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At least 703 records · Page 39Linked to original sources
PubMed1987

Enhancement of long-term potentiation by the calcium channel agonist Bayer K8644 in CA1 of the rat hippocampus in vitro.

The effect of the Ca agonist BAY K8644 was studied on long-term potentiation (LTP) of extracellular excitatory postsynaptic potentials in the stratum radiatum of CA1 of the hippocampus in vitro. LTP was evoked by brief trains of high-frequency stimulation applied to the stratum radiatum of CA1. 0.5% Ethanol, the vehicle used to dissolve BAY K8644, reduced LTP from 43% to 15%. An amount of 15 microM BAY K8644, in 0.5% ethanol, enhanced LTP from 13% in the ethanol control to 57%. The Ca channel antagonist verapamil did not alter control LTP, but did inhibit the potentiating action of BAY K8644 on LTP. It is postulated that the enhancement of LTP by BAY K8644 may occur through enhancement of Ca influx through voltage-dependent Ca channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

Phorbol ester-induced synaptic potentiation differs from long-term potentiation in the guinea pig hippocampus in vitro.

The relationship between the synaptic potentiations evoked by the protein kinase C activator phorbol-12,13-diacetate and by afferent tetanization has been examined in the CA1 region of the hippocampal slice preparation using extracellular recording. It has been found that the potentiation of the field excitatory postsynaptic potential produced by 1 microM phorbol ester does not affect the amount of long-term potentiation (LTP) that can be evoked by afferent tetanization, and vice versa. A dissociation between phorbol ester-induced and tetanus-induced potentiation is also indicated by the fact that only the former was associated with changes in paired-pulse facilitation. On the other hand, as previously described, higher concentrations (10 microM) of phorbol ester blocked the tetanus-induced potentiation. Since the total potentiation given by 10 microM phorbol ester and tetanization depended on the order of presentation of the potentiation-inducing stimuli, it appears that the blockade of LTP is, at least partly, independent of the phorbol ester-induced potentiation.

Action Potentials↗
PubMed1989

An in vitro study of the effect of lipoxygenase and cyclo-oxygenase inhibitors of arachidonic acid on the induction and maintenance of long-term potentiation in the hippocampus.

The effects on tetanus-induced long-term potentiation (LTP) of the lipoxygenase and phospholipase A2 inhibitor nordihydroguaiaretic acid (NDGA), and of the cyclo-oxygenase inhibitor indomethacin have been investigated in area CA1 of the hippocampal slice. In the presence of NDGA, tetanic stimulation of Schaffer collaterals produces an attenuated potentiation of the population excitatory postsynaptic potential (EPSP) lasting for less than 1 h. Indomethacin does not impair LTP of the EPSP. Neither drug significantly reduces LTP of the population spike. NDGA, but not indomethacin, reversibly reduces pre-established LTP. The results suggest a role for arachidonic acid or its lipoxygenase metabolites, but not its cyclo-oxygenase metabolites, in the induction and expression of tetanus-induced LTP in area CA1.

Action Potentials↗
PubMed1995

NMDA/R1-antisense oligonucleotide influences the early stage of long-term potentiation in the CA1-region of rat hippocampus.

We have studied the role of the N-methyl-D-aspartate (NMDA)/R1 receptor subunit in the mechanism of long-term potentiation (LTP) using an antisense-oligodeoxynucleotide strategy. Antisense-oligodeoxynucleotide (aDON; 10 nmol) or sense-oligodeoxynucleotide (sDON) were applied into the right ventricle of 7 week old male Wistar rats every 12 h for 3 days. Thereafter, in hippocampal slices extracellular field potential recordings were made from the CA1 region. LTP was induced by tetanization of the Schaffer collaterals. In slices of rats pretreated with aDON the initial potentiation of the population spike (POP-spike) was significantly smaller than in those from saline controls and naive animals. The impairment of potentiation lasted for about 50 min posttetanus. However, the potentiation of the field excitatory postsynaptic potentials (fEPSPs) was significantly influenced for 15 min. In slices of rats pretreated with sDON only a small, insignificant difference in POP-spike and fEPSP potentiation was seen compared to saline controls. In the group pretreated with aDON the specific binding of [3H]glutamate to the NMDA-receptor subtype of hippocampal membranes was reduced to about 63% in comparison with the group treated with sDON. These results indicate that DONs reached the target region when applied intraventricularly and were able to suppress the translation of mRNA of the NMDA/R1 receptor subunit. They further support the assumption of the essential role of the NMDA/R1 receptor subunit in the induction of LTP.

