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At least 1,135 records · Page 63Linked to original sources
PubMed1998

Bidirectional synaptic plasticity in the rat basolateral amygdala: characterization of an activity-dependent switch sensitive to the presynaptic metabotropic glutamate receptor antagonist 2S-alpha-ethylglutamic acid.

This study examines forms of activity-dependent synaptic plasticity in the basolateral amygdala in vitro and demonstrates that a brief high frequency stimulus (HFS) train can induce a switch in the direction of the enduring change in synaptic strength induced by subsequent low-frequency stimulation (LFS). LFS (1 Hz, 15 min) of the external capsule (EC) induced a persistent 1.7-fold enhancement in the amplitude of synaptic potentials recorded intracellularly in basolateral amygdala neurons. The enhancement occurred gradually during the stimulation and was maintained for >30 min after termination of the stimulus train. LFS-induced enduring synaptic facilitation was not affected by the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoate (APV; 100 microM). Brief high-frequency EC stimulation (HFS; 100 Hz, 1 sec) induced APV-sensitive short-term potentiation (2.5-fold) that generally decayed within 10 min. When LFS was applied after recovery from the short-term potentiating effect of HFS (HFS/LFS), there was an initial transient (<10 min) enhancement of the synaptic response followed by persistent synaptic depression (synaptic potential amplitude reduced by 22% at 30 min). This represents the first demonstration of stimulus-dependent long-lasting synaptic depression in the amygdala. Application of the presynaptic (group II) metabotropic glutamate receptor antagonist 2S-alpha-ethylglutamic acid (EGLU; 50 microM) prevented the HFS-dependent switch from synaptic facilitation to depression. Thus, LFS in the in vitro amygdala slice can induce either enduring synaptic potentiation or depression, depending on whether a priming HFS train has been applied. This experience-dependent switch, a novel form of metaplasticity, is not dependent on NMDA receptors but may require group II metabotropic glutamate receptors. In the amygdala, experiential modification of activity-dependent long-term synaptic plasticity adds flexibility to the ways in which synaptic strength can be modified and could play a role in diverse amygdala-dependent processes, including the formation, storage, and extinction of emotional memory and the regulation of epileptogenesis.

Amygdala↗
PubMed1976

Structural and functional changes in an identified cricket neuron after separation from the soma. II. Functional changes.

Physiological and behavioural effects of separation from the soma were examined in isolated arborization and isolated axon segments of an identified motor neuron in the Polynesian field cricket, Teleogryllus oceanicus. The identified neuron, the contralateral dorsal longitudinal motor neuron of the metathoracic ganglion (CDLM), has an arborization most of which lies contralateral to its soma within the ganglion. Midline lesions in the ganglion separated CDLM into a distal segment composed of the axon and most of the arborization, and a proximal segment made up of the remaining arborization, neurite and soma. Isolated axonal segments were produced by cutting the nerve containing the CDLM axon. The function of the neuron-muscle system composed of CDLM, its pre-synaptic inputs, and its innervated muscle bundle was examined in contrl and experimentally operated animals. Extracellular recording assessed function in the axon. Electrical or tactil stimulation was used to excite pre-synaptic inputs to the CDLM arborization. Intracellular recording determined changes in post-synaptic potentials and miniature end-plate potentials in the muscle bundle innervated by CDLM. Normal axonal conduction, competence to respond to pre-synaptic input, neuron-muscle transmission, and miniature end-plate potential appearance can remain in the isolated arborization preparation. Physiological viability is longer in the cricket isolated arborization than in other insect distal segments described. Survival times of axonal conduction and the competence of the isolated arborization to respond to pre-synaptic input are roughly correlated with disappearance of the whole distal segment at 100 or more postoperative days. A naturally-occurring breakdown of the metathoracic dorsal longitudinal muscles in Teleogryllus eventually prevents measurements of post-synaptic potentials and miniature end-plate potentials. Normal post-synaptic function mediated by the distal arborization is maintained up to this breakdown, to a maximum of 44 days postoperative. The distal axonal segment of CDLM degenerates physiologically within four days postoperative, a time course approximating that of degeneration in vertebrate peripheral nerve distal axons.

