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At least 469 records · Page 26Linked to original sources
PubMed1988

Proctolin potentiates synaptic transmission in the central nervous system of an insect.

1. Bursts of spike activity in the ventral nerve cord of the cockroach were elicited by mechanically stimulating the cercal organs. 2. In the presence of micromolar proctolin, the peak frequency and the duration of a burst were slowly but significantly increased. 3. In contrast, carbachol produced an immediate enhancement of spontaneous activity, but a potentiation of bursts was not seen. 4. It is proposed that proctolin functions as a neuromodulator in the terminal abdominal ganglion of the cockroach.

Animals↗
PubMed1990

Stable depression of potentiated synaptic responses in the hippocampus with 1-5 Hz stimulation.

Adult rats with two chronic stimulating electrodes in the Schaffer collateral/commissural system of the hippocampus and one recording electrode in the stratum radiatum (apical dendrites) of field CA1 were administered high-frequency stimulation (10 brief bursts at theta frequency) to produce long-term potentiation (LTP). 'Low frequency' stimulation (100 pulses at 1 Hz alone or followed by 250 pulses at 5 Hz) delivered 5-15 min later had no effect on LTP in 18% of the rats, caused a transient reversal in 18% of the group, but produced an apparent reversal of LTP for the remainder of a 1 h test session in 64% of the animals. LTP did not recover in animals tested 24 h later, at which point a second episode of high-frequency stimulation but without subsequent low-frequency stimulation was administered. This produced an LTP effect that persisted for a 1 h test session in 94% of the cases and that was still present in 86% of the animals tested 24 h later. Low-frequency stimulation applied prior to induction of LTP had no lasting effects on evoked responses not did it affect responses to a control stimulating electrode in those cases in which it reversed LTP. Possible implications of these results for hypotheses concerning the substrates of LTP and mechanisms of forgetting are discussed.

Action Potentials↗
PubMed1986

Antagonism of lateral olfactory tract synaptic potentials in rat prepyriform cortex slices.

Dose-response data were collected for the inhibition of the monosynaptic excitatory input onto prepyriform neurons from fibers of the rat lateral olfactory tract, using the potent antagonists of excitatory transmission, L(+)-2-amino-4-phosphonobutyrate (L(+)-AP4), kynurenate, N-(p-chlorobenzoyl)piperazine-2,3-dicarboxylate, and N-(p-bromobenzoyl)piperazine-2,3-dicarboxylate. Kynurenate and the piperazine derivatives blocked up to 80% of the synaptic response at doses of 1000 microM, with single-affinity dose-response curves. L(+)-AP4 blocked only 50% of the synaptic response at a dose of 1000 microM, with a multicomponent dose-response curve.

Aminobutyrates↗
PubMed1995

Differential sensitivity of NMDA receptor-mediated synaptic potentials to ethanol in immature versus mature hippocampus.

Pharmacologically isolated, NMDA receptor-mediated population EPSPs (pEPSPs) were evoked from area CA1 of hippocampal slices using electrical stimulation of the Schaffer collateral/commissural fiber pathway. Slices were prepared from rats aged 20-25 or 80-100 days. The inhibitory effects of a range of ethanol concentrations were assessed. While ethanol antagonized NMDA-mediated pEPSPs in slices from both age groups, it was significantly more potent against pEPSPs from immature versus mature hippocampi. In slices from mature animals, significant and consistent reduction of pEPSPs was observed only with the highest ethanol concentration (100 mM), whereas 10, 30, or 100 mM significantly reduced the amplitude of pEPSPs in slices from immature animals. These results indicate that NMDA-mediated synaptic activity in the hippocampus is more sensitive to the effects of ethanol in immature versus mature animals.

Age Factors↗
PubMed1997

Dopaminergic modulation of spinal neurons and synaptic potentials in the lamprey spinal cord.