Animals↗
PubMed1989

Nordihydroguaiaretic acid blocks the synaptic component of long-term potentiation and the associated increases in release of glutamate and arachidonate: an in vivo study in the dentate gyrus of the rat.

The dentate gyrus of anaesthetized rats was perfused with artificial cerebrospinal fluid while field responses evoked by stimulation of the perforant path were monitored. Perfusates were collected for analysis of endogenous glutamate, aspartate and arachidonate. In animals in which long-term potentiation was induced by tetanic stimulation, there was a sustained increase in the concentration of glutamate in the perfusate, and, less reliably, in aspartate, as previously reported by Bliss et al. (J. Physiol., Lond. 377, 391-408, 1986) and Errington et al. (Neuroscience 20, 279-284, 1987). The lipoxygenase and phospholipase A2 inhibitor nordihydroguaiaretic acid, when added to the perfusate 30 min before the tetanus, abolished both long-term potentiation of the population excitatory postsynaptic potential and the tetanus-induced increase in glutamate release. Long-term potentiation of the population spike was reduced but not abolished. There was also a sustained increase in the release of arachidonic acid following the induction of long-term potentiation which did not occur when induction was blocked by nordihydroguaiaretic acid. These results are discussed in the light of the possibility that arachidonic acid or one of its lipoxygenase metabolites may be the retrograde messenger which we have postulated is released from postsynaptic sites following tetanic stimulation to trigger increased transmitter release from presynaptic terminals.

Action Potentials↗
PubMed2006

The effect of estrogen and progesterone on spreading depression in rat neocortical tissues.

Although gender differences in the incidence of migraine with aura appear to be related to high circulating levels of ovarian hormones, the underlying mechanisms are not yet fully understood. Several studies have suggested a major role for spreading depression (SD) in the pathogenesis and symptomatology of migraine with aura. To investigate a possible role of SD in the association of high female hormones and attacks of migraine with aura, the effects of beta-estradiol and progesterone on SD were studied in rat neocortical tissues. Application of both hormones enhanced the repetition rate as well as the amplitude of SD in neocortical slices treated with hypotonic artificial cerebrospinal fluid. beta-Estradiol and progesterone also dose dependently increased the amplitude of SD induced by KCl microinjection. Both hormones exhibited a pronounced, persisting, and significant enhancement of long-term potentiation of the field excitatory postsynaptic potential in the neocortical tissues. The changes in SD characteristics in the presence of estrogen and progesterone may responsible for increased migraine with aura attacks associated by high female hormones. These hormones may exert their effects on SD via facilitation of synaptic transmission.

Animals↗
PubMed1997

PCCG-IV inhibits the induction of long-term potentiation in the dentate gyrus in vitro.

The effects of two ligands with previously established high and selective potency for metabotropic glutamate receptors (mGlu receptors) group II have been investigated on the high frequency stimulation (HFS) induced long-term potentiation of the field excitatory postsynaptic potential (EPSP) in the dentate gyrus of the rat hippocampus in vitro. The ligands investigated were (2S,1'S,2'S,3'R)-2-(2"-carboxy-3'-phenylcyclopropyl)glycine (PCCG-IV) and (R,S)-alpha-methyl-4-tetrazolylphenylglycine (MTPG). PCCG-IV (10 microM) strongly inhibited the induction of long-term potentiation of the field EPSP by high frequency stimulation. MTPG (50 microM) did not inhibit the induction of long-term potentiation, but prevented the inhibition of long-term potentiation induction by PCCG-IV. The inhibition of long-term potentiation induction by PCCG-IV is suggested to be due to an agonistic action on mGlu receptor group II, probably mGlu3 receptor, as the inhibition of long-term potentiation can be reversed by the application of MTPG, a well-known selective and potent antagonist of mGlu receptor group II.

