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At least 379 records · Page 21Linked to original sources
PubMed1993

Developmental changes in NMDA and non-NMDA receptor-mediated synaptic potentials in rat neocortex.

1. In vitro slices of frontal neocortex were prepared from rat pups 3-14 days of age. Whole-cell patch-clamp recordings were obtained from layer II-III cortical neurons, and measurements of passive membrane properties were made. The development of evoked synaptic excitation and inhibition was also examined with the use of current- and voltage-clamp techniques. 2. Pharmacological separation of excitatory synaptic activity into both N-methyl-D-aspartate (NMDA) and non-NMDA receptor-mediated components was accomplished by application of D(-)2-amino-5-phosphonovaleric acid (APV), D(-)2-amino-7-phosphonoheptanoic acid (AP7), and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Inhibitory synaptic events were described according to their reversal potentials and modulation by the GABAA receptor antagonist bicuculline methiodide (BMI). 3. Pups were grouped into three categories on the basis of age: postnatal day (PN) 3-5, PN 6-8, and PN 9-14. In slices from PN 3-5 pups, neurons exhibited high input resistances (Rn) and relatively low resting membrane potentials (RMP). Rns decreased, and RMPs became more negative with development. At all ages studied, current-voltage relationships measured in current clamp were relatively linear, with inward rectification observed in some neurons at hyperpolarized membrane potentials. Neurons in each group were capable of firing overshooting action potentials. 4. Local stimulation in layer IV-V at 0.033 Hz elicited depolarizing excitatory postsynaptic potentials (EPSPs) in neurons from all three age groups. In PN 3-5 neurons, EPSPs were characterized by a long duration and latency to peak. By PN 6-8, EPSPs had decreased significantly in both duration and latency-to-peak. Some neurons responded with a single-component EPSP, whereas others exhibited multicomponent EPSPs consisting of distinct early and late components. In PN 3-5 neurons, increasing the frequency of stimulation from 0.033 to 1 Hz resulted in an overall decrease in the amplitude of the entire EPSP, whereas in PN 6-8 neurons the main decrease was observed in the late EPSP. 5. Excitatory postsynaptic currents (EPSCs) recorded in both PN 3-5 and PN 6-8 neurons were shorter in duration than corresponding EPSPs and consisted of both early and late components. Early EPSCs routinely increased in amplitude with hyperpolarization at all ages. In PN 3-5 neurons, the voltage dependence of late EPSCs was variable. By PN 6-8, late EPSCs always exhibited a region of reduced amplitude from -45 to -90 mV. The reversal potential for both early and late EPSCs was near +10 mV.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed2000

Postnatal synaptic potentiation: delivery of GluR4-containing AMPA receptors by spontaneous activity.

To examine how functional circuits are established in the brain, we studied excitatory transmission in early postnatal hippocampus. Spontaneous neural activity was sufficient to selectively deliver GluR4-containing AMPA receptors (AMPA-Rs) into synapses. This delivery allowed non-functional connections to transmit at resting potentials and required NMDA receptors (NMDA-Rs) but not CaMKII activation. Subsequently, these delivered receptors were exchanged with non-synaptic GluR2-containing AMPA-Rs in a manner requiring little neuronal activity. The enhanced transmission resulting from this delivery and subsequent exchange was maintained for at least several days and required an interaction between GluR2 and NSF. Thus, this sequence of subunit-specific trafficking events triggered by spontaneous activity in early postnatal development may be crucial for initial establishment of long-lasting functional circuitry.

Animals↗
PubMed1982

Miniature synaptic potentials absent from motoneurons of intact spinal cord.

Intracellular recordings were made from lumbar motoneurons of decerebrate, paralyzed frogs with minimal surgical damage to the spinal cord. Detectable spontaneous synaptic activity was absent in most motoneurons, as compared with published in vitro recordings. Lesions of the thoracic cord increased the incidence of small spontaneously occurring potentials. This suggests that spontaneous quantal release of transmitter observed in isolated preparations is a consequence of presynaptic neuronal damage.

Animals↗
PubMed1990

Long-term synaptic potentiation in the amygdala.