It has been shown previously that dopamine-immunoreactive cells and processes are present in the lamprey spinal cord and that dopamine modulates the cycle period of fictive swimming. The present study was undertaken to further characterize the effects of dopamine on the cellular properties of lamprey spinal neurons and on inhibitory and excitatory postsynaptic potentials to determine how dopaminergic modulation may affect the central pattern generator for locomotion. Dopamine reduced the late afterhyperpolarization (late AHP) following the action potential of motoneurons, and in three types of sensory neurons: dorsal cells, edge cells, and giant interneurons. The late AHP was not reduced in lateral interneurons or CC interneurons, both of which are part of the central motor pattern generating neural network. The reduction of the late AHP in motoneurons, edge cells, and giant interneurons resulted in an increase in firing frequency in response to depolarizing current injection. In the six cell classes examined, no changes were observed in the resting membrane potential, input resistance, rheobase, spike amplitude, or spike duration after application of dopamine. The durations of action potentials broadened by application of tetraethylammonium in motoneurons and of calcium action potentials in dorsal cells and giant interneurons were decreased after bath application of 10 microM dopamine. The durations of tetrodotoxin-resistant, N-methyl-D-aspartate-induced membrane potential oscillations in lamprey spinal motoneurons were increased after bath application of 1-100 microM dopamine, due perhaps to reduced calcium entry and thus reduced Ca(2+)-dependent K+ current responsible for the repolarization of the membrane potential during each oscillation. Polysynaptic inhibitory postsynaptic potentials (IPSPs) elicited in lamprey spinal motoneurons by stimulation of the contralateral half of the spinal cord were reduced by bath application of 10 microM dopamine. Polysynaptic excitatory postsynaptic potentials were not reduced by dopamine. Monosynaptic IPSPs in motoneurons elicited by stimulation of single contralateral inhibitory CC interneurons and single ipsilateral axons were reduced by bath application of dopamine (10 microM). Monosynaptic IPSPs in CC interneurons elicited by stimulation of ipsilateral lateral interneurons, however, showed no change after application of dopamine. The lack of dopaminergic effect on the late AHP of the locomotor network neurons, lateral interneurons and CC interneurons, and the selective reduction of IPSPs from CC interneurons suggest that synaptic modulation may play an important role in dopaminergic modulation of cycle period during fictive swimming in the lamprey.

Animals↗
PubMed1985

Evidence that receptors mediating central synaptic potentials extend beyond the postsynaptic density.

Physiological recordings and computer simulations of unitary inhibitory postsynaptic potentials in the Mauthner cell of the goldfish central nervous system have been used to estimate the expected size of the postsynaptic receptor matrix at individual junctions. Simultaneous pre- and postsynaptic recordings were used to determine the kinetic parameters of the quantal responses under normal conditions and in the presence of strychnine, a competitive antagonist of glycine, which is the putative transmitter at these synapses. Calculations indicate that if the postsynaptic density, which has a radius of 0.1 micron, were to accommodate the population of channels estimated to be opened during a quantal response, the glycine binding site density in that region would be unrealistically high. Computer simulation of the quantal responses included transmitter diffusion, transmitter-receptor interactions, and channel activation under conditions including both normal and lowered binding site densities, the latter corresponding to the experimental data obtained with strychnine. The data indicate that the synaptic receptors involved in generating unitary responses are widely distributed to include regions located outside the junctional area, which directly faces the presynaptic release sites. We further suggest that the receptor matrix is surrounded by a restricted diffusional space; this geometrical organization may underlie the finding that response rise times are relatively independent of receptor binding site densities.

Action Potentials↗
PubMed1990

Synaptic potentials mediated by excitatory amino acid receptors in the nucleus accumbens of the rat, in vitro.

Focal stimulation of the dorsal regions of the nucleus accumbens of the rat, in vitro, evoked field potentials consisting of two negative waves. The first wave probably reflected electrical activation of the presynaptic fibres. This wave was resistant to excitatory amino acid antagonists and sulpiride. The second negative wave arose from a slower positive going component. These probably evince a population spike and field EPSP, respectively. Intracellular studies also indicated the occurrence of EPSP's and action potentials. The presumed field EPSP and population spike were reduced by kynurenic acid (IC50 approximately 300 microM) but not by AP5 nor sulpiride. When the Mg2+ was removed, the field EPSP was prolonged in a manner fully reversible by the addition of 30 microM D(-)AP5. These results indicate that focal stimulation within the nucleus accumbens may activate excitatory amino acid-ergic fibres that make synaptic contact with an indigenous population of neurones. The postsynaptic receptors were probably of a non-NMDA subtype. However NMDA receptor-mediated responses were evident upon removal of the Mg2+, suggesting that these receptors could also contribute to neuronal excitation under the appropriate physiological conditions.

