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At least 307 records · Page 17Linked to original sources
PubMed1980

Synaptic potentials in cat's lateral geniculate neurons during natural sleep with special reference to paradoxical sleep.

Juxtacellular DC recordings from lateral geniculate body (LGB) relay cells were performed in completely undrugged cats during natural sleep. Paradoxical sleep (P) was characterized by a decrease in synaptic (S) potentials and an increase in spike discharge as compared to slow wave sleep. During the P grouped discharges simultaneous with eye movements and cortical waves, a further decrease in S potentials accompanied by an increased cell excitability as indicated by the higher probability to elicit an antidromic spike occurred. The results suggest that the decrease of S potentials in P is not the result of presynaptic inhibition but that most of them reach firing level during the P grouped discharges.

Action Potentials↗
PubMed1990

Associative synaptic potentiation and depression: quantification of dissociable modifications in the hippocampal dentate gyrus favors a particular class of synaptic modification equations.

This report further characterizes associative long-term synaptic modification of the ipsilateral and contralateral synapses formed by the bilateral entorhinal cortical (EC) projection to the dentate gyrus (DG). The experimental model is the anesthetized hooded rat. The quantitative results qualify this system as a model for studying the rules of associative synaptic modification formulated in terms of individual synapses. Bilateral DG microelectrodes recorded both ipsilateral and contralateral EC-DG responses before and after brief, high-frequency EC conditioning stimulation. The weak contralateral pathway received high-frequency conditioning before, during, or after similar conditioning of the strong, converging ipsilateral pathway. Statistical analyses revealed two types of significant, dissociated synaptic modifications, which depend on the relationship of the ipsilateral and contralateral afferents. First, contralateral EC-DG responses potentiated or depressed when the converging ipsilateral responses concurrently either potentiated or remained unchanged. Second, contralateral EC-DG responses potentiated, depressed, or showed no change when the collateral ipsilateral responses concurrently either potentiated or remained unchanged. Correlation and contingency table analyses indicated that changes in the contralateral synaptic responses are not well predicted by changes at either neighboring synapses of the converging ipsilateral pathway or at synapses of the collateral ipsilateral pathway. The contingencies of associated pre- and postsynaptic activation determined by the conditioning paradigm, however, accurately predicted the altered synaptic responses of both ipsilateral and contralateral EC-DG pathways. The results imply that associative synaptic modification in the EC-DG system is specific to individual synapses and requires both appropriate presynaptic and postsynaptic activation. Because this system provides suitable controls for nonspecific effects of conditioning stimulation and because modification of neighboring synapses is dissociable, the EC-DG system can be used to study further those rules of activity-dependent associative modification that are formulated in terms of individual synapses. The discussion briefly considers published rules of synaptic modification, pointing out several rules that are not consistent with the experimental observations and one that agrees with the present results.

Animals↗
PubMed1995

Interactions between arachidonic acid and metabotropic glutamate receptors in the induction of synaptic potentiation in the rat hippocampal slice.

Perfusion of neither the metabotropic glutamate receptor agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD), nor arachidonic acid caused any long-term enhancement of synaptic transmission in the CA1 region of the rat hippocampal slice. However, co-perfusion of ACPD (50 microM) and arachidonic acid (10 microM) for 5 min induced a rapidly evoked and long-lasting enhancement of synaptic transmission. This enhancement persisted in the presence of D(-)-2-amino-5-phosphonopentanoic acid (40 microM) and is therefore independent of NMDA receptor activation. The potentiation was mimicked by perfusion of the phospholipase A2 activator melittin (10 micrograms/ml) for 5 or 10 min, or exogenous phospholipase A2 (1 microgram/ml) for 5 min, immediately before ACPD application. We propose a role for arachidonic acid in the induction of synaptic potentiation, possibly as a retrograde transmitter substance.

Animals↗
PubMed2000

Nicotinic acetylcholine receptor-mediated synaptic potentials in rat neocortex.

