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At least 433 records · Page 24Linked to original sources
PubMed2006

Calcium signaling pathways mediating synaptic potentiation triggered by amyotrophic lateral sclerosis IgG in motor nerve terminals.

Sporadic amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that affects particularly motoneurons. Several pieces of evidence suggested the involvement of autoimmune mechanisms mediated by antibodies in ALS. However, the significance of those antibodies in the disease and the underlying mechanisms are unknown. Here we showed that IgG purified from a group of sporadic ALS patients, but not familial ALS patients, specifically interact with the presynaptic membrane of motoneurons through an antigen-antibody interaction and modulated synaptic transmission. Immunoreactivity against nerve terminals showed strong correlation with synaptic modulation ability. In addition, several controls have ruled out the possibility for this synaptic modulation to be mediated through proteases or nonspecific effects. Effective IgG potentiated both spontaneous and asynchronous transmitter release. Application of pharmacological inhibitors suggested that activation of this increased release required a nonconstitutive Ca2+ influx through N-type (Cav2.2) channels and phospholipase C activity and that activation of IP3 and ryanodine receptors were necessary to both activate and sustain the increased release. Consistent with the notion that ALS is heterogeneous disorder, our results reveal that, in approximately 50% of ALS patients, motor nerve terminals constitutes a target for autoimmune response.

Adult↗
PubMed1993

[Effects of 6-OHDA lesions of the bilateral dorsal noradrenergic bundle on learning-dependent long-term synaptic potentiation in dentate gyrus].

In the present study, the role of NE in learning-dependent long-term potentiation (LdLTP) was investigated by examining the effects of 6-hydroxydopamine (6-OHDA) lesion made in the bilateral dorsal noradrenergic bundle on the changes of synaptic efficacy in dentate gyrus (DG) and related conditioned response during drinking conditioning. Bilateral injection of 6-OHDA (12 micrograms/4 microliters) into the dorsal noradrenergic bundle caused a continuous decrease of the amplitude of population spike (PS) reaching a value of 50 +/- 6.3% and 28 +/- 6.4% respectively at the 6th and the 12th day after injection of the drug. During this period of 7 days, the LdLTP could not be produced in spite of 20 trainings per day for a total of 140 trials, and the conditioned drinking response could not be established. The above results indicate that normal levels of norepinephrine in the hippocampus are necessary to the establishment of LdLTP in the DG and suggest that the development of LdLTP in the DG may be modulated by the nucleus locus ceruleus via the dorsal noradrenergic bundle.

Animals↗
PubMed1993

Co-administration of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid and arachidonic acid potentiates synaptic transmission in rat hippocampal slices.

Perfusion of the 1S,3R isomer of trans-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD, 50 microM), or arachidonic acid (10 microM), for 5 min produced only depression of the field excitatory postsynaptic potential recorded in the CA1 region of rat hippocampal slices from which the CA3 region had been removed. However, perfusion of t-ACPD and arachidonic acid in combination induced a rapid potentiation of the response which in 4/6 slices was maintained for at least 90 min.

Animals↗
PubMed1982

Vincamine: a psychogeriatric agent blocking synaptic potentiation in hippocampus.

The action of vincamine on the physiology of the CA1 region of the in vitro hippocampal slice preparation was investigated. At concentrations of 1, 10 and 100 microM, a five-minute perfusion with vincamine did not affect the synaptically-mediated activation of pyramidal neurons evoked by stimulation of the Schaffer-commissural fiber system. The effect of vincamine on the excitability of the pyramidal neurons was investigated by studying its effect on the antidromically-elicited field potential and the input-output relation of Schaffer-commissural fiber input. No effect on either of the two parameters was seen at a concentration of 100 microM of vincamine. Vincamine did, however, attenuate both the post-tetanic (PTP) and long-term potentiation (LTP) evoked by repetitive stimulation of the Schaffer-commissural fiber system. At a concentration of 100 microM of vincamine, PTP was significantly reduced and LTP was almost completely suppressed.