2-Amino-5-phosphonovalerate↗
PubMed1971

The time course of minimal excitory post-synaptic potentials evoked in spinal motoneurones by group Ia afferent fibres.

1. Group Ia EPSPs were recorded from lumbosacral motoneurones in anaesthetized cats after almost complete section of the relevant dorsal roots. The EPSPs were usually of small amplitude (median value of 230 muV) and an averaging device was used to improve the definition of their time course.2. From a total of over 500 averaged EPSPs a smaller number (342) were subjected to analysis. The other EPSPs were rejected either because they showed signs of multiple origin in the rising phase of their time course (see Methods) or because the resting membrane potential of the cell was less than 50 mV. All the selected EPSPs had their rise time (from the 10 to the 90% level) and half-width measured, and a semilogarithmic plot of their decay time course was made.3. 252 of the EPSPs showed an exponential decline in their later time course and the slope of this line was used to give an estimate of the membrane time constant. The range of the time constant for different motoneurones was 2.3-12.9 msec, with a mean value of 5.8 msec.4. In ten cells an EPSP was recorded which was judged to be generated exclusively by synaptic knobs located on the soma. On this assumption measurements of the normalized rise time, half-width and break point time were used to estimate alpha, rho(infinity) and L by the method suggested in Jack & Redman (1971b). The estimated value of alpha ranged from 18 to 65. A positive correlation was found between alpha and tau(m), indicating that for these EPSPs the duration of current injection was independent of the membrane time constant. The peak time of the wave form of current injection was between 0.1 and 0.25 msec. The estimates of rho(infinity) were not thought to be very accurate. A lower limit of 4 was assumed and the highest measured value was 12, but in three cells the time course of the EPSP could not be fitted even with a very high value of rho(infinity). Some possible explanations for this discrepancy are mentioned in the Discussion. The electrotonic length of the dendrites (L) was usually greater than 1.0 lambda and ranged between 0.75 and 1.5 lambda. Evidence for an open-circuit termination of the dendrites was found in some cells.5. The normalized values of the rise time and half-width were used to make an electrotonic distance allocation to the 246 EPSPs which were judged to be non-somatic. The method of allocation was not precise because individual values of rho(infinity) and L were not available for these motoneurones. Instead, a maximum possible range was assumed: for rho(infinity), 4-25; for L, 0.75-1.5. The range of alpha was also assumed, from 12 to 100. With these values the motoneurone model (Jack & Redman, 1971b) was used to set limits within which the normalized rise time and half-width of all EPSPs, generated by current at a single point, should lie. Twenty of the 246 EPSPs lay outside these boundary lines and hence they did not receive a distance allocation. The remaining 226 were assigned values between 0.2 and 1.6 lambda (in 0.2 lambda steps); the majority of the allocations (183) were to the proximal electrotonic part of the dendrites (0.2, 0.4 or 0.6 lambda). The relationship of these distance allocations to the histological results of Conradi (1969) is discussed.6. It is concluded that there is no good evidence against the view that the main time course of minimal Ia EPSPs can be explained by their generation by a brief pulse of synaptic current and subsequent passive spread.

Animals↗
PubMed1994

Involvement of AMPA receptors in trigeminal post-synaptic potentials recorded in rat abducens motoneurons in vivo.