Animals↗
PubMed1995

Development of excitatory and inhibitory postsynaptic potentials in the rat neocortex.

The postnatal development of synaptic potentials in the rat neocortex is characterized by the sequential appearance of functional excitatory and inhibitory synapses. Morphological and electrophysiological studies provided evidence that at early stages of development, pyramidal cells are extensively coupled to each other, presumably via gap junctions. Thus, immature neurons are able to communicate through pathways that are not available or only weakly expressed in the mature neocortex. During the very early postnatal period, excitatory synaptic inputs prevail. Excitatory postsynaptic potentials (EPSPs) are characteristically long in duration and show high sensitivity to frequent stimulation. Although spontaneous inhibitory postsynaptic potentials (IPSPs) and mature responses to exogenously applied gamma-aminobutyric acid (GABA) have been described during the first postnatal week, evoked IPSPs do not develop before postnatal day 10 (P10). During the period of maximum synaptogenesis (P11 to P20), GABA-mediated synaptic inhibition develops and pyramidal cells respond to afferent activation with efficient EPSPs and IPSPs. These postsynaptic potentials gradually mature during the late postnatal period. The delayed development of synaptic inhibition in the neocortex simultaneously promotes synaptic plasticity while increasing seizure susceptibility. On the one hand, the functional lack of synaptic inhibition during early stages of development enables a period of enhanced neuronal activity and augmented synaptic plasticity necessary to form proper synaptic connections. On the other hand, the absence of inhibitory control over excitatory processes increases the vulnerability of the developing neocortex to seizure activity during postnatal ontogenesis.

Aging↗
PubMed1979

Electrophysiological identification of two types of fibres in rat extraocular muscles.

1. The synaptic potentials and electrical properties of rat inferior rectus muscles were examined in vitro. 2. In most fibres the spontaneous synaptic activity consisted of typical miniature end-plate potentials which had a normal distribution of amplitudes and rather uniform time courses. Suprathreshold and maximal nerve stimulation evoked unitary end-plate potentials (e.p.p.s). The synaptic activity of these fibres could be recorded only in the innervation zone of the muscle. These fibres were identified as being focally innervated. 3. Focally innervated fibres gave action potentials upon direct and indirect stimulation. They had an effective resistance (Reff) of 1.62 +/- 0.22 M omega (mean +/- S.E., twenty-two fibres) and a time constant (tau m) of 3.8 +/- 0.4 msec (twenty-one fibres). Voltage-current curves in control saline were linear between membrane potentials of -50 to -140 mV. 4. In a small number of fibres the spontaneous synaptic activity consisted of miniature small-nerve junction potentials which had a skewed distribution of amplitudes with predominance of smaller voltages and time courses with a wide range of variation. Nerve stimulation evoked composite small-nerve junction potentials (s.j.p.s) which could be resolved into unitary components by varying the strength of stimulation. S.j.p.s had a higher threshold than e.p.p.s. Synaptic potentials could be recorded outside the innervation zone, at various sites along the muscle length. These fibres were recognized as being multiply innervated with polyneuronal innervation. 5. Multiply innervated fibres lacked action potentials had a large Reff of 6.0 +/- 1.1 M omega (six fibres) and a prolonged tau m of 29.8 +/- 4.8 msec. Reff show a moderate decrease to hyperpolarization and a rather large decrease to depolarization which denote, respectively, the presence of anomalous and delayed reactification. 6. It is concluded that rat extraocular muscles contain at least two populations of muscle fibres that in terms of synaptic activity and electrical properties are comparable to twitch fibres of other mammalian muscles and to slow or tonic fibres of amphibians.

Action Potentials↗
PubMed1990

The nature and causes of hippocampal long-term potentiation.

