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PubMed1996

The nitric oxide/cGMP pathway couples muscarinic receptors to the activation of Ca2+ influx.

Inward currents activated by 8-bromc-cGMP and by muscarinic agonist were compared in N1E-115 mouse neuroblastoma cells using perforated-patch voltage clamp and Fura-2 imaging. The cGMP analog activates a voltage-independent inward current that is carried at least in part by Ca2+ because it persists in Na(+)-free saline when Ca2+ is present and is blocked by external Mn2+ and Ba2+. The current is similar to the inward current that develops during stimulation of M1 muscarinic receptors, and the currents activated by agonist and by 8-bromo-cGMP are not additive, indicating that the same pathway is involved. Inhibition of cGMP production with NG-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of nitric oxide (NO)-synthase, prevents activation of Ca2+ current by agonist without affecting the content of intracellular Ca2+ stores or the ability of agonist to mobilize Ca2+. The inhibition is overcome by 8-bromo-cGMP. LY83583, a competitive inhibitor of guanylyl cyclase, reversibly blocks activation of Ca2+ current by agonist, again without affecting the content of Ca2+ stores or Ca2+ release. Rp-8-pCPT-cGMPS, an inhibitory analog of cGMP, also reduces the Ca2+ current and reduces Ca2+ influx during muscarinic activation. It is concluded that cGMP is the necessary and sufficient intermediate in the pathway linking muscarinic receptor occupancy to the activation of voltage-independent Ca2+ current. The pathway involves positive feedback. Calcium entering via voltage-independent channels preferentially stimulates NO-synthase, which leads to enhanced cGMP production and greater Ca2+ influx. Positive feedback may explain the rapid increase in cGMP that occurs during muscarinic receptor activation.

Animals↗
PubMed2001

Nitric oxide directly activates GABA(A) receptor function through a cGMP/protein kinase-independent pathway in frog pituitary melanotrophs.

The direct effects of nitric oxide (NO) donors and sulfhydryl-modifying agents on the GABA(A) receptor function were examined by perforated patch, whole-cell and single channel recordings in cultured frog melanotrophs. In amphotericin B-perforated cells incubated with the soluble guanylyl cyclase inhibitors LY 83583 and ODQ (10-4 M each), the NO donor sodium nitroprusside (SNP) (10(-3) M) reversibly increased the current evoked by GABA (5 x 10(-6) M). In the whole-cell configuration, internal application of the oxidizing agent H2O2 (0.05%) potentiated the GABA-evoked current while the reducing agent 2-mercaptoethanol (5 x 10(-3) M) slightly decreased the current amplitude. In inside-out patches, GABA (2 x 10(-7) M) triggered single channel bursts of openings. Incubation with the NO donors SNP or DEA/NO (10(-4) M each) enhanced the open probability of the GABA(A) receptor channel but did not modify the chloride reversal potential and did not affect the conductance states. The oxidizing agents H2O2 (0.05%) or DTNB (10-4 M) mimicked the stimulatory effect of the NO donors on the open probability while the reducing compounds 2-mercaptoethanol (5 x 10(-3) M) or DTT (10(-4) M) markedly attenuated the channel activity. Potentiation of the GABA-induced single channel activity by SNP or H2O2 was blocked by 2-mercaptoethanol. Similarly, the potentiating effect produced by DEA/NO or DTNB on the open probability was reversed by DTT. In outside-out patches, incubation with SNP also significantly enhanced the open probability of single channels activated by GABA (10(-6) M). These data indicate that, in frog pituitary melanotrophs, NO potentiates the GABA-evoked current independently of the cGMP/protein kinase pathway. The effect of NO can be accounted for by S-nitrosylation/oxidation of thiol groups either directly on the GABA(A) receptor subunits or on a regulatory protein tightly associated with the GABA(A) receptor.

Aminoquinolines↗
PubMed1975

Crossed pathways from the entorhinal area to the fascia dentata. I. Normal in rabbits.