The manner in which the circuitry of the amygdala computes its suspected mnemonic functions has been a mystery, partly because the cytoarchitectual complexity of this nuclear group has impeded the necessary cellular analysis. Here we report in vitro methods and results that may help elucidate cellular learning mechanisms in amygdala neurons. The amygdala brain slice preparation was combined with the single-electrode clamp (SEC) technique for intracellular analysis of membrane properties and synaptic responses. With respect to the active and passive membrane properties, we found considerable diversity among the population of cells that were sampled in the lateral and basolateral nuclei (n = 85). Synaptic inputs to these neurons were studied by stimulating the external capsule (EC), which was shown to produce a complex response that typically consisted of an excitatory followed by an inhibitory component. Based on several criteria, the excitatory component appeared to reflect a monosynaptic connection from the EC. One immediate goal was to discover whether the excitatory component displays the phenomenon of long-term potentiation (LTP)--a persistent increase in synaptic strength that can be induced by brief periods of the appropriate synaptic stimulation. Indeed, we found that high-frequency (100 Hz) stimulation of the EC induced LTP in 80% of the cells from which suitable recordings were obtained (n = 20). This finding of LTP in the amygdala is significant in regard to current efforts to explore linkages between this use-dependent form of synaptic plasticity and rapid kinds of associative learning.

Amygdala↗
PubMed1993

Calcitonin gene-related peptide potentiates synaptic responses at developing neuromuscular junction.

Protein phosphorylation is important in synaptic transmission and plasticity. At the neuromuscular junction, phosphorylation of acetylcholine (ACh) receptor-channels increases the rate of agonist-induced channel desensitization. In contrast, potentiation of ACh channel activity through protein phosphorylation has not been described. We report here that calcitonin gene-related peptide (CGRP), a neuropeptide present at presynaptic motor nerve terminals, enhances the postsynaptic response at developing neuromuscular junctions by increasing the burst duration of embryonic ACh channels. The effect of CGRP on these ACh channels is mimicked by dibutyryl-cyclic AMP and by cAMP-dependent protein kinase (PKA) and prevented by a specific peptide inhibitor of PKA. Moreover, postsynaptic inhibition of PKA reduced the amplitude and decay time of spontaneous synaptic currents, suggesting that endogenous CGRP may act as a potentiating factor during the early phase of synaptogenesis.

Acetylcholine↗
PubMed1984

Characterization of synaptic potentials in hindlimb extensor motoneurons during L-DOPA-induced fictive locomotion in acute and chronic spinal cats.

Intracellular recordings were carried out in extensor hindlimb motoneurons during L-DOPA-induced fictive locomotion from acute and chronically spinalized cats. It was demonstrated that motoneurons in chronic animals exhibited irregularly occurring, high frequency discharges within a given burst of a spike train, and sporadic membrane potential depolarizations and hyperpolarizations correlated with extensor and flexor nerve filament activity, respectively, during the locomotor cycle. In contrast, motoneurons recorded from acute cats demonstrated smooth membrane potential fluctuation and regularly occurring low frequency spike discharges. These results indicate that the pharmacologically activated central pattern generator (CPG) for locomotion in young adult chronic cats spinalized at two weeks of age produces disorganized locomotor-like patterns in the absence of sensory feedback. It is suggested that the above-mentioned characteristics of membrane potential fluctuations and spike discharges are not due to alterations in the motoneuron membrane properties, but instead are due to changes in the inputs to the motoneurons.

Animals↗
PubMed1990

[Effect of scopolamine and picrotoxin on the learning-dependent long-term synaptic potentiation].

The purpose of this study was to investigate the effects of microinjection of scopolamine, a M-cholinergic antagonist and picrotoxin, a GABA-ergic antagonist into the rat hippocampal CA3 area on the learning-dependent long-term potentiation (LDLTP) during the establishment, extinction and re-establishment of conditioned drinking response. Following stimulation of the perforant path, field potentials of hippocampal CA3 of freely moving rats were recorded. The results were as follows: the synaptic efficacy and the development of LDLTP in hippocampal CA3 were depressed significantly by scopolamine, but the extinction of LDLTP was accelerated. Picrotoxin significantly enhanced synaptic efficacy and facilitated the development of LDLTP, but it depressed the extinction of LDLTP. Meanwhile, the establishment or extinction of drinking conditioning was correspondingly depressed or accelerated. Moreover, the development of LDLTP and its extinction preceded the development and extinction of drinking conditioning. The results provide further evidence indicating that LDLTP might be one of the neuronal mechanisms underlying behavioral learning and memory. Moreover, it seems that M-cholinergic receptors and GABA-ergic receptors in rat hippocampal CA3 area are involved in the development and retention of LDLTP.

Animals↗
PubMed1999

Synaptic potentiation induced by a protein factor in cultured cerebral neurons.

