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PubMed1991

Neuropharmacology of the muscarinic antagonist telenzepine in myenteric ganglia of the guinea-pig small intestine.

Intracellular recording methods were used to investigate the actions of the putative M1 muscarinic receptor antagonist telenzepine on the electrical and synaptic behavior of myenteric neurons. Telenzepine had no effect on resting membrane potential, input resistance, excitability and antidromic potentials in both AH/type 2 and S/type 1 neurons, when applied in concentrations of 0.1-2000 nM, although higher concentrations (10-100 microM) did have a significant non-specific effect on the postsynaptic membrane. Micromolar concentrations of telenpzepine (1-2 microM) had no effect on excitatory responses to substance P, vasoactive intestinal peptide, the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium or the nicotinic action of acetylcholine. Nicotinic fast excitatory postsynaptic potentials were also unaffected by 2 microM telenzepine. In contrast, at submicromolar concentrations (100 nM), telenzepine abolished responses to either muscarine or the muscarinic component of the acetylcholine response. The excitatory effect of muscarine at postsynaptic M1 receptors was dose dependently inhibited by telenzepine (0.1-1000 nM) at concentrations which had no effect on the electrical properties of the cells. This effect was slowly reversible, usually requiring more than 60 min for significant recovery. The threshold dose of telenzepine as an antagonist of the muscarinic depolarization in AH/type 2 neurons was in the range of 0.1-1 nM. The IC50 concentration of telenzepine needed to abolish the response was 8.5 nM. A small proportion of stimulus-evoked slow excitatory postsynaptic potentials in both AH/type 2 and S/type 1 cells were abolished by 1 microM telenzepine, while the majority of them remained unaffected, indicating that some slow excitatory postsynaptic potentials are mediated by the muscarinic action of released acetylcholine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

The effects of angiotensin IV analogs on long-term potentiation within the CA1 region of the hippocampus in vitro.

Within the brain-renin angiotensin system, it is generally assumed that angiotensin peptide fragments shorter than angiotensins II and III, including angiotensin IV (AngIV), are inactive. This belief has been challenged by the recent discovery that AngIV, and AngIV-like analogs, bind with high affinity and specificity to a putative angiotensin binding site termed AT4. In the brain these sites include the hippocampus, cerebellum, and cerebral cortex, and influence associative and spatial learning tasks. The present study investigated the effects of two AngIV analogs, Nle1-AngIV (an AT4 receptor agonist) and Nle1-Leual3-AngIV (an AT4 receptor antagonist), on long-term potentiation (LTP). Field excitatory postsynaptic potentials (fEPSPs) were recorded from the CA1 stratum radiatum following stimulation of the Schaffer collateral pathway. Activation of AT4 receptors by Nle1-AngIV enhanced synaptic transmission during low-frequency test pulses (0.1 Hz), and increased the level of tetanus-induced LTP by 63% over that measured under control conditions. Paired stimulation before and during infusion of Nle1-AngIV indicated no change in paired-pulse facilitation (PPF) as a result of AT4 receptor activation suggesting that the underlying mechanism(s) responsible for Nle1-AngIV-induced increase in synaptic transmission and LTP is likely a postsynaptic event. Further, applications of Nle1-Leual3-AngIV prior to, but not 15 or 30 min after, tetanization prevented stabilization of LTP. These results extend previous findings from behavioral data in that AT4 receptor agonists and antagonists are capable of activating, and inhibiting, learning and memory pathways in the hippocampus, and suggest that the AT4 receptor subtype is involved in synaptic plasticity.

Angiotensin II↗
PubMed1996

Felbamate decreases synaptic transmission in the CA1 region of rat hippocampal slices.