Alanine↗
PubMed1997

Comparative in vivo and in vitro studies with the potent GABAB receptor antagonist, CGP 56999A.

CGP 56999A ([3-[1-(R)-[(3-cyclohexylmethyl)hydroxyphosphinyl]-2-(S)- hydroxy-propyl] amino]ethyl]-benzoic acid) is a potent GABAB receptor antagonist showing much more pronounced convulsant features in mice than do other previously studied GABAB receptor antagonists. The goal of this study was to elucidate the physiological mechanisms underlying this effect. In mice a dose of 0.6 mg/kg intraperitoneal (i.p.) CGP 56999A elicited behavioral activation and stereotypy with periods of intensive scratching and grooming. At 1 mg/kg i.p. most mice displayed myoclonic seizure-like episodes lasting several min. Pretreatment with the lower dose of 0.6 mg/kg i.p. also induced seizures after treatment with a subthreshold dose of pentylenetetrazole (40 mg/kg i.p.). In rats a dose of 3 mg/kg CGP 56999A (i.p.) induced convulsions of tonic-clonic nature. Intracellular sharp microelectrode recordings from rat cortical neurons in slices revealed no paroxysmal actions of CGP 56999A (10 microM). Similar to other GABAB receptor antagonists, CGP 56999A suppressed the late inhibitory postsynaptic potential (i.p.s.p.), but had no effect on the excitatory postsynaptic potential (e.p.s.p.) in the cortex. In cortical slices exposed to picrotoxin (10 microM), the compound evoked pronounced, spontaneous and intense epileptiform discharges. In conclusion, these findings demonstrated that the convulsive feature of the potent GABAB receptor antagonist, CGP 56999A, may be due to suppression of the late i.p.s.p., which becomes apparent in the intact brain only, whereas this action remains undetected in untreated brain slices. This remarkable discrepancy between in vitro and in vivo may be a consequence either of disruption of neuronal circuits during slice preparation or of the pronounced hyperpolarization of pyramidal neurons, at least in the case of cortical slice preparations.

Animals↗
PubMed1997

Z-321, a prolyl endopeptidase inhibitor, augments the potentiation of synaptic transmission in rat hippocampal slices.

The present study investigated the effects of arginine-vasopressin (AVP) and (1-[3-(2-indanylacetyl)-L-thioprolyl] pyrrolidine (Z-321), an inhibitor of prolyl endopeptidase (PEP; (EC 3.4.21.26)) which degrades AVP in vitro, on the short-lasting potentiation of the field excitatory postsynaptic potentials (EPSP) coupled with a weak tetanus. The EPSP, after the electrical stimulation of the Schaffer collateral/commissural pathway, were recorded in the CA1 region of rat hippocampal slices. AVP at 10(-8) M and Z-321 at 10(-4) M augmented the potentiation induced by the weak tetanus; the magnitude of the post-tetanic potentiation of the EPSP was enhanced and the potentiation lasted for 60 min. In contrast, the racemic D-thioprolyl compound of Z-321, which virtually lacks any inhibitory effects on PEP, failed to affect the potentiation at 10(-4) M. The facilitatory effect of Z-321 was reversed by the application of [d(CH2)5,Tyr(Me)2]AVP (10(-8) M), an antagonist of the AVP V1 receptors, indicating that the effect of Z-321 was mediated through the V1 receptors. These findings suggest that Z-321 augmented the potentiation due to its inhibitory influence on the AVP degradation by PEP.

Animals↗
PubMed1997

Involvement of M2 receptor in an enhancement of long-term potentiation by carbachol in Schaffer collateral-CA1 synapses of hippocampal slices.