1. We reported in a previous paper that long-lasting enhancement of spontaneous excitatory post synaptic currents (SEPSCs) in cultured chick cerebral neurons was induced by exposure to a conditioned medium (CM) prepared by Mg(2+)-free treatment of neurons. This suggested that the CM contained a diffusible factor(s) for the potentiation. 2. In this paper, the factor(s) was shown to be a protein(s) by heat and trypsin treatment of the CM. 3. The factor induced the potentiation within 5 min, but it was not required for maintenance of increased SEPSCs. 4. The factors in CM induced the potentiation without protein synthesis. 5. Protein synthesis at least in postsynaptic neurons, was indispensable to induce the potentiation by the Mg(2+)-free condition.

Animals↗
PubMed1973

The amplitude, time course and charge of unitary excitatory post-synaptic potentials evoked in spinal motoneurone dendrites.

1. Group Ia e.p.s.p.s were recorded from lumbosacral motoneurones in anaesthetized cats after almost complete section of the appropriate dorsal roots. The cable parameters of these same motoneurones were obtained from the voltage response to a brief intracellular current pulse, as described in Iansek & Redman (1973).2. A total of thirty-three e.p.s.p.s, recorded in thirty different motoneurones, were analysed. E.p.s.p.s which were recorded in motoneurones which were not studied using an intracellular current pulse, or in which the resting membrane potential fell below 50 mV, were not considered. Also, e.p.s.p.s whose time course indicated more than one synaptic site of origin were not analysed. The selected e.p.s.p.s were plotted on a semilogarithmic amplitude scale, and their 10-90% rise time, half-width and peak amplitudes were measured.3. Using the previously determined values of the cable parameters L, rho(infinity) and tau(m), the rise time and half-width of each e.p.s.p. were used to determine the synaptic location (X), and the synaptic current time course (alpha). Twenty-seven e.p.s.p.s had time courses which allowed a value of X and alpha to be determined within the constraints of the measured cable parameters. The remaining six e.p.s.p.s either required an extension of the dendritic cable to be localized, or their time course was not compatible with a brief synaptic current.4. The synaptic locations lie in the range 0 (soma) to 1.25 space constants. When expressed as a fraction of the length of the dendritic cable, all but four of the twenty-seven e.p.s.p.s were located on the proximal half of the dendrites.5. The time to peak of synaptic current for each e.p.s.p. ranged from 30 to 390 musec, although a majority (70%) lay in the range 50 to 200 musec. There was no significant correlation between time to peak of synaptic current and synaptic location.6. The peak amplitude of e.p.s.p.s at the soma showed no significant correlation with synaptic location.7. The peak amplitude, and the cable parameters for each e.p.s.p. were used to compute the time course and amplitude of each e.p.s.p. at its point of generation on various fractions of the total dendritic cable, using the results derived in Redman (1973). These calculations showed the greatly increased rate of decay of e.p.s.p.s at their point of generation. Assuming that the synaptic input was restricted to one tenth of the total dendritic tree, the range of peak amplitudes at the synaptic site was from less than 100 muV (soma) to 20 mV.8. The net inward positive charge crossing the synaptic junction was calculated from the voltage-time integral of the e.p.s.p., as was the net outward positive charge crossing the soma membrane. These calculations showed that dendritic synapses caused up to ten times more net charge to be displaced across the synaptic junction than did synapses on or near to the soma, for similar durations of synaptic current. Similarly, dendritic synapses were generally more effective than somatic synapses in displacing charge across the soma membrane. It was concluded that the average quantal content in the conductance change at dendritic synapses is significantly greater than for somatic synapses.9. Some implications of the results for general integrative mechanisms in dendrites are discussed.

Animals↗
PubMed1982

Long-term synaptic potentiation in the superior cervical ganglion.

Brief tetanic stimulation of the preganglionic nerves to the superior cervical ganglion enhances the postganglionic response to single preganglionic stimuli for 1 to 3 hours. This long-term potentiation of transmission through the ganglion is apparently not attributable to a persistent muscarinic action of the preganglionic neurotransmitter, acetylcholine, since neither the magnitude nor the time course of the phenomenon is reduced by atropine. The decay of long-term potentiation can be described by a first-order kinetic process with a mean time constant of 80 minutes. We conclude that long-term potentiation, once considered a unique property of the hippocampus, is in fact a more general feature of synaptic function. This form of synaptic memory may significantly influence information processing and control in other regions of the nervous system, including autonomic ganglia.

Animals↗
PubMed1998

Synaptic potentials mediated via alpha-bungarotoxin-sensitive nicotinic acetylcholine receptors in rat hippocampal interneurons.