The antiepileptic drug felbamate (FBM) is known to block N-methyl-D-aspartate receptor-mediated responses and to decrease voltage-sensitive Na+ and Ca+2 channels. The present work was aimed at investigating the actions of FBM on synaptic potentials in the hippocampus, a region frequently involved in epileptic discharges. In rat hippocampal slices, application of FBM (100-1300 microM, 10 min) elicited a concentration-dependent, fully reversible decrease in amplitude of electrically evoked population spikes recorded extracellularly from the CA1 pyramidal cell layer. In intracellular recordings, FBM (50-300 microM) decreased the amplitude of excitatory postsynaptic potentials and reduced the probability of firing action potentials upon synaptic activation. Action potential frequency adaptation (accommodation), which typically limits repetitive firing in CA1 pyramidal cells, was increased. By using a paired-pulse protocol, FBM (300 microM) depressed the amplitude of paired excitatory postsynaptic potentials, without affecting the facilitation of the second response. In nominally Mg(+2)-free solution, FBM (100 microM) blocked N-methyl-D-aspartate receptor-mediated synaptic excitatory postsynaptic potentials isolated by the presence of 10 microM 6-nitro-7-sulfamoylbenzo(f)quinoxaline hydrochloride, a selective alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor antagonist, and 10 microM bicuculline or 25 microM picrotoxin. This effect was not reversed by the addition of 300 microM Gly. All these effects contribute to decrease excitatory synaptic transmission and are likely to limit neuron recruitment and propagation of epileptic discharges.

Animals↗
PubMed1997

Regulation of synaptic efficacy by coincidence of postsynaptic APs and EPSPs.

Activity-driven modifications in synaptic connections between neurons in the neocortex may occur during development and learning. In dual whole-cell voltage recordings from pyramidal neurons, the coincidence of postsynaptic action potentials (APs) and unitary excitatory postsynaptic potentials (EPSPs) was found to induce changes in EPSPs. Their average amplitudes were differentially up- or down-regulated, depending on the precise timing of postsynaptic APs relative to EPSPs. These observations suggest that APs propagating back into dendrites serve to modify single active synaptic connections, depending on the pattern of electrical activity in the pre- and postsynaptic neurons.

Action Potentials↗
PubMed1987

Presynaptic and postsynaptic effects of histamine and histamine agonists in the superior cervical ganglion of the rat.

Extracellular and intracellular recording techniques were used to study the effects of histamine and the histamine agonists [impromidine (IMP) and 2-thiazolylethylamine (2-TH)] on synaptic transmission in the superior cervical ganglion of the rat in vitro. At the concentrations employed (up to 10(-5) M) these compounds did not produce detectable effects on the electrical properties of the postsynaptic neurons. Histamine produced a dose-dependent reduction in the amplitude of the extracellularly-recorded presynaptic and postsynaptic compound action potential. The H2 receptor agonist impromidine reduced only the postganglionic compound action potential. Cimetidine, a specific H2 receptor antagonist, produced parallel shifts in the log dose-response curves for impromidine. Impromidine also reduced the average size of the evoked excitatory postsynaptic potential. The reduction of the mean amplitude of the excitatory postsynaptic potential was due to a decrease in the amount of acetylcholine (ACh) liberated by each preganglionic volley (mean quantal content, m) and a diminution in quantal size. The H1 receptor agonist, 2-TH produced a dose-dependent increase in the presynaptic and postsynaptic compound action potential and in m. The increase in m was not associated with changes in quantal size. The H1 antagonists, pyrilamine and promethazine, did not prevent facilitation of ganglionic transmission induced by 2-TH. It is concluded that histamine H1 and H2 receptors exist on preganglionic axons, or terminals in sympathetic ganglia of the rat. Activation of H1 receptors facilitates release of ACh whereas H2 receptor activation results in depressed release.

Action Potentials↗
PubMed1991

Persistent enhancement of transmitter release accompanying long-term potentiation in the guinea pig hippocampus.

In order to examine temporal changes in enhancement of transmitter release during long-term potentiation (LTP), we examined amplitude fluctuation of excitatory postsynaptic potentials (EPSPs) for longer periods than 2 h after tetanic stimulation (up to 4 h in the longest observation). The relative magnitude of excitatory postsynaptic potentiation (EPSP) fluctuation (coefficient of variation, CV) reduced throughout the observation periods in association with an increase in EPSP amplitude after tetanic stimulation. The reciprocals of squared CVs (= mean2/variance) were almost in proportion to the magnitude of LTP, and the ratio of 1/CV2 and the LTP magnitude did not change significantly for up to 4 h. These findings suggest that a prolonged enhancement of transmitter release from presynaptic terminals underlies LTP, and the relative contribution of this presynaptic enhancement does not change significantly for 2 h (maybe up to 4 h, or longer) after tetanic stimulation.

