiation of both orthodromic population spike and excitatory postsynaptic potential evoked in the LPP, but not in adjacent medial perforant path. PLO17 ([N-MePhe3-D-Pro4]morphiception; 0.3 or 1 microM), a mu opioid agonist, reduced the threshold for LTP and increased the amount of LTP in the LPP. PLO17 also reduced recurrent inhibition and enhanced an N-methyl-D-aspartate (NMDA) receptor-mediated component in single pulse-evoked field potentials in the LPP. The effects of PLO17 were antagonized by 1 microM naloxone and the NMDA receptor antagonist D-2-amino-5-phosphonovaleric acid (100 microM). These findings suggest that endogenous opioids released during high frequency stimulation play an important role in the induction of LTP at the LPP synapses. A mu receptor-mediated disinhibition which increases current flow through NMDA channels may contribute to the opioid enhancement of LTP in the dentate gyrus.

2-Amino-5-phosphonovalerate↗
PubMed1998

Inhibition by [Arg8]-vasopressin of long term potentiation in guinea pig hippocampal slice.

We examined the effects of [Arg8]-vasopressin (AVP) on long term potentiation (LTP) of the field excitatory postsynaptic potentials at CA1 and CA3 synapses in adult guinea pig hippocampal slices. AVP (10 nM) depressed the magnitude of LTP without any effects on basal responses at both synaptic pathways. The depressive effect by AVP at CA1 synapses appears to be receptor-mediated since it was inhibited by an AVP V1-receptor antagonist, [Pmp1,Tyr(Me)2]-AVP. From these results, AVP may play an inhibitory role on the induction of LTP via V1 receptors in the guinea pig hippocampus.

Animals↗
PubMed1985

A morphological investigation of thalamic neurons by intracellular HRP staining in cats.

Morphological analysis of 77 neurons in the ventroanterior (VA), ventrolateral (VL), ventromedial (VM), and central lateral (CL) nuclei was performed by intracellular HRP staining in combination with electrophysiological studies. The neurons were classified into four groups according to either electrophysiological or morphological criteria, i.e., 20 relay neurons (18 thalamocortical (T-C) and two thalamocaudate (T-Cd) relay neurons), 17 projection neurons, 36 unidentified neurons, and four presumed interneurons. All 36 unidentified neurons had morphological features similar to those of relay and projection neurons. All neurons except four presumed interneurons had dendrites sparsely covered with spinelike appendages. Most of their dendrites displayed a spherically radiating branching pattern, and a few showed a tufted or linearly oriented pattern. Sizes of somata and dendritic radii were compared in entopeduncular (Ent)-responsive (n = 25) and cerebellar (CN)-responsive groups (n = 37) in VA, VL, and VM nuclei. The soma size was similar in VL (18-21 X 29-34 micron) and VM (15-19 X 29-31 micron), but in VA, CN-responsive neurons (15 X 30 micron) seemed to be smaller than Ent-responsive ones (22 X 36 micron). The largest dendritic field of neurons in each thalamic nucleus was similar in both groups. They were about 250-320 micron in radius. Diameters of axons were also compared but no statistically significant difference was detected (i.e., 1.5 +/- 0.3 (mean +/- S.D.) micron for the Ent group and 1.7 +/- 0.5 micron for the CN group). Three types of axonal trajectories were noted, i.e., neurons projecting their axons dorsolaterally, ventrolaterally, or horizontally. Fourteen neurons out of 37 relay and projection neurons gave off several fine distal axon collaterals in the thalamic reticular nucleus, and one T-Cd, three projection, and one unidentified neurons gave off proximal axon collaterals near the soma-dendritic domain in addition to those in the thalamic reticular nucleus. Four neurons classified as presumed interneurons had smaller somata (9-13 X 18-23 micron) and varicose dendrites. Three of them received Ent-induced inhibitory postsynaptic potentials (IPSPs) or CN-induced excitatory postsynaptic potentials (EPSPs). Several presumed axon terminals were found to cover the soma of an adjacent neuron, which seemed to indicate their inhibitory nature. The proximal axon collaterals in the ventral thalamic nuclei may consist of local inhibitory circuits with presumed interneurons in addition to other inhibitory circuits with thalamic reticular neurons.

Animals↗
PubMed1993

Paroxysmal long-lasting depolarizations in cultured hippocampal neurons are generated by activation of NMDA and non-NMDA receptors.