We examined effects of carbachol (CCh), muscarinic receptor agonist, on long-term potentiation (LTP) of field excitatory postsynaptic potential (fEPSP) at Schaffer collateral-CA1 synapse of guinea pig hippocampal slices using extracellular recording technique. Application of 0.1 microM CCh to the slices significantly augmented the magnitude of LTP without significant change in the amplitude of pretetanus fEPSP. The enhancement of LTP by 0.1 microM CCh was significantly attenuated by 0.1 microM AF-DX 116, M2 receptor antagonist, but not by 0.1 microM pirenzepine, M1 receptor antagonist. Ten micromolar of carbachol reduced the amplitude of pretetanus fEPSP, while the magnitude of LTP was significantly larger than that in control slices to which tetanus was applied in a stimulus intensity producing pretetanus fEPSPs with an amplitude comparable to those during administration of 10 microM CCh. Neither 0.1 microM pirenzepine nor 0.1 microM AF-DX 116 had significant effect on the enhancement of LTP by 10 microM CCh. These results suggest that the induction of LTP at Schaffer collateral-CA1 synapse was enhanced through the activation of M2 receptors by CCh at a lower concentration.

Animals↗
PubMed1995

D1/D5 receptor agonists induce a protein synthesis-dependent late potentiation in the CA1 region of the hippocampus.

Agonists of the dopamine D1/D5 receptors that are positively coupled to adenylyl cyclase specifically induce a slowly developing long-lasting potentiation of the field excitatory postsynaptic potential in the CA1 region of the hippocampus that lasts for > 6 hr. This potentiation is blocked by the specific D1/D5 receptor antagonist SCH 23390 and is occluded by the potentiation induced by cAMP agonists. An agonist of the D2 receptor, which is negatively coupled to adenylyl cyclase through G alpha i, did not induce potentiation. Although this slow D1/D5 agonist-induced potentiation is partially independent of N-methyl-D-aspartate receptors, it seems to share some steps with and is occluded by the late phase of long-term potentiation (LTP) produced by three repeated trains of nerve stimuli applied to the Schaffer collateral pathway. Similarly, the D1/D5 antagonist SCH 23390 attenuates the late phase of the LTP induced by repeated trains, and the D1/D5 agonist-induced potentiation is blocked by the protein synthesis inhibitor anisomycin. These results suggest that the D1/D5 receptor may be involved in the late, protein synthesis-dependent component of LTP in the hippocampal CA1 region, either as an ancillary component or as a mediator directly contributing to the late phase.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1997

Block of LTP in rat hippocampus in vivo by beta-amyloid precursor protein fragments.

The effects of beta-amyloid precursor protein (beta-APP) fragments on plasticity of glutamtatergic synaptic transmission were examined in the hippocampus of urethane anaesthetized rats. I.c.v. injection of beta-amyloid (A beta) 1-40 and 1-42 and the C-terminal fragment CT105 greatly shortened the duration of high frequency stimulation-induced long-term potentiation (LTP) of field excitatory postsynaptic potentials in the CA1 area. Whereas in vehicle injected animals LTP was stable over a 5 h recording period, doses of these peptides (A beta 1-40, 0.4 and 3.5 nmol; A beta1-42, 0.01 nmol; CT105, 0.05 nmol) which did not affect baseline synaptic transmission abolished LTP within 3-5 h. The reduced duration of this form of synaptic plasticity may contribute to the cognitive deficits in Alzheimer's disease.

Amyloid beta-Protein Precursor↗
PubMed2001

Effects of anisomycin on LTP in the hippocampal CA1: long-term analysis using optical recording.

Long-term potentiation (LTP) in the hippocampal CA1 region and in the dentate gyrus consists of different stages: early LTP lasting minutes or several hours, and late LTP lasting longer than 4 h. It has been suggested that the late phase of LTP is dependent on protein synthesis. However, the experimental results of the effects of protein synthesis inhibitors are still confusing. We applied optical recording techniques to rat hippocampal slices, and re-evaluated the effects of a protein synthesis inhibitor, anisomycin, on LTP. Using a voltage-sensitive oxonol dye, NK3630 (RH482), LTP in the CA1 region could be monitored optically for a long-term period (7-8 h). In the presence of anisomycin, the potentiation of the EPSP (excitatory postsynaptic potential) lasted about 2-3 h, followed by a gradual decline in the signal amplitude. Statistically, significant effects of anisomycin were observed 6 h after LTP induction for 100 Hz tetanus and 8 h after LTP induction for 400 Hz tetanus. These results suggest that the early phase of LTP is independent of protein synthesis, while the late phase of potentiation (> 3-5 h) depends on protein synthesis.