Animals↗
PubMed1993

N-methyl-D-aspartate stimulates the dephosphorylation of the microtubule-associated protein 2 and potentiates excitatory synaptic pathways in the rat hippocampus.

We have studied the effect of brief (50-150 s) applications of N-methyl-D-aspartate (10-100 microM) on the phosphorylated state of the microtubule-associated protein 2 in slices of rat hippocampus. Following a similar experimental protocol we also studied the pattern of excitatory postsynaptic potentials intracellularly recorded in CA1 pyramidal cells elicited by stimulation of the Schaffer collateral-commissural pathway. N-Methyl-D-aspartate treatment produced a marked and specific dephosphorylation of the cytoskeletal microtubule-associated protein 2, which was not due to enhanced proteolytic activity. Dephosphorylation of the microtubule-associated protein 2 affects mainly the tubulin-binding domain of the molecule and seems to be a consequence of the activation of the Ca2+/calmodulin-dependent phosphatase calcineurin, as it is partially inhibited by calmidazolium but not by okadaic acid. A few minutes after N-methyl-D-aspartate treatment we observed a 23 +/- 17% increase in the amplitude of the monosynaptic excitatory postsynaptic potential recorded in the cells and the appearance of a large polysynaptic excitatory postsynaptic potential. Both effects lasted for several tens of minutes. The late polysynaptic potential was not observed when the CA3 and CA1 subfields were surgically separated. Our results indicate that the N-methyl-D-aspartate receptor activation leads to the dephosphorylation of the microtubule-associated protein 2 via a Ca2+/calmodulin phosphatase, probably calcineurine. This may, in turn, participate in the potentiation of synaptic efficacy.

Animals↗
PubMed2002

Intersegmental neuronal pathways in sacrococcygeal spinal cord (S3-Co3) activated by electrical stimulation of tail muscle nerves with low threshold in low spinal cats.

The aim of this study was to elucidate the neuronal pathways mediating propriospinal reflexes of the tail with special reference to the intersegmental connections between group I muscle afferents and motoneurons. Experiments were performed on 25 unanesthetized, spinalized (L1) cats of both sexes. The effects of electrical stimulation of the afferents embedded in different levels of the following muscles: m. extensor caudae medialis (ECM), m. extensor caudae lateralis (ECL), m. flexor caudae longus (FCL), and m. flexor caudae brevis (FCB), were observed in tail motoneurons in the first or second coccygeal (Co1 or Co2) spinal segment. Stimulation of group I muscle afferents from the cranial parts of the tail muscles produced predominantly excitatory postsynaptic potentials. In ECM and FCB, some motoneurons had significant excitatory effects exerted by group I afferent inputs from homonymous and/or synergistic muscles during vertical tail movement, and some motoneurons had predominately excitatory effects from antagonistic muscles during vertical tail movement. Excitatory effects in ECL and FCL motoneurons occurred more often and were larger in size after stimulating the ipsilateral tail muscles than after stimulating the contralateral tail muscles. The stimulation of group I muscle afferents from the caudal parts of the tail muscles produced predominantly inhibitory effects. The shortest neuronal pathways for excitatory postsynaptic potentials and inhibitory postsynaptic potentials were mono- and disynaptic neuronal pathways, respectively. The results of the present experiments suggest that continuous tail movements along the tail are performed by group I reflex pathways.

Afferent Pathways↗
PubMed1987

Postsynaptic membrane shifts during frequency potentiation of the hippocampal EPSP.