Action Potentials↗
PubMed1986

Induction of synaptic potentiation in hippocampus by patterned stimulation involves two events.

Electrical stimulation of axons in the hippocampus with short high-frequency bursts that resemble in vivo activity patterns produces stable potentiation of postsynaptic responses when the bursts occur at intervals of 200 milliseconds but not 2 seconds. When a burst was applied to one input and a second burst applied to a different input to the same target neuron 200 milliseconds later, only the synapses activated by the second burst showed stable potentiation. This effect was observed even when the two inputs innervated completely different regions of the postsynaptic cells; but did not occur when the inputs were stimulated simultaneously or when the second burst was delayed by 2 seconds. Intracellular recordings indicated that the first burst extended the decay phase of excitatory postsynaptic potentials evoked 200 milliseconds later. These results suggest that a single burst of axonal stimulation produces a transient, spatially diffuse "priming" effect that prolongs responses to subsequent bursts, and that these altered responses trigger spatially restricted synaptic modifications. The similarity of the temporal parameters of the priming effect and the theta rhythm that dominates the hippocampal electroencephalogram (EEG) during learning episodes suggests that this priming may be involved in behaviorally induced synaptic plasticity.

Animals↗
PubMed1986

Low concentrations of penicillin reveal rhythmic, synchronous synaptic potentials in hippocampal slice.

Field and intracellular recordings were used to examine the effects of varying concentrations of penicillin on synchronous CA3 activity in guinea pig hippocampal slices. In addition to the high-amplitude bursts, extracellular recordings in the distal apical dendrites (700-1200 microns from the soma) revealed biphasic mini field potentials (MFPs) which were not evident at the soma in 2000 IU/ml. A long-lasting (76 ms) field potential (A potential) with a waveform similar to the positive component of the MFP initiated the bursts. The cellular correlate of the positive component of the MFP and of the A potential appeared to be an EPSP and that of the negative component of the MFP and IPSP. Reductions of penicillin concentration below 2000 IU/ml (3.4 mM) decreased the burst rate and amplitude and increased burst threshold. At concentrations below 250 IU/ml the bursts were blocked and the MFPs increased in amplitude and occurred rhythmically at a mean frequency of 2.6 Hz. At intermediate concentrations the bursts arose from the rhythmic background. This activity more closely resembles that recorded with electroencephalography in human epileptic foci than does the high-dose penicillin preparation and may provide a better model of epileptiform discharge.

Action Potentials↗
PubMedDate not supplied

Complex composition of synaptic potentials of the rubrospinal neurons to corticofugal impulses.

Complex, multicomponent excitatory postsynaptic potentials (EPSPs) of the red nucleus rubrospinal neurons evoked by stimulation of the sensorimotor cortex and associative field of the parietal cortex were studied in acute experiments on pentobarbitalized cats by the intracellular recording technique. Complex cortical EPSPs were recorded in two-thirds of the studied number of neurons. Monosynaptic nature of the first two components of EPSPs evoked by corticofugal impulses propagating at an average velocity of 18.5 ms and 7.5 ms was revealed. Participation of the corticospinal input in the genesis of EPSPs mentioned was revealed by selective activation of corticospinal fibers on the level of medullary pyramids as well as by studying peculiarities of their interaction with effects of cortical stimulation. It was shown that both corticospinal and corticorubral (predominantly slow conducting) neurons participate in the genesis of the first two components of complex EPSPs.

Animals↗
PubMed1976

The effect of polarizing currents on unitary Ia excitatory post-synaptic potentials evoked in spinal motoneurones.

1. Depolarizing and hyperpolarizing currents were applied to motoneurones in which unitary Ia e.p.s.p.s were evoked. The results concentrate on those e.p.s.p.s which had time courses which were compatible with somatically located synapses. 2. No reversal of these e.p.s.p.s was observed. Depolarizing currents up to 150 nA simply reduced the peak amplitude. 3. Hyperpolarizing currents caused little, if any, increase in the peak amplitude of the e.p.s.p. The time course of decay became briefer as the membrane was hyperpolarized. 4. Changes in decay time course of the e.p.s.p. which accompanied depolarization and hyperpolarization could be attributed to changes in membrane conductances, rather than to changes in synaptic current time course. 5. The failure of the e.p.s.p. to increase with hyperpolarization was shown to be due to the failure of the synaptic current to increase, rather than to the shunting of anomalous rectification. 6. Chemical and electrical transmission are evaluated against these results and those of the preceding papers.