The entorhinal area projects to the Ammon's horn and the fascia dentata by way of the medial and lateral perforant paths that originate in the medial and lateral part of that area, respectively. The two tracts terminate at different laminar levels in the molecular layers of the ipsilateral hippocampal regio inferior and fascia dentata. Using the Fink-Heimer technique, each of the perforant paths in the normal rabbit is now shown to innervate the antero-dorsal extremes of the Ammon's horn and fascia dentata in both hemispheres. The crossed and uncrossed components of each path innervate homotopic zones on each side. This bilateral innervation contrasts with the situation in the rat where only very weak crossed components exist. Degeneration particles in the fascia dentata contralateral to a lesion of the perforant paths diminish in number along the course of the fibers as they proceed away from the midline, but are traceable for several millimeters. Crossed fibers are shown to pass from one hemisphere into the other directly through the fused molecular layers of the fasciae dentatae. The bilateral innervation in the rabbit indicates that even though the axons of the perforant paths are highly specific with respect to the class of neuron and the dendritic segments upon which they form synapses, they apparently do no possess a mechanism by which they can distinguish between the receptive fields in the two hemispheres. It is concluded that during ontogeny the perforant path fibers from both sides most likely compete for available synaptic sites in the rostral part of their terminal fields and that their relative amounts in the two hemispheres is governed by spatial and temporal factors.

Animals↗
PubMed1995

Transesophageal echocardiographically guided atrial transseptal catheterization in patients with normal-sized atria: incidence of complications.

The incidence of cardiac complications from atrial transseptal catheterization has never been quantified in patients with normal-sized atria. Series defining the complication rate are derived from diseased hearts with structural changes that may alter the complication rate of the procedure. The generation of a standardized incidence of perforation in a population of structurally normal atria has important implications. A total of 46 atrial transseptal catheterizations guided by transesophageal echocardiography (TEE) for radiofrequency ablation of left-sided accessory pathways was performed in 42 patients during a 3-year period (1990-1993). Clinical and echocardiographic data were analyzed, with special attention given to TEE reports pre- and post-transseptal catheterization. Only one complication occurred in the 46 procedures (2.2%): a perforation of the left atrium that led to pericardial effusion and cardiac tamponade. In a small series of patients with normal sized atria, we have demonstrated that TEE-guided transseptal catheterization in a procedure with a low complication rate.

Adult↗
PubMed2000

Impairment of hippocampal long-term potentiation by Alzheimer amyloid beta-peptides.

Although it is generally believed that amyloid beta (Abeta) peptides contribute to the pathogenesis of Alzheimer's disease, the precise role of these peptides in the development of memory loss of Alzheimer's disease, has not been fully understood. The present study examined the effect of several synthetic Abeta peptides on long-term potentiation (LTP), a cellular model of learning and memory, in rat hippocampal slices. Brief perfusion of slices with low concentrations (200 nM or 1 microM) of Abeta(1-42), Abeta(1-40) or their active fragment Abeta(25--35) significantly inhibited LTP induction without affecting the basal synaptic transmission and posttetanic potentiation in the dentate medial perforant path. A similar effect of Abeta(25-35) was also observed in the Schaffer collateral-CA1 pathway. When comparing actions of several Abeta variants derived from Abeta(25-35), the N-terminal sequence of Abeta(25-35) was found necessary for inhibiting LTP. In addition, Abeta variants lacking neurotoxic action and aggregating property were also able to block LTP, suggesting that this effect was neurotoxicity independent. Our findings demonstrated that subneurotoxic concentrations of Abeta peptides could strongly suppress long-term synaptic plasticity in the hippocampus. Such an effect might underlie the memory deficits seen in Alzheimer's disease before neuronal cell loss.

Amyloid beta-Peptides↗
PubMed1987

Field potential evidence for long-term potentiation of feed-forward inhibition in the rat dentate gyrus.

Trains of high-frequency stimulation to the perforant path cause (i) long-term potentiation (LTP) of the population excitatory post-synaptic potential (EPSP), (ii) a lasting increase in the population spike, and (iii) a lasting alteration of the relationship between the EPSP and population spike (E-S relationship), consisting of a decreased x-intercept and decreased slope of the linear regression. To compare the thresholds of these changes, we applied a series of trains, increasing in duration from below LTP threshold. The EPSP potentiated with about the same low threshold as the reduction in E-S slope, whereas the reduction in E-S x-intercept required longer trains. In the second experiment, LTP of the EPSP was reduced by concurrent high-frequency stimulation of the commissural input and a lasting reduction of the population spike height was observed. In a third experiment, picrotoxin, an antagonist of gamma-aminobutyric acid (GABA)-mediated inhibition, blocked the decrease in slope of the E-S relationship which normally accompanies LTP. These results imply that perforant path/granule cell LTP is normally accompanied by long-term potentiation of a feed-forward inhibitory pathway which may involve interneurones.