1. In some classes of central neurons, repetitive synaptic stimulation induces substantial changes in the postsynaptic membrane, in conjunction with robust frequency potentiation of the excitatory postsynaptic potential (EPSP). However, the nature and time course of these postsynaptic membrane shifts, or their possible contributions to EPSP frequency potentiation (e.g., by altering driving force or current pathways), have not been examined extensively. We therefore studied the simultaneous patterns of change in composite EPSP amplitude, postsynaptic input resistance (Rin), and postsynaptic membrane potential during a 4-min train of 10-Hz monosynaptic stimulation in CA1 neurons of hippocampal slices. Slices were maintained in media containing either control (4 mM) or high (6.5 mM) concentrations of K+. 2. Potentiation of the EPSP, hyperpolarization of the membrane, and a decline of Rin, all developed rapidly during 10-Hz synaptic stimulation; these responses reached maximal levels by 5-15 s of the stimulation train. In most cells, a membrane depolarization phase occurred between 15 and 45 s of stimulation, followed by rehyperpolarization by 1 min of stimulation. During the depolarization phase, both EPSP potentiation and the decline in Rin remained near maximal. No significant differences were seen as a function of K+ concentrations. 3. These results show that hyperpolarization is not invariably associated temporally with EPSP frequency potentiation. Moreover, if driving force and membrane conductance changes are assumed to be approximately similar in large dendrites and soma, then the increase in driving force due to membrane hyperpolarization was not sufficient to account for the three- and fourfold increases in EPSP amplitude seen during frequency potentiation. Further, based on similar assumptions and on dendritic models of EPSP attenuation, the decline in Rin should reduce EPSP amplitude at the dendritic synaptic site and, to a proportionately greater extent, at the soma. 4. Studies in which the membrane was hyperpolarized with injected current to approximately the IPSP reversal potential, or in which bicuculline methiodide was applied to the slices, indicated that depression of the IPSP by repetitive stimulation did not account for frequency potentiation of EPSP amplitude. 5. These data are therefore consistent with the conclusion that the frequency potentiation of composite EPSPs in central neurons depends on presynaptic mechanisms, rather than on generalized postsynaptic changes. However, our findings do not rule out localized postsynaptic changes in receptors or spines as possible contributing factors.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2000

Laminar differences in recurrent excitatory transmission in the rat entorhinal cortex in vitro.

Paired intracellular recordings were used to investigate recurrent excitatory transmission in layers II, III and V of the rat entorhinal cortex in vitro. There was a relatively high probability of finding a recurrent connection between pairs of pyramidal neurons in both layer V (around 12%) and layer III (around 9%). In complete contrast, we have failed to find any recurrent synaptic connections between principal neurons in layer II, and this may be an important factor in the relative resistance of this layer in generating synchronized epileptiform activity. In general, recurrent excitatory postsynaptic potentials in layers III and V of the entorhinal cortex had similar properties to those recorded in other cortical areas, although the probabilities of connection are among the highest reported. Recurrent excitatory postsynaptic potentials recorded in layer V were smaller with faster rise times than those recorded in layer III. In both layers, the recurrent potentials were mediated by glutamate primarily acting at alpha-amino-3-hydroxy-5-methyl-4-isoxazole receptors, although there appeared to be a slow component mediated by N-methyl-D-aspartate receptors. In layer III, recurrent transmission failed on about 30% of presynaptic action potentials evoked at 0.2Hz. This failure rate increased markedly with increasing (2, 3Hz) frequency of activation. In layer V the failure rate at low frequency was less (19%), and although it increased at higher frequencies this effect was less pronounced than in layer III. Finally, in layer III, there was evidence for a relatively high probability of electrical coupling between pyramidal neurons. We have previously suggested that layers IV/V of the entorhinal cortex readily generate synchronized epileptiform discharges, whereas layer II is relatively resistant to seizure generation. The present demonstration that recurrent excitatory connections are widespread in layer V but not layer II could support this proposal. The relatively high degree of recurrent connections and electrical coupling between layer III cells may be a factor in it's susceptibility to neurodegeneration during chronic epileptic conditions.

2-Amino-5-phosphonovalerate↗
PubMed2002

Effects of methylphenidate on the inhibitory postsynaptic potential in rat locus coeruleus neurons.