In primary cultures of hippocampal neurons from the embryonic rat, spontaneous depolarizations lasting up to 6 sec and resembling paroxysmal depolarization shifts (PDSs) appeared after 11 days in vitro. These depolarizations are presumably generated by synaptic events, because: (1) both their appearance and duration are independent of membrane potential, (2) the amplitudes of the underlying currents depend monotonically on membrane potential, and (3) they are reversed at the reversal potential of the excitatory postsynaptic potentials (EPSPs). In addition, PDSs disappeared reversibly when sodium-dependent action potentials were blocked by tetrodotoxin (10 microM) and when synaptic transmission was reduced by elevated Mg2+ (5 mM). Further, the fact that these depolarizations can appear simultaneously in two neurons in paired recordings also points to a synaptic origin. Inhibition of glutaminergic synaptic transmission by kynurenic acid (50 microM) and the NMDA-antagonist D-2-amino-5-phosphonovaleric acid (APV; 50 microM) led to a marked shortening of the depolarizations. This blocking effect of kynurenic acid and APV and comparison with the currents elicited by locally applied glutamate or NMDA provide evidence for an activation of both types of glutamate receptors to induce PDSs. The role of alteration of glutaminergic synaptic transmission in the induction and maintenance of these depolarizations is discussed in the context of results from the literature on the appearance of PDSs in cultures grown under chronic blockade of glutamate receptors.

2-Amino-5-phosphonovalerate↗
PubMed1985

Long-term potentiation and 4-aminopyridine.

Long-term potentiation (LTP) of excitatory postsynaptic potentials (epsp's) was investigated with extracellular field potential recording in hippocampal slices from rats. In the presence of 100 microM 4-aminopyridine (4-AP) the probability of eliciting LTP was unchanged or increased; the extent of potentiation was not significantly different from normal. During LTP saturation, 4-AP further enhanced the epsp. These data are inconsistent with an involvement of A-current reduction in LTP.

4-Aminopyridine↗
PubMed1985

Tongue-muscle-controlling motoneurons in the Japanese toad: topography, morphology and neuronal pathways from the 'snapping-evoking area' in the optic tectum.

As a step to clarifying the neural bases for the visually-guided prey-catching behavior in the toad, special attention was paid to the flipping movement of the tongue. Tongue-muscle-controlling motoneurons were identified antidromically, and their topographical distribution within the hypoglossal nucleus, the morphology, and the neuronal pathways from the optic tectum including the 'snapping-evoking area' (see below) to these motoneurons were investigated in paralyzed Japanese toads using intracellular recording techniques. The morphology of motoneurons innervating the tongue-protracting or retracting muscles (PMNs or RMNs respectively) was examined by means of intracellular-staining (using HRP/cobaltic lysine) and retrograde-labeling (using cobaltic lysine) methods. Both PMNs and RMNs showed an extensive spread of the branching trees of dendrites; 4 dendritic fields were distinguished: lateral/ventrolateral, dorsal/dorsolateral, medial, and in some motoneurons, contralateral dendritic fields, although there was a tendency for the dorsal/dorsolateral dendritic field to be less extensive in the PMNs than in the RMNs. The axons of both PMNs and RMNs arose from thick dendrites, ran in a ventral direction without any axon-collaterals branching off, and then entered the hypoglossal nerve. The PMNs and RMNs were distributed topographically within the hypoglossal nucleus; the RMNs were located rostrally within the nucleus, whereas the PMNs were located more caudally within it. In about 3/4 of the RMNs tested, depolarizing potentials [presumably the excitatory postsynaptic potentials (EPSPs)], on which action potentials were often superimposed, were evoked by electrical stimuli applied to the nerve branch innervating the tongue protractor. These EPSPs were temporally facilitated when the electrical stimuli were applied at short intervals (10 ms). Both PMNs and RMNs showed hyperpolarizing potentials (IPSPs) in response to single electrical stimuli of various intensities (10-200 microA) applied to the 'snapping-evoking area' (lateral/ventrolateral part of the optic tectum) on either side. These IPSPs were facilitated after repetitive electrical stimulations at short intervals (10 ms) and of weaker intensities (down to 10 microA); i.e., a temporal facilitation of the IPSPs was observed. On the other hand, large and long-lasting EPSPs which prevailed over the underlying IPSPs were evoked after repetitive electrical stimulations (a few pulses or more) at short intervals (10 ms) and of stronger intensities (generally 90 microA or more); thus, a temporal facilitation of the EPSPs was also observed.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1982

Black widow spider venom: excitatory action on hippocampal neurons.

Electrical activities of thin hippocampal sections of the guinea pig were studied in vitro during and after administration of black widow spider venom (BSV). In CA3 neurons, BSV induced spontaneous discharges which were suppressed by Co2+ or Mn2+. During BSV administration, trains of potential changes resembling excitatory postsynaptic potentials (EPSPs) were recorded intracellularly. The EPSP-like potentials were blocked by TTX. BSV seems to induce impulses in presynaptic fibers or terminals and thereby facilitates release of neurotransmitters.

Animals↗