In the neocortex, fast excitatory synaptic transmission can typically be blocked by using excitatory amino acid (EAA) receptor antagonists. In recordings from layer II/III neocortical pyramidal neurons, we observed an evoked excitatory postsynaptic potential (EPSP) or current (EPSC) in the presence of EAA receptor antagonists (40-100 microM D-APV+20 microM CNQX, or 5 mM kynurenic acid) plus the GABA(A)-receptor antagonist bicuculline (BIC, 20 microM). This EAA-antagonist resistant EPSC was observed in about 70% of neurons tested. It had a duration of approximately 20 ms and an amplitude of 61.5+/-6.8 pA at -70 mV (n=35). The EAA-antagonist resistant EPSC current-voltage relation was linear and reversed near 0 mV (n=23). The nonselective nicotinic acetylcholine receptor (nAChR) antagonists dihydro-beta-erythroidine (DH beta E, 100 microM) or mecamylamine (50 microM) reduced EPSC amplitudes by 42 (n=20) and 33% (n=9), respectively. EPSC kinetics were not significantly changed by either antagonist. Bath application of 10 microM neostigmine, a potent acetylcholinesterase inhibitor, prolonged the EPSC decay time. EAA-antagonist resistant EPSCs were observed in the presence of antagonists of metabotropic glutamate, serotonergic (5-HT(3)) and purinergic (P2) receptors. The EAA-antagonist resistant EPSC appears to be due in part to activation of postsynaptic nAChRs. These results suggest the existence of functional synaptic nAChRs on pyramidal neurons in rat neocortex.

2-Amino-5-phosphonovalerate↗
PubMed1978

Impaired synaptic potentiation processes in the hippocampus of aged, memory-deficient rats.

A series of neurophysiological experiments was performed on the Schaffercommissural system of the hippocampus of aged and young anesthetized Fischer rats. The aged Fisher rats were previously found to exhibit retention performance deficits. No obvious differences were found between aged and young animals in amplitude, latency, stimulation threshold, or wave forms of typical synaptic responses when these were elicited by control (0.3 Hz) stimulation pulses. Further, the temporal curves of facilitation during a paired-pulse series were not different in aged and young animals. However, aged and young synapses showed consistently different responses during repetitive stimulation. Synapses of aged animals were deficient in frequency potentiation processes during 12 Hz stimulation; and the aged animals exhibited a delayed rise of post-tetanic synaptic potentiation following a 5 sec, 100 Hz stimulation train. Moreover, aged synapses 'exhausted' more rapidly during continuous 4 Hz stimulation. Throughout these studies a biphasic pattern of potentiation was observed during repetitive stimulation (brief potentiation, depression, renewed potentiation). Aged animals were deficient primarily in development of the second phase of potentiation. This pattern suggests an age-related impairment of some secondary process of potentiation, leading to an increased tendency to synaptic depression during and after stimulation. The possibility that the impaired hippocampal synaptic plasticity may be related to reported deficient behavioral plasticity in the aged animals is considered.

Action Potentials↗
PubMed2000

Enhanced synaptic potentiation in transgenic mice expressing presenilin 1 familial Alzheimer's disease mutation is normalized with a benzodiazepine.

Mutations in presenilin 1 (PS1) are the most common causes of familial Alzheimer's disease (FAD). We examined synaptic physiology in hippocampal brain slices of transgenic mice expressing the FAD-linked PS1 deletion of exon 9 variant. Basal excitatory transmission and paired-pulse facilitation in PS1 mutant mice were unchanged. Short- and long-term potentiation of excitatory transmission following high-frequency stimulation were greater in transgenic mice expressing mutant PS1. Mutants had enhanced synaptic inhibition, which may be a compensatory change offsetting an abnormally sensitized plasticity of excitatory transmission. Increasing inhibitory transmission in mutant animals even more with a benzodiazepine reverted synaptic potentiation to the levels of controls. These results support the potential use of benzodiazepines in the treatment of familial Alzheimer's disease.

Alzheimer Disease↗
PubMed1995

Excitatory synaptic potentials dependent on metabotropic glutamate receptor activation in guinea-pig hippocampal pyramidal cells.