One of the most fascinating features of the hippocampus is its capacity for plasticity. Long-term potentiation (LTP), a stable facilitation of synaptic potentials after high-frequency synaptic activity, is very prominent in hippocampus and is a leading candidate memory storage mechanism. Here, we discuss the nature and causes of LTP and relate them to endogenous rhythmic neuronal activity patterns and their potential roles in memory. Anatomical studies indicate that LTP is accompanied by postsynaptic structural modifications while pharmacological studies strongly suggest that LTP is not due to an increase in presynaptic transmitter release. In field CA1, LTP induction appears to be triggered by a postsynaptic influx of calcium through NMDA receptor-linked channels. Possible roles of several calcium-sensitive enzyme systems in LTP are discussed and it is argued that activation of a calcium-dependent protease (calpain) could produce the structural changes linked to LTP. Rhythmic bursting activity is highly effective in inducing LTP and it is argued that the endogenous hippocampal theta rhythm plays a role in LTP induction in vivo. Finally, studies indicate that LTP and certain types of memory share a common pharmacology and the use of electrical brain stimulation as a sensory cue suggests that LTP develops when the significance of that cue is learned.

Action Potentials↗
PubMed1978

Pentobarbital: differential postsynaptic actions on sympathetic ganglion cells.

The frog sympathetic ganglion has been used as a model to elucidate the cellular mechanism of barbiturate anesthesia. Anesthetic concentrations of pentobarbital markedly reduced the fast nicotinic excitatory postsynaptic potential while having no effect on the slow excitatory postsynaptic potential or slow inhibitory postsynaptic potential, even though all three synaptic potentials depend on the presynaptic release of acetylcholine. A similar differential effect was seen for nicotinic and muscarinic responses to exogenously applied agonists, while the depolarizing action of gamma-aminobutyric acid (GABA) was enhanced. These results indicate that pentobarbital has remarkably selective actions on the sympathetic ganglion and further indicate that blockade of ganglionic transmission by anesthetic concentrations of pentobarbital can be entirely explained by a postsynaptic action. The present results strengthen the concept that pentobarbital anesthesia results from a postsynaptic blockade of central excitatory synapses which increase sodium conductance coupled with a postsynaptic enhancement of GABA-mediated synaptic inhibition.

Animals↗
PubMed1996

Repeated administration of pentylenetetrazol alters susceptibility of rat hippocampus to primed-burst stimulation: evidence from in vitro study on CA1 of hippocampal slices.

The effectiveness of theta pattern primed-bursts (PBs) on development of primed-burst (PB) potentiation was investigated in hippocampal CA1 of pentylenetetrazol-kindled rats. Experiments were carried out in the hippocampal slices from control and kindled rats at two post-kindling periods, i.e., 48-144 h (early phase) and 30-33 days (long-lasting phase). Field potentials (population excitatory post-synaptic potential, pEPSP) were recorded at stratum radiatum following stimulation of the stratum fibers. theta pattern primed-bursts were delivered to stratum radiatum and PB potentiation was assessed. The results showed that 48-144 h after kindling, PB potentiation in CA1 of kindled slices is significantly greater than control slices. In contrast, 30, 33 days after kindling PB potentiation was not observed and the pEPSP slope was depressed after PBs delivery, which lasted at least 60 min. Our results suggest that shortly after kindling, PB potentiation can be more readily induced while one month later, it is more difficult ot elicit. These findings may help to explain the behavioral deficits seen with the kindling model of epilepsy.

Animals↗
PubMed1995

The serotonergic inhibitory postsynaptic potential in prepositus hypoglossi is mediated by two potassium currents.

Synaptic inhibition mediated by the activation of potassium channels has been reported from several types of neurons. In each case, despite mediation by different neurotransmitters, the K+ conductance underlying the synaptic potential is activated by a G protein and inwardly rectifies. We report here a second K+ current that contributes to synaptic inhibition. Intracellular recordings were made from guinea pig nucleus prepositus hypoglossi in vitro, where we have described a 5-HT-mediated IPSP. Voltage-clamp analysis of the current induced by applied 5-HT revealed two separate conductances: an inwardly rectifying, rapidly activating K+ current (IIR) and an outwardly rectifying, slowly activating K+ current (IOR). IIR was blocked by extracellular Ba2+ (200 microM) and TEA+ (126 mM). IOR was insensitive to this concentration of Ba2+ and TEA+, but was inhibited by Cd2+ and intracellular BAPTA, indicating Ca dependence. Single focal electrical stimuli evoked a 5-HT-mediated IPSP, or under voltage clamp, an inhibitory postsynaptic current (IPSC). Ba2+ blocked only a component of this IPSC, which corresponded to the current caused by IIR. When multiple stimuli were applied (to prolong the release of transmitter), the time-dependent current IOR was more fully activated, resulting in an augmentation of the IPSC. We conclude that the IPSC is caused by both currents and that its amplitude can be modulated by the degree to which IOR is activated. This represents a mechanism by which synaptic responses can be potentiated.