Animals↗
PubMed1995

The perforant path projection to hippocampal area CA1 in the rat hippocampal-entorhinal cortex combined slice.

1. The perforant path projection from layer III of the entorhinal cortex to CA1 of the hippocampus was studied within a hippocampal-entorhinal combined slice preparation. We prevented contamination from the other main hippocampal pathways by removal of CA3 and the dentate gyrus. 2. Initially the projection was mapped using field potential recordings that suggested an excitatory sink in stratum lacunosum moleculare with an associated source in stratum pyramidale. 3. However, recording intracellularly from CA1 cells, stimulation of the perforant path produced prominent fast GABAA and slow GABAB IPSPs often preceded by small EPSPs. In a small number of cells we observed EPSPs only. 4. CNQX blocked excitatory and inhibitory responses. This indicated the presence of an intervening excitatory synapse between the inhibitory interneurone and the pyramidal cell. 5. Focal bicuculline applications revealed that the major site of GABAA inhibitory input was to stratum radiatum of CA1. 6. The inhibition activated by the perforant path was very effective at reducing simultaneously activated Schaffer collateral mediated EPSPs and suprathreshold-stimulated action potentials. 7. Blockade of fast inhibition increased excitability and enhanced slow inhibition. Both increases relied upon the activation of NMDA receptors. 8. Perforant path inputs activated prominent and effective disynaptic inhibition of CA1 cells. This has significance for the output of hippocampal processing during normal behaviour and also under pathological conditions.

2-Amino-5-phosphonovalerate↗
PubMed1999

Time-dependent changes in striatal glutamate synapses following a 6-hydroxydopamine lesion.

The goal of this study was to investigate changes in glutamatergic synapses in the striatum of rats at two different time-points following a unilateral injection of 6-hydroxydopamine into the medial forebrain bundle. One month following this lesion of the nigrostriatal pathway, there was an increase (70%) in the mean percentage of asymmetrical synapses within the dorsolateral striatum containing a discontinuous, or perforated, postsynaptic density, possibly suggesting an increase in glutamatergic activity. This was correlated, in the same brain region, with a decrease (44%) in the density of glutamate immunoreactivity within nerve terminals associated with all asymmetrical synapses and also with those terminals associated with a perforated postsynaptic density. These morphological changes were consistent with an increase (>two-fold) in the basal extracellular level of striatal glutamate, as measured by in vivo microdialysis. The density of GABA immunolabeling within symmetrical nerve terminals was increased (25%) at this one month time-period. Dopamine levels within the lesioned striatum were >99% depleted. However, at three months, while an increase in the mean percentage of striatal perforated synapses was maintained, a significant increase (50%) in the density of striatal nerve terminal glutamate immunolabeling within all asymmetrical synapses and those associated with a perforated postsynaptic density was observed. This was correlated with a small, but significant, decrease (32%) in the basal extracellular level of striatal glutamate. The density of GABA immunolabeling within nerve terminals associated with a symmetrical contact remained elevated at this three month time-period, while striatal dopamine levels remained depleted. While the density of nerve terminal GABA immunolabeling remained elevated at both the one and three month time-periods, there appeared to be a differential effect on glutamatergic synapses. The in vivo microdialysis data suggest that glutamate synapses were more active at a basal level at one month and become less active compared to the control group at the three month time-period. These data suggest that there are compensatory changes in glutamatergic synapses within the striatum following a 6-hydroxydopamine lesion that appear to be independent of the level of striatal dopamine or GABA. We propose that changes in the activity of the thalamo-cortico-striatal pathway may help to explain the differential time-course change in striatal glutamatergic synaptic activity.

Animals↗
PubMed2000

Amygdalo-entorhinal inputs to the hippocampal formation in relation to schizophrenia.