The pharmacology of trigeminal excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of the vibrissal pad was investigated in vivo in rat abducens motoneurons using intracellular recordings combined with microionophoretic applications of excitatory amino acid agonists [alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), NMDA, kainate] and a selective non-NMDA receptor antagonist (GYKI-52466). Intravenous applications of GYKI-52466 were also performed during synaptic and amino acid excitations. GYKI-52466, applied intravenously or microionophoretically, reversibly antagonized AMPA-induced depolarizations and trigeminal EPSPs in rat abducens motoneurons without affecting NMDA and kainate responses. The inhibition of AMPA-induced depolarizations was similar following i.v. and ionophoretic applications of GYKI-52466. Intravenous applications of GYKI-52466 (0.3-4 mg/kg) reversibly and dose-dependently reduced trigeminal EPSPs, which could be totally suppressed at the highest doses of GYKI-52466 (2-4 mg/kg). The antagonist effect, which developed very quickly, could last several minutes and recovered gradually. The effect of GYKI-52466 on the EPSPs and AMPA responses were compared in the same motoneurons. The partial inhibition of trigeminal EPSPs during microionophoretic applications of GYKI-52466 was probably due to the distribution of the synapses in the dendritic arborization of abducens motoneurons. Our results show that AMPA receptors are involved in the generation of trigeminal EPSPs in rat abducens motoneurons in vivo.

Abducens Nerve↗
PubMed1995

Activation of Metabotropic Glutamate Receptors in Conjunction with Postsynaptic Depolarization Triggers a Long-Term Depression of the N-Methyl-D-Aspartate Receptor-Mediated Synaptic Potential in the Rat Hippocampus.

The mechanism responsible for long-term depression (LTD) of pharmacologically isolated N-methyl-D-aspartate (NMDA) receptor-mediated excitatory postsynaptic potential (EPSP(NMDA)) was studied. Intracellular recordings were made from CA1 cells of rat hippocampal slices in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (10 &mgr;M) and picrotoxin (50 &mgr;M), which block non-NMDA and GABA(A) receptors, respectively. Intracellular injections of depolarizing pulses (500 ms, 0.3-0.7 nA) at 1 Hz for 5 min in the absence of synaptic stimulation caused a persistent increase in the amplitude of EPSP(NMDA). However, coupling postsynaptic depolarization with synaptic activity induced LTD. The EPSP(NMDA) LTD could be blocked by L-2-amino-3-phosphonopropionic acid (50 &mgr;M) or (RS)-alpha-methyl-4-carboxyphenylglycine (200 &mgr;M), specific antagonists for metabotropic glutamate receptors (mGluR). Furthermore, application of trans-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD, 50 &mgr;M), a specific mGluR agonist, in conjunction with postsynaptic depolarizing elicited LTD. In contrast, the mGluR agonists quisqualate or t-ACPD when given alone produced a sustained enhancement of EPSP(NMDA). Finally, coupled depolarization did not evoke LTD in slices pretreated with the protein kinase C (PKC) inhibitor calphostin c (60 nM). The present results demonstrate that activation of mGluR is necessary for the induction of LTD of EPSP(NMDA) and suggest that NMDA receptors are subject to bidirectional regulation by mGluR. Furthermore, the induction of LTD is likely to involve the stimulation of PKC. Copyright 1995 S. Karger AG, Basel

Journal Article↗
PubMed2005

Muscarinic acetylcholine receptor activation enhances hippocampal neuron excitability and potentiates synaptically evoked Ca(2+) signals via phosphatidylinositol 4,5-bisphosphate depletion.

Using single cell Ca(2+) imaging and whole cell current clamp recordings, this study aimed to identify the signal transduction mechanisms involved in mACh receptor-mediated, enhanced synaptic signaling in primary cultures of hippocampal neurons. Activation of M(1) mACh receptors produced a 2.48 +/- 0.26-fold enhancement of Ca(2+) transients arising from spontaneous synaptic activity in hippocampal neurons. Combined imaging of spontaneous Ca(2+) signals with inositol 1,4,5-trisphosphate (IP(3)) production in single neurons demonstrated that the methacholine (MCh)-mediated enhancement required activated G(q/11)alpha subunits and phospholipase C activity but did not require measurable increases in IP(3). Electrophysiological studies demonstrated that MCh treatment depolarized neurons from -64 +/- 3 to -45 +/- 3 mV and increased action potential generation. Depletion of plasma membrane phosphatidylinositol 4,5-bisphosphate (PIP(2)) enhanced neuronal excitability and prolonged the action of MCh. These studies suggest that, in addition to producing the second messengers IP(3) and diacylglycerol, mACh receptor activation may directly utilize PIP(2) hydrolysis to regulate neuronal excitability.

Animals↗
PubMed2001

Cholinergic synaptic potentials in the supragranular layers of auditory cortex.