Animals↗
PubMed1988

Regulation of intraganglionic synapses among rabbit parasympathetic neurones.

1. The response of parasympathetic neurones to the removal of preganglionic innervation was studied in the ciliary ganglia of adult rabbits. After section of the preganglionic oculomotor nerve, individual ciliary neurones were characterized electrophysiologically by intracellular recording, and morphologically by intracellular injection of horseradish peroxidase. 2. Within the first 24-48 h after nerve section, only two of fifty-nine neurones responded to antidromic stimulation of the postganglionic ciliary nerve with synaptic potentials. This result indicates that synaptic connections between principal neurones are rare in normal ganglia. 3. One week after denervation, however, excitatory postsynaptic potentials were recorded in thirty-nine out of fifty-three cells examined. Thus there is a rapid and extensive formation of intraganglionic connections after denervation. Morphological analysis of these ganglion cells showed numerous fine processes arising from the cell bodies and dendrites; such neurites were not present among control neurones. Many of these newly formed processes appeared to form synapses on neighbouring cells. 4. A similar proportion of neurones (about two-thirds of the cells) showed antidromically evoked excitatory postsynaptic potentials 2 weeks after denervation. Dendrites were still longer and more complex than controls at this time. After several months the morphology and prevalence of intraganglionic connections returned to normal as the ganglion became reinnervated. 5. Thus, denervation of rabbit ciliary ganglion cells induces the rapid formation of large numbers of functional synaptic connections among ganglion cells. It is postulated that local regulatory factors govern connections between parasympathetic ganglion cells. After denervation, these trophic signals are no longer modulated by presynaptic axons and they exert a stimulus for sprouting and synapse formation among this population of cholinergic neurones.

Action Potentials↗
PubMed2003

Spike-timing-dependent plasticity and relevant mutual information maximization.

Synaptic plasticity was recently shown to depend on the relative timing of the pre- and postsynaptic spikes. This article analytically derives a spike-dependent learning rule based on the principle of information maximization for a single neuron with spiking inputs. This rule is then transformed into a biologically feasible rule, which is compared to the experimentally observed plasticity. This comparison reveals that the biological rule increases information to a near-optimal level and provides insights into the structure of biological plasticity. It shows that the time dependency of synaptic potentiation should be determined by the synaptic transfer function and membrane leak. Potentiation consists of weight-dependent and weight-independent components whose weights are of the same order of magnitude. It further suggests that synaptic depression should be triggered by rare and relevant inputs but at the same time serves to unlearn the baseline statistics of the network's inputs. The optimal depression curve is uniformly extended in time, but biological constraints that cause the cell to forget past events may lead to a different shape, which is not specified by our current model. The structure of the optimal rule thus suggests a computational account for several temporal characteristics of the biological spike-timing-dependent rules.

Action Potentials↗
PubMed1998

Theta oscillations in somata and dendrites of hippocampal pyramidal cells in vivo: activity-dependent phase-precession of action potentials.