Action Potentials↗
PubMed1981

Long-term facilitation of excitatory synaptic transmission in single motor cortical neurones of the cat produced by repetitive pairing of synaptic potentials and action potentials following intracellular stimulation.

The effects of postsynaptic firing activity on excitatory postsynaptic potentials (EPSPs) were studied in the motor cortex of anaesthetized cats. Postsynaptic firing was induced by 1-5 nA cathodal current pulses via the recording intracellular microelectrode, while EPSPs were elicited by thalamic, callosal, pyramidal tract and somatosensory stimuli. In 102 cells, EPSP-spike stimulus pairs were applied with 0.2-1/sec frequency and 10-100 msec interstimulus intervals. In 42 neurones, reversible facilitation of paired EPSPs appeared lasting from 4 to 47 min. The synaptic facilitation in most cases was accompanied by membrane depolarization and an increase in input resistance. The effectiveness of current induced action potentials upon test EPSPs provided evidence for the postsynaptic localization of plastic changes occurring in conditioning experiments.

Action Potentials↗
PubMed1984

Characteristics of a slow hyperpolarizing synaptic potential in rat hippocampal pyramidal cells in vitro.

An orthodromically evoked late hyperpolarizing potential (LHP) was studied using intracellular recording techniques in rat hippocampal CA1 pyramidal cells in vitro. Several tests indicated that the LHP is not blocked by GABA antagonists, but rather comprises the initial portion of the stimulation-induced burst afterhyperpolarization (AHPs) produced in the presence of these antagonists. Bath application of magnesium (Mg) or 8-bromo adenosine 3',5'-cyclic monophosphate (cAMP), or intracellular injection of ethyleneglycol-bis (beta-amino-ethylether)-N,N'-tetraacetic acid (EGTA) blocked the late portion of the AHPs, at times when the early portion was only slightly or not at all affected. The late part of the AHPs was also associated with the voltage-dependent components of the burst, whereas the early part was not. Both the early part of the burst AHPs and the LHP in standard saline have similar time courses and dependence on membrane potential. The LHP was nullified by hyperpolarization of the membrane in extracellular potassium concentrations [( K]o) of 5.4 mM and below and could be reversed in [K]o above 5.4 mM. The apparent reversal potential for the LHP followed shifts in [K]o as predicted by the Nernst equation and is, therefore, probably a K-dependent potential. No specific antagonist of the LHP from among several K conductance blockers was found, however. An alternative hypothesis, that the LHP might be an electrogenic pump effect was not supported. Ouabain depressed the LHP; however this effect was probably nonspecific and due, in part, to a ouabain-induced increase in [K]o. Decreasing temperature in the range 37-22 degrees C prolonged but did not block the LHP. The LHP was enhanced by increases in extracellular calcium concentration and depressed by high [Mg]o or cadmium. It was associated with a small (14%) decrease in total resting input resistance. In cells depolarized to approximately 0 mV, regenerative voltage-dependent potentials were blocked; however, an LHP still occurred. The LHP was not found to be dependent on the excitatory postsynaptic potential (EPSP). With weak stimuli LHP and EPSP amplitudes were uncorrelated and the EPSP was more resistant than the LHP to block by high [Mg]o. The LHP continued to occur when the EPSP was reversed in depolarized cells. The LHP may be mediated by interneuronal circuitry within a slice. In GABA antagonists the LHP occasionally occurred spontaneously at regular intervals.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Participation of voltage-gated conductances on the response succeeding inhibitory synaptic potentials in the crayfish slowly adapting stretch receptor neuron.