Receptive-field plasticity within the auditory neocortex is associated with learning, memory, and acetylcholine (ACh). However, the interplay of elements involved in changing receptive-fields remains unclear. Herein, we describe a depolarizing and a hyperpolarizing potential elicited by repetitive stimulation (20-100 Hz, 0.5-2 sec) and dependent on ACh, which may be involved in modifying receptive-fields. These potentials were recorded, using whole cell techniques, in layer II/III pyramidal cells in the rat auditory cortex in vitro. Stimulation at low stimulus intensities can give rise to a hyperpolarizing response and stimulation at higher stimulus intensities can elicit a depolarizing response. The depolarizing response had a reversal potential of -35 mV, and was reduced by the combination of AMPA/kainate and NMDA glutamate receptor antagonists (AMPA/kainate: CNQX, DNQX, and GYKI 52466; NMDA: APV, MK-801) and by the muscarinic ACh receptor antagonist atropine. The hyperpolarizing response had a reversal potential of -73 mV and could be reduced by atropine, GABA(A) receptor antagonists (bicuculline and a Cl(-) channel blocker picrotoxin), and to a small extent a GABA(B) receptor antagonist (saclofen). This suggests that the hyperpolarizing response is likely to be mediated by ACh acting on GABAergic interneurons. Extracellular recordings, also made from layer II/III of cortical slices, yielded a negative-going potential which was reduced by ionotropic glutamate receptor antagonists (same as above) and by the ACh receptor antagonists atropine and scopolamine, suggesting that this potential was the extracellular representation of the depolarizing response.

Acetylcholine↗
PubMed1993

Trichloroethanol potentiates synaptic transmission mediated by gamma-aminobutyric acidA receptors in hippocampal neurons.

We have examined the actions of trichloroethanol (TCEt), the active metabolite of the general anesthetic chloral hydrate, on responses mediated by gamma-aminobutyric acid (GABA)A receptors in response to application of exogenous GABA and activation of endogenous GABAergic transmission, by using hippocampal neurons in cell culture and in brain slices. In the presence of TCEt, Cl- current activated by exogenous GABA was both enhanced in amplitude and prolonged, leading to a net increase in total charge passing through GABAA receptor channels. Prolongation of GABA-activated current increased in magnitude in a concentration-dependent manner from 0.2 to 10 mM TCEt. Inhibitory postsynaptic currents produced at synapses between pairs of cultured GABAergic neurons or by activation of interneurons in hippocampal slices were also prolonged by TCEt, at concentrations from 0.5 to 10 mM. Application of TCEt at concentrations of 1 mM and above produced a small amplitude current which was directed outwardly at -40 mV in neurons in which methylsulfate or gluconate was the major intracellular anion and directed inwardly in neurons filled with Cl-. Our observations indicate that TCEt potentiates GABAergic transmission; presumably by potentiating the function of GABAA receptors in a manner similar to barbiturate or steroid anesthetics. This action is likely to contribute to the general anesthetic effect of TCEt which occurs after chloral hydrate administration.

Action Potentials↗
PubMed2006

Persistent enhancement of neuron-glia signaling mediated by increased extracellular K+ accompanying long-term synaptic potentiation.

Neuron-glia signaling is important for neural development and functions. This signaling may be regulated by neuronal activity and undergo modification similar to long-term potentiation (LTP) of neuronal synapses, a hallmark of neuronal plasticity. We found that tetanic stimulation of Schaffer collaterals (Sc) in the hippocampus that induced LTP in neurons also resulted in LTP-like persistent elevation of Sc-evoked slow depolarization in perisynaptic astrocytes. The elevated slow depolarization in astrocytes was abolished by NMDA receptor antagonist and K(+) channel inhibitors, but not by Ca(2+) chelator BAPTA loaded in the recorded astrocytes, suggesting involvement of an increased extracellular K(+) accumulation accompanying LTP of neuronal synapses. The increased K(+) accumulation and astrocyte depolarization after LTP induction may reduce the efficiency of glial glutamate transporters, which may contribute to the enhanced synaptic efficacy. The neuronal activity-induced persistent enhancement of neuron-glia signaling may thus have important physiological relevance.

2-Amino-5-phosphonovalerate↗