Effects of methylphenidate (MPH), an agent used clinically for the treatment of children presenting the attention-deficit/hyperactivity disorder (AD/HD), on synaptic transmission in the rat locus coeruleus (LC) were examined by intracellular recording methods. Bath-application of MPH (30 nM-3 microM) increased the amplitude of the inhibitory postsynaptic potential (IPSP), while it did not change the amplitude of the excitatory postsynaptic potential (EPSP). MPH increased the time-to-peak and the half-decay time of the IPSP in LC neurons. MPH increased the amplitude of spontaneous IPSP: individual spontaneous IPSPs merged one into the other so as to produce regular, long-lasting waves of hyperpolarization. Clonidine (10 nM), a selective agonist for alpha 2-adrenoceptors, depressed the IPSP without affecting the EPSP in LC neurons. The results suggest that MPH enhances inhibitory synaptic transmission in the rat LC by depressing the norepinephrine (NE) re-uptake system.

Animals↗
PubMed1987

Tiletamine is a potent inhibitor of N-methyl-aspartate-induced depolarizations in rat hippocampus and striatum.

N-methyl-D,L-aspartate (NMA) antagonists are of potential value in the treatment of epilepsy and ischemia, but commonly utilized compounds are of low potency and poorly penetrate the brain. Tiletamine hydrochloride is a lipophilic and potent veterinary anesthetic. This study shows tiletamine to be similar to ketamine and to phencyclidine, agents known to interact with the NMA receptor. Effects of tiletamine on synaptic transmission and on direct excitatory responses to exogenous amino acids were examined in rat hippocampal and striatal slices. In striatal slices, tiletamine inhibited the NMA-mediated, but not the spontaneous, release of [3H]acetylcholine, with an IC50 of 70 nM. In hippocampal CA1 cells, 3 microM tiletamine in the perfusate reversibly blocked the intracellularly recorded responses to ionophoretically applied NMA, but not to glutamate, quisqualate and kainate. Tiletamine, 3 to 100 microM, had no effect on the orthodromically elicited excitatory postsynaptic potential, action potential amplitude or duration, resting membrane potential, or input resistance. In Mg++-free perfusate, the excitatory postsynaptic potential was greatly augmented to give a paroxysmal depolarization shift and was reversibly blocked by 10 microM tiletamine. Our results show that tiletamine is a potent and reversible antagonist of NMA-mediated responses without itself having major effects in low concentrations on normal membrane and synaptic pyramidal cell properties.

Acetylcholine↗
PubMed1993

Laryngeal afferent inputs to the nucleus of the solitary tract.

The following study was undertaken to examine the integration of laryngeal afferent inputs within the nucleus of the solitary tract (NTS), the primary site of termination of laryngeal afferent fibers. Intracellular recordings were obtained from 63 cells that responded to electrical stimulation of the superior laryngeal nerve (SLN) with an excitatory postsynaptic potential (EPSP; n = 49), an excitatory-inhibitory postsynaptic potential (EPSP-IPSP) sequence (n = 13), or an IPSP (n = 1). Mechanical stimulation of laryngeal mechanoreceptors revealed a variety of response patterns (e.g., slowly and rapidly adapting depolarizations or hyperpolarizations). Two types of response to increasing SLN stimulus frequency were observed. In 11 cells SLN-evoked EPSP amplitude at 10 Hz was only 47 +/- 4% of the amplitude at 1 Hz, while in 6 cells EPSP amplitude at 10 Hz was virtually identical (93 +/- 3%) to that at 1 Hz. Time-dependent inhibitory interactions occurred between SLN inputs to NTS neurons at intervals between 50 and 400 ms and in the absence of any change in membrane potential. NTS neuronal responses to brief activation of laryngeal mechanoreceptors correspond well to discharge patterns described for individual laryngeal mechanoreceptors. Frequency-dependent filtering and time-dependent inhibitory interactions might modify NTS neuronal responses during more intense stimulation of laryngeal afferents.

Afferent Pathways↗
PubMed1996

Metabotropic glutamate receptor subtype agonists facilitate long-term potentiation within a distinct time window in the dentate gyrus in vivo.