This chapter reviews recent postmortem studies of schizophrenic brain and discusses the potential role of the amygdala in the induction of hippocampal abnormalities in this disorder. Based on available evidence, sectors CA4, CA3, and CA2, but not CA1, show preferential changes in schizophrenic subjects, although the most pronounced changes have been found in CA3 and CA2. It seems likely that the amygdala would contribute in some way to the induction of abnormalities along the trisynaptic pathway via its direct input to sectors CA3 and CA2, as well as an indirect one that involves the entorhinal cortex and its perforant path projection to the area dentata. The postmortem findings reported to date have been integrated into a working model in which decreases of inhibitory GABAergic modulation are invoked to explain the observation from a recent PET scan study (Heckers et al., 1999) that baseline metabolic activity in the hippocampus of schizophrenics is increased. In addition, however, the apparent inability of schizophrenics to increase metabolic activity in the hippocampus when challenged with a memory retrieval task may reflect a disturbance of disinhibitory modulation postulated herein to occur in sector CA3, a key relay point along the trisynaptic pathway. Overall, it seems plausible that an increase of excitatory activity entering the hippocampus from the basolateral complex via both direct and indirect pathways may make a significant contribution to the pathophysiology of schizophrenia.

Afferent Pathways↗
PubMed1987

Barbiturate effects on hippocampal excitatory synaptic responses are selective and pathway specific.

Barbiturate actions on excitatory synaptic responses in CA 1 and dentate regions of hippocampal slices were studied to determine whether different effects occur on anatomically distinct synaptic pathways. Pentobarbital facilitated transmission between stratum radiatum inputs and CA 1 neurons at low concentrations (0.02-0.08 mM) and produced postsynaptic depression at higher concentrations. Only depression was observed for stratum oriens inputs to CA 1 and perforant path inputs to dentate granulae neurons. The (+) isomer of pentobarbital was approximately four times more potent than the (-) isomer of racemic mixture. Phenobarbital (0.04-0.12 mM) produced only depression of synaptic responses in CA 1 and dentate pathways. Comparison of effect on field excitatory postsynaptic potentials and population spike responses indicated that the barbiturates act at selective and pathway-specific sites. The results provide further evidence for specific cellular and membrane recognition sites for barbiturate action.

Action Potentials↗
PubMed2006

Postsynaptic mechanisms are essential for forskolin-induced potentiation of synaptic transmission.

It has been demonstrated that stimulation of protein kinase A (PKA) results in enhanced synaptic transmission in the hippocampus and other brain areas. To investigate mechanisms of the PKA-mediated potentiation of synaptic transmission, we used rat hippocampal embryonic cultures. In low-density cultures, paired recordings under the perforated patch demonstrated that 15-min forskolin treatment produced long-lasting potentiation of evoked excitatory postsynaptic currents (eEPSCs) mediated by the cAMP/PKA pathway. eEPSC amplitudes increased to 240 +/- 10% of baseline after 15 min of forskolin treatment (early). After forskolin washout, eEPSCs declined to a potentiated level. Potentiation was sustained for > or = 85 min after forskolin washout and, 60 min after forskolin washout, constituted 152 +/- 7% of baseline (late potentiation). Disruption of presynaptic processes with the whole cell configuration and internal solution containing PKA inhibitor peptide did not affect forskolin-induced potentiation. Disruption of postsynaptic processes, in contrast, impaired early potentiation and abolished late potentiation. Study of mEPSCs confirmed the contribution of postsynaptic mechanisms. Forskolin-induced enhancement of mEPSC frequency observed under the perforated patch was attenuated by the whole cell configuration. Forskolin also induced an increase of mEPSC amplitudes in the perforated patch, but not in the whole cell, experiments. Potentiation of eEPSCs was not activity dependent, persisting in the absence of stimulation. NMDA receptor blockade did not abolish forskolin-induced potentiation. In summary, we demonstrate that forskolin-induced potentiation of eEPSCs was mediated by postsynaptic mechanisms, presumably by upregulation of AMPA receptors by phosphorylation.

Animals↗
PubMed2005

Pulse stimulation with odors or IBMX/forskolin potentiates responses in isolated olfactory neurons.