Theta frequency field oscillation reflects synchronized synaptic potentials that entrain the discharge of neuronal populations within the approximately 100-200 ms range. The cellular-synaptic generation of theta activity in the hippocampus was investigated by intracellular recordings from the somata and dendrites of CA1 pyramidal cells in urethane-anesthetized rats. The recorded neurons were verified by intracellular injection of biocytin. Transition from non-theta to theta state was characterized by a large decrease in the input resistance of the neuron (39% in the soma), tonic somatic hyperpolarization and dendritic depolarization. The probability of pyramidal cell discharge, as measured in single cells and from a population of extracellularly recorded units, was highest at or slightly after the negative peak of the field theta recorded from the pyramidal layer. In contrast, cyclic depolarizations in dendrites corresponded to the positive phase of the pyramidal layer field theta (i.e. the hyperpolarizing phase of somatic theta). Current-induced depolarization of the dendrite triggered large amplitude slow spikes (putative Ca2+ spikes) which were phase-locked to the positive phase of field theta. In the absence of background theta, strong dendritic depolarization by current injection led to large amplitude, self-sustained oscillation in the theta frequency range. Depolarization of the neuron resulted in a voltage-dependent phase precession of the action potentials. The voltage-dependent phase-precession was replicated by a two-compartment conductance model. Using an active (bursting) dendritic compartment spike phase advancement of action potentials, relative to the somatic theta rhythm, occurred up to 360 degrees. These data indicate that distal dendritic depolarization of the pyramidal cell by the entorhinal input during theta overlaps in time with somatic hyperpolarization. As a result, most pyramidal cells are either silent or discharge with single spikes on the negative portion of local field theta (i.e., when the somatic region is least polarized). However, strong dendritic excitation may overcome perisomatic inhibition and the large depolarizing theta rhythm in the dendrites may induce spike bursts at an earlier phase of the extracellular theta cycle. The magnitude of dendritic depolarization is reflected by the timing of action potentials within the theta cycle. We hypothesize that the competition between the out-of-phase theta oscillation in the soma and dendrite is responsible for the advancement of spike discharges observed in the behaving animal.

Action Potentials↗
PubMed1995

Non-involvement of the redox site of NMDA receptors in bidirectional synaptic plasticity in the CA1 area of the rat hippocampus in vitro.

We have examined the effects of the redox reagent 5,5'-dithiobis-2-nitrobenzoic acid (DTNB) on synaptic potentials recorded extracellularly from the CA1 area in hippocampal slices following low frequency stimulation (LFS) and tetanic stimulation (TS). Application of DTNB (200 microM) neither changed synaptic responses, nor prevented the expression of TS-induced long-term potentiation of synaptic responses and their depotentiation by LFS. Conversely, in naive slices, LFS still induced long-term depression of synaptic responses following application of DTNB. This depression could be subsequently reversed with a TS. It is concluded that the redox state of N-methyl-D-aspartate receptors does not affect the expression of long-term potentiation and depression of synaptic responses.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1967

Synaptic noise as a source of variability in the interval between action potentials.

The source of variability in the interval between action potentials has been identified in a class of cat spinal motoneurons. The observed random fluctuations in membrane potential (synaptic noise) together with an empirical description of spike generation accurately predict the statistical structure of variability observed to occur in the neuron's discharge.

Action Potentials↗
PubMed2005

Dynamics of learning-induced cellular modifications in the cortex.

This aim of this review is to describe the dynamics of learning-induced cellular modifications in the rat piriform (olfactory) cortex after olfactory discrimination learning and to describe their functional significance to long-term memory consolidation. The first change to occur is in the intrinsic properties of the neurons. One day after learning, pyramidal neurons show enhanced neuronal excitability. This enhancement results from reduction in calcium-dependent conductance that mediates the post burst after-hyperpolarization. Such enhanced excitability lasts for 3 days and is followed by a series of synaptic modifications. Several forms of long-term enhancement in synaptic connections between layer II pyramidal neurons in the piriform cortex accompany olfactory learning. Enhanced synaptic release is indicated by reduced paired-pulse facilitation. Post-synaptic enhancement of synaptic transmission is indicated by reduced rise time of post-synaptic potentials and formation of new synaptic connections is indicated by increased spine density along dendrites of these neurons. Such modifications last for up to 5 days. Thus, olfactory discrimination rule learning is accompanied by a series of cellular modifications which occur and then disappear at different times. These modifications overlap partially, allowing the maintenance of the cortical system in a 'learning mode' in which memories for specific odors can be acquired rapidly and efficiently.