1. Intracellular and extracellular recordings of CA1 and CA3 neurones were performed in guinea-pig hippocampal slices to examine synaptic activities dependent on metabotropic glutamate receptors (mGluRs). 2. Long burst activities were elicited by 4-aminopyridine in the presence of ionotropic glutamate receptor and GABAA receptor blockers (6-cyano-7-nitroquinoxaline-2,3-dione and 3-(RS-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid, and picrotoxin). Long bursts were also elicited by alpha-dendrotoxin. 3. Long bursts consisted of a 5-25 s depolarization with overriding action potentials and occurred rhythmically at intervals ranging from 1 to 20 min. Long bursts were generated in a population of CA3 neurones and the synchronized output elicited long bursts in CA1 cells. Depolarizing potentials underlying long bursts in CA1 cells had a reversal potential of -14.8 +/- 5.1 mV. 4. Long burst-associated depolarizations in CA1 neurones were suppressed by local application of L-(+)-2-amino-3-phosphonopropionic acid (L-AP3) and of the phenylglycine derivatives (+)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG), S-4-carboxyphenylglycine (S-4CPG) and S-4-carboxy-3-hydroxyphenylglycine (S-4C3HPG). (-)-MCPG or atropine application did not affect the long burst-associated depolarization. 5. Bath perfusion of (+)-MCPG (0.5 mM), S-4CPG (0.5 mM), S-4C3HPG (0.5 mM) or L-AP3 (1 mM) blocked the occurrence of long bursts. 6. The results suggest that the long burst-associated depolarizations are synaptic potentials dependent on mGluR activation. Activation of mGluRs may also be involved in the generation of synchronized long bursts in the CA3 region.

Action Potentials↗
PubMed1981

Giant synaptic potential hypothesis for epileptiform activity.

According to one hypothesis, the paroxysmal depolarizing shift observed in the penicillin model of epilepsy results from a giant excitatory postsynaptic potential. This hypothesis has recently been questioned, primarily because it has never been subjected to rigorous experimental examination. Four quantitative predictions were derived from this hypothesis and tested in CA3 pyramidal neurons of the hippocampus. The four critical predictions concern the behavior of the paroxysmal depolarizing shift under current- and voltage-clamp conditions as a function of membrane potential. The experiments confirmed all four predictions.

Action Potentials↗
PubMed1987

Long-term potentiation in the hippocampus using depolarizing current pulses as the conditioning stimulus to single volley synaptic potentials.

The conditions responsible for the associative properties of long-term potentiation (LTP) were examined in the CA1 region of the hippocampal slice preparation. Intracellularly recorded EPSPs resulting from single-volley stimulation at low frequency (0.15-0.1 Hz) in the stratum radiatum or oriens were paired with depolarizing current pulses (50-100 msec) injected through the recording microelectrode. It is shown that these EPSPs, when paired with pulses of sufficient magnitude, become potentiated. This potentiation generally reached a peak after 20-30 pairing events and could outlast the conditioning period by more than 1 hr. It was specific to the paired input, was blocked by 2-amino-5-phosphonovalerate (APV) and was largely blocked by prior homosynaptic tetanization (and vice versa). In experiments performed with picrotoxin (PTX) in the bath, EPSPs were potentiated using 2-4 nA current pulses, with somewhat higher values in normal solution. The effective current pulses, in both normal and PTX solution, produced a repetitive spike discharge of 7-11 spikes (per 100 msec), and within this range, higher frequencies were associated with larger potentiations. However, since similar degrees of EPSP potentiation were observed following blockade of spike activity by intracellular QX-314, spike activity was not the primary conditioning factor. For the potentiation to appear, the EPSP had to occur together with the current pulse or precede it by less than about 100 msec. No potentiation was observed when the EPSP immediately succeeded the pulse. The results suggest that the cooperativity aspect of LTP is related to a need for sufficient postsynaptic depolarization.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1998

Arachidonic acid metabolites and the synaptic potentiation evoked by activation of metabotropic glutamate receptors.

We have previously shown that coapplication of arachidonic acid (10 microM) and (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD, 50 microM) evokes an enhancement of synaptic transmission in the CA1 region of the rat hippocampal slice. Here we have investigated whether the metabolites of arachidonic acid are implicated in this potentiation. Inclusion of the cyclo-oxygenase inhibitor indomethacin (10 microM) did not block the potentiation induced by coapplication of arachidonic acid and ACPD. However, the presence of either the cyclo-, lipo- and epoxygenase inhibitor 5,8,11,14-eicosatetraynoic acid (ETYA, 20 microM), or the lipoxygenase inhibitor nordihydroguaiaretic acid (10 microM), prevented the long-lasting enhancement. The results suggest that the lipoxygenase and epoxygenase metabolites of arachidonic acid may be involved in the induction of this form of synaptic potentiation.

5,8,11,14-Eicosatetraynoic Acid↗