1. We examined the contribution of voltage-gated conductances to inhibitory postsynaptic potential (IPSP) effects under current clamp in silent and spiking slowly adapting stretch receptor neurons (SN1s) in the slow receptor muscle of the crayfish Procambarus. The receptor exemplifies the simplest inhibitory neural circuit, with one presynaptic and one postsynaptic neuron. The effects of synaptic inhibition were compared with the outcome of hyperpolarizing current pulses. Because pulse effects were exclusively due to postsynaptic mechanisms, an estimation of the synaptic or extrasynaptic origin of the results of IPSP was possible. 2. Inhibition by single IPSPs increased gradually with the time elapsed from the preceding spike in 60% of the spiking SN1s. However, early IPSP arrivals were exclusively excitatory in the rest of the cases. Inhibition was restricted to a single expanded SN1 interspike interval, but the early excitation and the postinhibitory rebound lasted several intervals. Rebound was invariably present; it was the only consequence of IPSPs in silent receptors and could be extremely long lasting (> 25 s). 3. The membrane potential of the SN1 neuron was clamped at hyperpolarized values (greater than -65 mV) by prolonged IPSP barrages at high rate (> 20/s). A prominent depolarizing sag and a gradual reduction of the IPSP amplitude were observed with prolonged presynaptic stimulation. There were subthreshold IPSP amplitude oscillations consisting of gradual increases and decreases of the post-IPSP peak depolarization at lower presynaptic rates. IPSP amplitude variations (< or = 10 mV) were primarily due to larger local responses. 4. Essentially all IPSP effects were mimicked by hyperpolarizing pulses. Sag was also evoked by pulses and was accompanied by a gradual conductance increase preceded by a brief initial drop. Sag and rebound were markedly reduced by Cs+ (2 mM) and tetrodotoxin (1 microM) and less by Ba2+ (5 mM) or tetraethylammonium (25 mM) superfusion. Both were somewhat decreased by acetylcholine (30 microM), which also markedly depolarized and accelerated firings, results which were usually reduced by atropine (10 microM). 5. In conclusion, IPSP and hyperpolarizing pulse effects were essentially identical, implying that extrasynaptic membrane properties were decisive. Interestingly, net excitatory consequences were usual, effectively increasing sensitivity and reducing the sensory threshold. Pharmacological evidence is provided suggesting that the hyperpolarization-activated current, IQ, and also probably the K+ M-current, the A-current, and the low-threshold, persistent Na+ conductances participate in sag and rebound genesis.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Isoproterenol potentiates synaptic transmission primarily by enhancing presynaptic calcium influx via P- and/or Q-type calcium channels in the rat amygdala.

The effects of selective beta-adrenergic receptor agonist isoproterenol (Iso) on neuronal excitability and synaptic transmission were investigated in brain slices of rat amygdala. Iso (15 microM) produced a long-lasting enhancement of the EPSP that was not blocked by pretreatment with 20 microM D-2-amino-5-phosphonovalerate (D-APV) alone or D-APV in combination with kynuretic acid (1 mM). The sensitivity of postsynaptic neurons to the glutamate receptor agonist AMPA was unchanged by Iso pretreatment. Superfusion of Iso reversibly blocked the after-hyperpolarization (AHP) that followed a depolarizing current pulse and caused more action potential firing. Intracellular application of a selective inhibitor of the catalytic subunit of cAMP-dependent protein kinase A blocked the effect of Iso on the AHP, whereas Iso-induced potentiation was entirely normal in the same neuron. In addition, Iso decreased the magnitude of paired-pulse facilitation, which is consistent with a presynaptic mode of action. Substituting the Mg2+ for Ca2+ in the medium completely abolished the Iso-induced enhancement of the EPSP. The effect of Iso also was blocked by low concentrations of omega-agatoxin-IVA, but not by nifedipine or omega-conotoxin-GVIA. These results suggest that Iso enhances synaptic transmission in the amygdala via a presynaptic site of action: the mechanism underlying the potentiating effect likely is attributable to an increased Ca2+ influx through P- and/or Q-type Ca2+ channels.

Action Potentials↗