Trans-azetidine-2,4-dicarboxylic acid (ADA) is a putative selective agonist of group 1 metabotropic glutamate receptors. It has been shown previously that application of ADA prior to a short-term potentiation-inducing high-frequency tetanus facilitates long-term potentiation in vivo. In order to examine the role of metabotropic glutamate receptors in this response, we studied the effect of ADA in the dentate gyrus of the rat when applied after high-frequency tetanus to the perforant path. A comparison was made with the effects of the metabotropic glutamate receptor group 1 agonist 3,5-dihydroxyphenylglycine. Drugs were applied via a cannula implanted in the lateral cerebral ventricle. Both population spike amplitude and field excitatory postsynaptic potential were measured. Weak tetanization produced a short-term potentiation of field excitatory postsynaptic potential and population spike which decayed to baseline values by 90 min, and was unaffected by vehicle injections. Application of ADA (20 mM/5 microliters) or 3,5-dihydroxyphenylglycine (4mM/5 microliters) 5 min after high-frequency tetanus facilitated short-term potentiation into a long-term potentiation which lasted over 24 h. (R,S)-alpha-Methyl-4-carboxyphenylglycine (200 mM/5 microliters), a metabotropic glutamate receptor antagonist, when applied prior to high-frequency tetanus and ADA or 3,5-dihydroxyphenylglycine, completely inhibited this effect. ADA applied 10,15,20 and 25 min after high-frequency tetanus also facilitated short-term potentiation into long-term potentiation, but the magnitude of long-term potentiation was smaller than than produced by ADA given 5 min after tetanus. Similar effects were seen with 3,5-dihydroxyphenylglycine applied 25 min after high-frequency tetanus. When (R,S)-alpha-methyl-4-carboxyphenylglycine was applied prior to high-frequency tetanus and ADA or 3,5-dihydroxyphenylglycine applied 30 min after high-frequency tetanus, or after short-term potentiation decay, elicited no facilitation of long-term potentiation. These results indicate that a distinct time window for the enhancement by ADA and 3,5-dihydroxyphenylglycine of short-term potentiation into long-term potentiation occurs in the dentate gyrus in vivo. This suggests that metabotropic glutamate receptor activation in long-term potentiation occurs within a finite period of time and may be mediated by group 1 metabotropic glutamate receptors. Furthermore, it suggests that metabotropic glutamate receptor modulation of N-methyl-D-aspartate receptors does not account for the role of metabotropic glutamate receptors in long-term potentiation.

Animals↗
PubMed1996

Interactions between ethanol, endogenous adenosine and adenosine uptake in hippocampal brain slices.

Previous studies have suggested that ethanol (EtOH) can inhibit the transport of adenosine (ADO) into cells, and that ADO may be an important mediator of the effects of EtOH in the brain. Nevertheless, there have been few functional studies of EtOH-ADO interactions at the cellular level in the brain that support this hypothesis. In the present study, the effects of EtOH were compared with those of other more well-characterized ADO uptake inhibitors, using evoked field excitatory postsynaptic potentials in the rat hippocampal slice preparation as a measure of changes in extracellular ADO. As has been reported previously, the ADO uptake inhibitor dipyridamole (DIPY) depresses the amplitude of field excitatory postsynaptic potentials responses in a dose-dependent, theophylline-reversible manner, suggesting that, by inhibiting ADO transport, DIPY significantly increases the concentration of extracellular ADO. Nitrobenzylthioinosine, which inhibits a different ADO transporter that has been reported to be selectively affected by EtOH, had no significant effect on its own, but produced a weak inhibitory effect when combined with DIPY. When tested alone, EtOH (20 and 100 mM) produced variable effects on the field excitatory postsynaptic potentials response, but overall did not have a statistically significant effect. Unlike nitrobenzylthioinosine, EtOH did not produce a significant depression of evoked responses when combined with DIPY. These experiments demonstrate that, although EtOH may inhibit the nitrobenzylthioinosine-sensitive ADO transporter, intoxicating concentrations do not produce large enough changes in extracellular ADO in hippocampal slices to be detectable using electrophysiological response measures.

Adenosine↗
PubMed1982

Effect of substance P on colonic mechanoreceptors, motility, and sympathetic neurons.