Animals↗
PubMed2003

Chronic neurotrophin-3 strengthens synaptic connections to motoneurons in the neonatal rat.

We report that neurotrophin-3 (NT-3), delivered chronically via fibroblasts implanted intrathecally into neonatal rats, can facilitate synaptic transmission in the spinal cord. A small collagen plug containing NT-3-secreting fibroblasts was placed on the exposed dorsal surface of the spinal cord (L1) of 2-d-old rats; controls received beta-galactosidase-secreting fibroblasts. After 6 hr to 12 d of survival, synaptic potentials (EPSP) elicited by two synaptic inputs, L5 dorsal root and ventrolateral funiculus (VLF), were recorded intracellularly in L5 motoneurons in vitro. Preparations treated with NT-3 implants exhibited enhanced monosynaptic synaptic transmission from both inputs, which persisted over the entire testing period. Unlike acute enhancement of transmission by NT-3 (Arvanian and Mendell, 2001a), the chronic effect could occur at connections not normally eliciting an NMDA receptor-mediated response at the time of NT-3 exposure. Using susceptibility to blockade of the NMDA receptor by Mg2+ and APV, we confirmed that chronic treatment with NT-3 did not enhance NMDA receptor activity at these connections. Cords treated with chronic NT-3 also transiently displayed polysynaptic components activated by VLF that were blocked by the NMDA receptor antagonist APV. These novel NMDA receptor-mediated potentials may reflect changes in interneurons near the site of fibroblast implantation. We conclude that chronic NT-3 enhances the potency of segmental and descending projections via mechanisms different from those underlying acute changes.

Animals↗
PubMed2004

The combination of nicotine with the D2 antagonist raclopride or the weak D4 antagonist L-745,870 generates a clozapine-like facilitation of NMDA receptor-mediated neurotransmission in pyramidal cells of the rat medial prefrontal cortex.

Clozapine and other atypical, but not typical, antipsychotic drugs (APDs), facilitate both dopaminergic and N-methyl-D-aspartate (NMDA) receptor-mediated glutamatergic transmission in the medial prefrontal cortex (mPFC), which is thought to improve cognition. Switching schizophrenic patients from typical APDs to clozapine may reduce their cigarette smoking. Here, we tested whether nicotine, which facilitates dopamine release, also facilitates NMDA receptor-mediated neurotransmission in the mPFC, when given alone or in combination with a D(2,3) antagonist, raclopride, or a D4 antagonist, 3-(4-[4-chlorophenyl]piperazin-1-yl)methyl-1H-pyrrolo[2,3b]pyridine (L-745,870), using intracellular recording in pyramidal cells of the rat mPFC. Neither nicotine nor raclopride or L-745,870 alone altered NMDA-induced currents in these cells. However, combining nicotine with raclopride or L-745,870 facilitated these currents. Similarly to clozapine the combination of nicotine with raclopride or L-745,870 also markedly potentiated evoked excitatory post-synaptic potentials in the mPFC. Our results support the idea that intense smoking in schizophrenia may represent a form of self-medication with nicotine.

Analysis of Variance↗
PubMed1989

Excitatory amino acid receptors mediate slow synaptic transmission in turtle cerebellum.

In the isolated turtle cerebellum intracellular recordings from Purkinje cell dendrites and somata reveal novel slow excitatory synaptic potentials evoked by activation of climbing fiber (CF) or parallel fiber (PF) inputs. Classical fast excitatory synaptic responses to CF and PF stimulation are followed by large, slow excitatory postsynaptic potentials (sEPSPs) which are associated with an increase in conductance and are enhanced by hyperpolarization. Both sEPSPs are blocked by the excitatory amino acid (EAA) antagonist kynurenate, but not by DL-2-amino-5-phosphonovalerate (AP-5). The EAA receptor antagonist L-amino-4-phosphonobutyric acid (L-AP-4) reversibly blocked the PF-sEPSP without affecting the CF-sEPSP. Two novel slow synaptic potentials mediated by excitatory amino acid receptors can therefore be observed in turtle cerebellum which may play an important role in synaptic integration.

Action Potentials↗