Many odor responses are mediated by the adenosine 3',5'-cyclic monophosphate (cAMP) pathway in which the cAMP-gated current is amplified by Ca2+-dependent Cl- current. In olfactory neurons, prolonged exposure to odors decreases the odor response and is an adaptive effect. Several studies suggest that odor adaptation is linked to elevated intracellular Ca2+. In the present study, using the perforated configuration of the patch clamp technique, we found that repetitive odor stimulation elicits a potentiation of the subsequent responses in olfactory neurons. This potentiation is mimicked by stimulating the cAMP pathway and does not appear to be related to phosphorylation of ion channels since protein kinase inhibitors could not block it. Our data suggest that local increases in [Ca2+]i via activation of the cAMP pathway mediate the pulse-elicited potentiation. In the first odor application, entry of Ca2+ through cyclic nucleotide-gated channels appears to be buffered. Repetitive stimulation allows local increases in [Ca2+]i, recruiting more Ca2+-dependent Cl- channels with each subsequent odor pulse.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Differential effects of benzodiazepine receptor agonists on hippocampal long-term potentiation and spatial learning in the Morris water maze.

The amnesic effect of benzodiazepine drugs has been well documented, though the mechanisms mediating this effect are unknown. Long-term potentiation (LTP) has been proposed as a mechanism by which information is stored in the mammalian central nervous system. This experiment sought to determine if benzodiazepines impair mnemonic processes by blocking LTP. Rats implanted with a stimulating electrode in the perforant path and a recording electrode in the dentate gyrus were given high-frequency stimulation after the administration of either chlordiazepoxide (5 mg/kg), diazepam (5 mg/kg) or CL 218,872 (10 mg/kg). None of these drugs completely blocked the induction of LTP as measured by changes in the magnitude of the population spike amplitude, though CL 218,872 significantly suppressed potentiation over the duration of recording (24 h). Moreover, the potentiation observed in diazepam-treated rats returned to baseline after 24 h. Two weeks after the last recording, the same implanted rats were given their previous drug and dose and then tested for spatial learning ability in the Morris water maze. Each drug resulted in a severe impairment of spatial learning, but had no effect on cue learning. Two days later, in the absence of drugs, the same rats readily acquired a reversed platform location. Together these results suggest that CL 218,872 may impair spatial learning by suppressing LTP in the perforant path but that chlordiazepoxide and diazepam can impair spatial learning in the absence of LTP suppression in this pathway.

Animals↗
PubMed1998

Evidence for involvement of the cGMP-protein kinase G signaling system in the induction of long-term depression, but not long-term potentiation, in the dentate gyrus in vitro.

The involvement of the cGMP-protein kinase G (PKG) signaling pathway in the induction of long-term depression (LTD) and long-term potentiation (LTP) was investigated in the medial perforant path of the dentate gyrus in vitro. Low-frequency stimulation (LFS)-induced LTD of field EPSPs was inhibited by bath perfusion of the selective soluble guanylyl cyclase inhibitor 1H-[1,2,4] oxadiazolo[4,3, -a]quinoxalin-1-one (ODQ). LFS-induced LTD of EPSPs and whole-cell patch-clamped EPSCs was also blocked by bath perfusion and postsynaptic intracellular injection, respectively, of the selective PKG inhibitor KT5823. Elevation of intracellular cGMP by perfusion of the cGMP phosphodiesterase inhibitor zaprinast resulted in induction of LTD of field EPSPs and EPSCs. Occlusion experiments showed mutual inhibition between LFS-induced LTD and zaprinast-induced LTD. The zaprinast-induced LTD of field EPSPs was inhibited by perfusion of ODQ and KT5823. In addition, zaprinast-induced LTD of EPSCs was inhibited by postsynaptic application of KT5823. Glutamate receptor stimulation, especially that of metabotropic glutamate receptors (mGluRs), was required for zaprinast-induced LTD, because cessation of test stimulation or perfusion with the mGluR antagonist (+)-alpha-methyl-4-carboxyphenylglycine (MCPG) inhibited zaprinast-induced LTD. No inhibitory effect of ODQ or KT5823 on the induction of LTP of EPSPs or EPSCs was found. These data indicate that the cGMP-guanyly cyclase-PKG signaling pathway in the dentate gyrus is essential for induction of LTD, although not of LTP, in the dentate gyrus.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1998

Response to change is facilitated by a three-neuron disinhibitory pathway in the tiger salamander retina.