Intracellular recording techniques were used in vitro to analyze the effects of substance P (SP) on synaptic transmission and electrical properties of sympathetic neurons in the inferior mesenteric ganglion (IMG) of the guinea pig. Intraluminal pressure-recording techniques were used to study the effects of SP on colonic motility. Superfusion of the ganglia with SP (10(-7) to 10(-6) M) depolarized the cell soma (2--12 mV) and increased cell input resistance (8--11 M omega). These effects converted synchronous excitatory postsynaptic potentials, in response to electrical stimulation of preganglionic nerves, and asynchronous excitatory postsynaptic potentials, in response to activation of colonic mechanoreceptors, to action potentials. Administration of SP to only the colon increased basal intraluminal pressure and the frequency and amplitude of phasic changes in intraluminal pressure. These changes increased mechanoreceptor synaptic input to neurons in the IMG. We conclude that SP facilitates synaptic transmission along noradrenergic pathways and increases colonic motility.

Animals↗
PubMed2002

Electrical behaviour of interleukin-1 beta (IL-1 beta) and prostaglandin-E2 (PGE2) on colonic myenteric neurones.

Abstract Intracellular recordings were used to examine the effects on electrical and synaptic behaviour of interleukin (IL)-1beta and prostaglandin E2(PGE2) on myenteric neurones of the guinea-pig colon. Application of IL-1beta and PGE2resulted in a concentration-dependent slow depolarization with enhanced spike discharge in, respectively, 45% (21/47) and 83% (33/41) of the impaled colonic neurones. Administration of IL-1beta in three neurones (6%) elicited a hyperpolarization. Responses remained during tetrodotoxin application, indicative of a direct effect of both substances on the impaled neurones. The effects of IL-1beta remained in the presence of indomethacine, a prostaglandin synthase inhibitor. Responses were seen in both nitric oxide synthase- and choline acetyl transferase-immunoreactive neurones. IL-1beta evoked a 26% reduction of the fast excitatory postsynaptic potential. These results indicate that the application of IL-1beta and PGE2evoke direct excitatory actions on a subset of myenteric neurones. For IL-1beta, direct inhibition and presynaptic inhibition of the fast excitatory postsynaptic potential has also been found. In the distal colon, responses to IL-1beta are not mediated through PGE2pathways.

Animals↗
PubMed2000

Re-evaluation of phorbol ester-induced potentiation of transmitter release from mossy fibre terminals of the mouse hippocampus.

To investigate the mechanisms by which phorbol esters potentiate transmitter release from mossy fibre terminals we used fura dextran to measure the intraterminal Ca2+ concentration in mouse hippocampal slices. A phorbol ester, phorbol 12,13-diacetate (PDAc), potentiated the field excitatory postsynaptic potential (fEPSP) slope. PDAc also enhanced the stimulation-dependent increase of [Ca2+]i in the mossy fibre terminal (Delta[Ca2+]pre). The magnitude of the PDAc-induced fEPSP potentiation (463+/-57% at 10 microM) was larger than that expected from the enhancement of Delta[Ca2+]pre (153+/-5%). The Delta[Ca2+]pre was suppressed by omega-agatoxin IVA (omega-AgTxIVA, 200 nM), a P/Q-type Ca2+ channel-specific blocker, by 31%. The effect of PDAc did not select between omega-AgTxIVA-sensitive and -resistant components. The PDAc-induced potentiation of the fEPSP slope was partially antagonized by the protein kinase C (PKC) inhibitor bisindolylmaleimide I (BIS-I, 10 microM), whereas the Delta[Ca2+]pre was completely blocked by BIS-I. Although the BIS-I-sensitive fEPSP potentiation was accompanied by a reduction of the paired-pulse ratio (PPR), the BIS-I-resistant component was not. Whole-cell patch clamp recording from a CA3 pyramidal neuron in a BIS-I-treated slice demonstrated that PDAc (10 microM) increased the frequency of miniature excitatory postsynaptic currents (mEPSCs, 259+/-33% of control) without a noticeable change in their amplitude (102+/-5% of control). These results suggest that PKC potentiates transmitter release by at least two distinct mechanisms, one Delta[Ca2+]pre dependent and the other Delta[Ca2+]pre independent. In addition, some phorbol ester-mediated potentiation of synaptic transmission appears to occur without activating PKC.

Action Potentials↗