Animals↗
PubMed1983

delta 9-Tetrahydrocannabinol and cannabidiol: dose-dependent effects on evoked potentials in the hippocampal slice.

The effects of (-) trans-delta 9-tetrahydrocannabinol (THC) and its metabolite cannabidiol (CBD) were investigated on evoked responses in the CA1 and dentate gyrus regions of the guinea pig transverse hippocampal slice. In both areas orthodromically evoked responses were enhanced by 10(-7) M THC, while 10(-6) M THC caused depression. Antidromic responses were not significantly affected. Antidromically-evoked inhibition in the CA1 region was decreased at low doses and unaffected at higher doses, while the facilitation by orthodromic interaction was unaffected at both dose ranges. The early part of the orthodromic field potential corresponding to the excitatory postsynaptic potential (EPSP) was enhanced at 10(-7) M in both areas. CBD (10(-6) M) decreased facilitation in CA1, and caused delayed excitation in the dentate granule layer. This study supports the conclusion that the biphasic effects of THC are dose dependent.

Anesthetics↗
PubMed1988

The involvement of nonspiking cells in long-term potentiation of synaptic transmission in the hippocampus.

In guinea pig hippocampal slices, stimulation of stratum radiatum during depolarization (with intracellular current injections) of nonspiking cells (presumed to be glia) in the apical dendritic area of CA1 pyramidal neurons resulted in a subsequent long-term potential of intracellularly recorded excitatory postsynaptic potentials as well as extracellularly recorded population spikes in the CA1 area. Tetanic stimulation of stratum radiatum resulted in a subsequent prolonged depolarization of the presumed glial cells, and this depolarization was smaller when the tetanus was given during the presence of 2-amino-5-phosphonovalerate or when the slices were exposed to Ca2+-free medium containing Mn2+ and Mg2+. These results suggest that glial depolarization is involved as one of the steps in generating long-term potentiation.

Action Potentials↗
PubMed1983

Action potential in neurons of motor nerve net of Cyanea (Coelenterata).

Neurons of the motor nerve net of the jellyfish Cyanea were impaled with microelectrodes for intracellular recordings. The cells have conventional, negative resting potentials and produce variable-amplitude action potentials with complex waveforms. The variability and complexity of these spikes is due to the superimposition of two classes of Ca2+-dependent potentials on an otherwise fast, clean action potential. Repetitive stimulation and ionic manipulation reveal that most superimposed potentials are chemically induced excitatory postsynaptic potentials (EPSPs). These account for the complexity and variability of the action potential. The remaining potential is interpreted as a Ca2+ component of the action potential. The action potential is a Na+-dependent but tetrodotoxin- (TTX) insensitive event. Repolarization is achieved by two pharmacologically distinct mechanisms: a tetraethylammonium- (TEA) and 4-amino-pyridine- (4-AP) sensitive K+ efflux and a delayed, Ca2+-activated, K+ efflux. The latter is responsible for the afterhyperpolarization that follows the action potential. The results indicated that these neurons are physiologically conventional. This is interesting in view of the phylogenetic primitiveness of the preparation and important, since it means that this preparation can provide generally useful information on chemical synaptic physiology.

4-Aminopyridine↗
PubMed1989

Role of extracellular space in hyperosmotic suppression of potassium-induced electrographic seizures.