Exogenous application of acetylcholine elicits inward currents in hippocampal interneurons that are mediated via alpha-bungarotoxin-sensitive nicotinic acetylcholine receptors, but synaptic responses mediated via such receptors have never been reported in mammalian brain. In the present study, EPSCs were evoked in hippocampal interneurons in rat brain slices by electrical stimulation and were recorded by using whole-cell voltage-clamp techniques. Nicotinic EPSCs were isolated pharmacologically, using antagonists to block other known types of ligand-gated ion channels, and then were tested with either alpha-bungarotoxin or methyllycaconitine, which are selective antagonists for nicotinic acetylcholine receptors that contain the alpha7 receptor subunit. Each antagonist proved highly effective at reducing the remaining synaptic current. Evoked alpha7-mediated nicotinic EPSCs also were desensitized by superfusion with 1 microM nicotine, had extrapolated reversal potentials near 0 mV, and showed strong inward rectification at positive potentials. In several interneurons, methyllycaconitine-sensitive spontaneous EPSCs also were observed that exhibited a biphasic decay rate very similar to that of the alpha7-mediated evoked response. These studies provide the first demonstration of a functional cholinergic synapse in the mammalian brain, in which the primary postsynaptic receptors are alpha-bungarotoxin-sensitive nicotinic acetylcholine receptors.

Aconitine↗
PubMed2001

PKC and CaMKII dependent synaptic potentiation in cultured cerebral neurons.

We have reported that the long-lasting potentiation of spontaneous excitatory postsynaptic currents (SEPSCs) was induced by a Mg(2+)-free treatment in cultured chick cerebral neurons and a factor(s) extracellularly released during the treatment could induce the potentiation by itself. In this paper, protein kinase C (PKC) and calcium/calmodulin-dependent protein kinase type II (CaMKII) but not protein kinase A (PKA) were reported to contribute to the potentiation mechanism during a step between the activation of the N-methyl-D-aspartate receptors by the Mg(2+)-free treatment and the secretion of the protein factor(s).

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1985

Thyrotropin-releasing hormone mimics descending slow synaptic potentials in rat spinal motoneurons.

Thyrotropin-releasing hormone (TRH) produced a depolarization in lumbar motoneurons of neonatal rats. The depolarization by TRH persisted after extracellular Ca2+ was replaced by Mg2+ or Mn2+, indicating its direct action upon motoneurons. Stimulation of the ventral descending tract at the lower thoracic segment evoked slow excitatory postsynaptic potentials (e.p.s.ps) lasting 20-30 s in every motoneuron. Both the TRH-induced depolarization and descending slow e.p.s.p. were accompanied by a decrease in input conductance of motoneurons. When the membrane potential of the motoneuron was shifted, both the TRH-induced depolarization and slow e.p.s.p. became larger in amplitude during depolarization and smaller during hyperpolarization. However, they could not be reversed in polarity by hyperpolarization. During the depolarization of motoneuron produced by TRH application, the slow e.p.s.p. was markedly reduced in amplitude, suggesting the involvement of identical ionic mechanisms in the two responses. After incubation of the isolated spinal cord with antisera to TRH, the depolarizing response produced by TRH as well as the descending slow e.p.s.p. was greatly diminished. In contrast, monosynaptic reflexes evoked by dorsal root stimulation remained unchanged under this condition. These results suggest that TRH serves as a neurotransmitter mediating the descending slow e.p.s.p. in motoneurons.

Animals↗
PubMed2005

The retrograde spread of synaptic potentials and recruitment of presynaptic inputs.

Lateral excitation is a mechanism for amplifying coordinated input to postsynaptic neurons that has been described recently in several species. Here, we describe how a postsynaptic neuron, the lateral giant (LG) escape command neuron, enhances lateral excitation among its presynaptic mechanosensory afferents in the crayfish tailfan. A lateral excitatory network exists among electrically coupled tailfan primary afferents, mediated through central electrical synapses. EPSPs elicited in LG dendrites as a result of mechanosensory stimulation spread antidromically back through electrical junctions to unstimulated afferents, summate with EPSPs elicited through direct afferent-to-afferent connections, and contribute to recruitment of these afferents. Antidromic potentials are larger if the afferent is closer to the initial input on LG dendrites, which could create a spatial filtering mechanism within the network. This pathway also broadens the temporal window over which lateral excitation can occur, because of the delay required for EPSPs to spread through the large LG dendrites. The delay allows subthreshold inputs to the LG to have a priming effect on the lateral excitatory network and lowers the threshold of the network in response to a second, short-latency stimulus. Retrograde communication within neuronal pathways has been described in a number of vertebrate and invertebrate species. A mechanism of antidromic passage of depolarizing current from a neuron to its presynaptic afferents, similar to that described here in an invertebrate, is also present in a vertebrate (fish). This raises the possibility that short-term retrograde modulation of presynaptic elements through electrical junctions may be common.

Afferent Pathways↗