Most retinal ganglion cells respond only transiently, for approximately 150 msec at the onset and termination of a light flash. The responses are transient because it has been shown that bipolar-to-ganglion cell transmission is truncated after 150 msec by a feedback inhibition to bipolar cell terminals. The feedback inhibition itself must be delayed by approximately 150 msec to allow the initial bipolar-ganglion cell transmission. This study identifies a three-component serial synaptic pathway from glycinergic amacrine cells to GABAergic amacrine cells to bipolar cell terminals as one source of this delay. We used perforated and whole-cell patch-clamp recordings to measure the timing of light responses in amacrine, bipolar, and ganglion cells under control and glycine and GABA receptor-blocked conditions. Our results suggest that, after a light flash, a population of glycinergic amacrine cells responds first, inhibiting a population of GABAergic amacrine cells for approximately 150 msec. The GABAergic amacrine cells feed back to bipolar terminals, but only after the 150 msec delay, allowing the bipolar terminals to excite ganglion cells for the first 150 msec. Blocking the glycinergic amacrine cell activity with strychnine allows the GABAergic system to become active earlier. GABAergic amacrine cells then inhibit release from bipolar cells earlier. Under these conditions, the ganglion cell response to change would be decreased.

Animals↗
PubMed1977

Lamellar organisation in the rat hippocampus.

A series of experiments was conducted in the urethane anaesthetised rat to determine the organisation of some hippocampal pathways in this species, using stimulating and recording microelectrodes to elicit and record pupulation spikes. It was found that the mossy fibres, alvear fibres and perforant path were clearly arranged in a lamellar fashion. Lamellar organisation could not be demonstrated for the afferents in the stratum radiatum which include the Schaffer collaterals. It was concluded that hippocampal organisation in this species essentially resembles that in the rabbit and cat.

Animals↗
PubMed1983

[Short- and long-term potentiation in the afferent pathways of the hippocampus in the newborn rabbit].

Field potentials were recorded from dendritic and cell body layers of CA1 and dentate regions in newborn rabbits. Responses were evoked by electrical stimulation of the collateral Schaffer system and the perforant path with paired (a 15-100 ms interstimulus interval) and rhythmical stimuli (20-40/c, 3-5 s). Short-term potentiation in the tests with paired stimulation and posttetanic potentiation (up to 3 h) were observed in the CA1 area beginning from the first postnatal day and in the later maturing fascia dentata beginning from 8-10th days, i.e. when neuronal reactions to stimulation of the appropriate afferent pathways first appeared.

Afferent Pathways↗
PubMed2002

[IL-1beta stimulates alpha-smooth muscle actin expression through JNK/p38 signal pathway in cultured rat mesangial cells].

To investigate the role of intracellular mitogen activated protein kinase (MAPKs, ERK, JNK and p38) signal pathways in IL-1beta -stimulated alpha-smooth muscle actin (alpha-SMA) expression in rat mesangial cells (rMC), alpha-SMA-promoter gene was transfected into rMC by electro-perforation method and the promoter activity was assayed after IL-1beta (10 ng/ml) stimulation. Protein expression of alpha-SMA was assayed by Western blot. The results were compared between the groups stimulated by IL-1beta with or without PD98059 and SB203580, which are thought to block ERK and p38 pathway, respectively. Dominant-negative-JNKK plasmid was co-transfected in rMC to block JNK pathway. The spatial distribution of alpha-SMA and microfilament-like structure was observed by a confocal laser scanning microscope or an electric microscope. After 6 or 24 h of incubation with IL-1beta, rMC underwent a phenotypic change, which was represented by up-regulation of alpha-SMA promoter activity and protein expression. An increase in alpha-SMA and microfilament-like structure was found around the cell nucleus. Block of JNK and/or p38 pathway greatly inhibited IL-1beta -induced alpha-SMA expression, and the block of p38 pathway also suppressed the basal level of alpha-SMA expression. In contrast, ERK pathway had no influence on the process. It is, therefore, concluded that IL-1beta -stimulated expression of alpha-SMA is due to its protein synthesis and cytoskeleton re-organization in activated rMC. Intracellular signal regulation of alpha-SMA expression seems to be mediated mainly by JNK/p38 pathways, but ERK appears to have no effect on the process.

Actins↗