1. Focal electrographic seizures arose in the CA1 region of rat hippocampal slices bathed in elevated (8.5 mM) external potassium [( K+]o). High [K+]o also induced spontaneous interictal bursts that originated in area CA3 and propagated to CA1. To examine the contribution to electrographic seizure initiation of excitatory mechanisms that are influenced by extracellular volume, we studied the effect of hyperosmotic expansion of interstitial volume on seizure occurrence, interictal bursts, and excitatory synaptic transmission. The tissue electrical resistance was also measured leading up to and during seizures. 2. Media made 5-30 mosmol/kg hyperosmotic by addition of agents restricted to the extracellular space (mannitol, sucrose, raffinose, L-glucose, dextran) rapidly and reversibly abolished [K+]o-induced spontaneous CA1 seizures in 86% of slices tested. However, similar increases in osmolality effected by agents that access the intracellular compartment (D-glucose, glycerol) did not influence electrographic seizure occurrence. Hyperosmotic changes with plasma membrane impermeable compounds, but not permeable compounds, produced significant concentration-dependent decreases (1-10%) in the electrical resistance of CA1 stratum pyramidale. Because tissue resistance is proportional to extracellular volume, these results suggest that hyperosmotic suppression of electrographic seizures is associated with expansion of the extracellular space in hippocampal slices. 3. Measurement of electrical resistance of the CA1 stratum pyramidale during spreading depression and electrographic seizure revealed an increase in tissue resistance to 122% and 108% of control, respectively. Furthermore, a slight (approximately 2%) but significant increase in electrical resistance gradually occurred over the 20 s immediately preceding seizure generation. The observed increase in tissue resistance suggests extracellular space is decreased during these events. 4. Hyperosmolality did not alter CA3 interictal burst frequency. However, burst intensity, estimated from the total length of the burst waveform, was significantly reduced in both the CA3 (83% control) and CA1 region (67% control) when osmotic changes were imposed by plasma membrane impermeant compounds. Additionally, media made hypoosmotic by removal of 7.5 mM NaCl reversibly increased burst intensity. 5. High [K+]o potentiated excitatory synaptic transmission and excitatory postsynaptic potential (EPSP) spike coupling.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Metabotropic glutamate receptor dependent EPSP and EPSP-spike potentiation in area CA1 of the submerged rat hippocampal slice.

1. We reexamined the important areas of conflict in (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid [(1S,3R)-ACPD]-induced potentiation of the field excitatory postsynaptic potential (EPSP) and, for the first time, investigated the role of mGluRs in EPSP-spike (E-S) coupling. 2. (1S,3R)-ACPD (10 microM) bath applied for 20 min consistently induced a long-lasting potentiation of the dendritic EPSP in area CA1 of submerged rat hippocampal slices, which was considerably faster in onset than described previously. 3. This effect was not associated with any change in presynaptic fiber volley but was dependent on both an intact CA3 connection, because removal of area CA3 blocked (1S,3R)-ACPD-induced potentiation, and also on functional N-methyl-D-aspartate (NMDA) receptors, because (1S,3R)-ACPD-induced potentiation was blocked by inclusion of the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (AP5; 50 microM). 4. (1S,3R)-ACPD induced a long-lasting potentiation of the population spike (PS) amplitude that was consistently larger than that of the EPSP measured in the cell body area. This EPSP-PS (E-S) potentiation was blocked by inclusion of the gamma-aminobuturic acid-A (GABAA) receptor antagonist, picrotoxin (50 microM). 5. E-S potentiation induced by high-frequency stimulation (HFS), which was of the same magnitude as that induced by (1S,3R)-ACPD, was blocked by the mGluR-selective antagonist (+)-alpha-methyl-4-carboxyphenylglycine (+MCPG; 250 microM). +MCPG also blocked HFS-induced long-term potentiation (LTP) of the EPSP measured in the cell body. 6. These results suggest that (1S,3R)-ACPD-induced potentiation is NMDA receptor dependent, contrary to some previous findings, and provide further evidence that both synaptic and E-S potentiation induced by (1S,3R)-ACPD share common mechanisms of expression with HFS-induced LTP. The data emphasize the important role of mGluRs in induction of EPSP LTP and E-S potentiation.

Animals↗