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PubMed1972

Quantal components of the inhibitory synaptic potential in spinal mononeurones of the cat.

1. Monosynaptic i.p.s.p.s were produced in spinal motoneurones of the cat by stimulation of a pool of interneurones following chronic degeneration of descending tracts and primary afferent fibres in the lumbosacral cord.2. Monosynaptic i.p.s.p.s so evoked by supramaximal stimuli often showed a fluctuation in amplitude with occasional failures of response.3. When two successive stimuli were applied at a short interval, the mean amplitude of the second i.p.s.p.s was greater than that of the first. This facilitation was associated with a decrease in the number of failures, a decrease in the coefficient of variation of the amplitude distribution and an increase in the probability of occurrences of large i.p.s.p.s.4. A statistical analysis of the i.p.s.p. amplitude fluctuation showed that the monosynaptic i.p.s.p. is composed of discrete unit potentials evoked with a certain probability in a manner described by a binomial law.5. The application of strychnine decreased the mean amplitude of i.p.s.p.s with little change in the coefficient of variation of the i.p.s.p. amplitude distribution.6. It is concluded that the release of inhibitory transmitter occurs in quantal steps and that strychnine blocks primarily the post-synaptic receptors for the inhibitory transmitter.

Animals↗
PubMed1985

Synaptic potentials in motoneurons during fictive swimming in spinal Xenopus embryos.

Embryos spinalized at the 3rd to 6th postotic myotome and immobilized in 10(-4) M tubocurarine can respond to a brief skin stimulus with motor root activity suitable for swimming. Embryos spinalized at the more caudal levels give shorter episodes of fictive swimming. We have previously described the synaptic inputs to motoneurons during fictive swimming in intact embryos (23). In the present paper we look to see if similar synaptic inputs are present in spinal embryos and are therefore spinal in origin. All motoneuron firing during fictive swimming is associated with a tonic depolarization that falls away slowly once firing stops, is increased by hyperpolarizing current, and is reduced by depolarizing current. A slow depolarizing potential evoked by lower levels of skin stimulation has similar properties and rate of fall. In 1-2 mM PDA, an excitatory amino acid antagonist, only a small remnant of the depolarization remains, and motoneuron firing stops. The NMDA antagonist 50 microM APV reduces the depolarization less but also blocks firing. Motoneurons fire one spike per swimming cycle, in phase with nearby motor root discharge. Spikes are preceded by a depolarizing prepotential. This increases with hyperpolarizing current, which can block the spike to reveal an underlying depolarizing potential. In phase with motor root discharge on the opposite side of the body, motoneurons receive a midcycle inhibitory postsynaptic potential, which increases with depolarizing current, decreases with hyperpolarizing current, and is blocked by 10(-6) M strychnine. Strychnine, 5 X 10(-7) M, leads first to broadening of motor root bursts then to loss of the alternating swimming pattern of activity, which is replaced by synchronous bursts on both sides of the body. We conclude that the synaptic inputs to motoneurons during fictive swimming in spinal embryos are very similar in properties and pharmacology to those in intact embryos. These inputs, including the tonic depolarization always associated with motoneuron firing during swimming, must be at least partly spinal in origin.

Amino Acids↗
PubMed1993

Pairing of pre- and postsynaptic activities in hippocampal CA1 neurons induces long-term modifications of NMDA receptor-mediated synaptic potential.

An in vitro slice preparation of rat hippocampus was used to study the long-term modifications of pharmacologically isolated N-methyl-D-aspartate (NMDA) receptor-mediated excitatory postsynaptic potential (EPSPNMDA). Intracellular recordings were made from CA1 pyramidal cells in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) and picrotoxin (50 microM) which block non-NMDA and GABAA receptors, respectively. Pairing of low-frequency EPSPNMDA with postsynaptic depolarization induced a long-term depression (LTD) of EPSPNMDA. The maximal reduction of EPSPNMDA amplitude amounted to 81.3% of the control 1 min after the pairing. When low-frequency synaptic stimulation was paired with strong postsynaptic depolarization, a long-term potentiation (LTP) of EPSPNMDA could be induced. These results suggest that the induction of long-term modifications of EPSPNMDA has at least a postsynaptic component.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1993

Use-dependent modification of a slow NMDA receptor-mediated synaptic potential in rat amygdalar slices.

A single stimulus applied to the endopyriform nucleus evoked in 35 of the 101 basolateral amygdaloid (BLA) neurons a slow excitatory postsynaptic potential (s-EPSP) of varying latencies. The s-EPSP could be graded by changing the stimulus intensity and, on reaching the threshold, triggered action potentials. At stimulus intensity just subthreshold for evoking a spike, the s-EPSP has an average amplitude of 16.3 +/- 1.4 mV, a time to peak of 25.7 +/- 3.8 ms, and a duration of 124 +/- 14 ms. The s-EPSP was reversibly blocked by DL-2-amino-5-phosphonovaleate (DL-APV) or ketamine, indicating its mediation through N-methyl-D-aspartate (NMDA) receptor activation. However, the s-EPSP was not able to follow stimulus frequency of 1 Hz, suggesting that APV-sensitive s-EPSP is probably generated by a polysynaptic pathway. The s-EPSP was greatly enhanced by synaptic stimulation in the presence of bicuculline or in Mg(++)-free solution leading to the genesis of paroxysmal depolarizing shift (PDS). The s-EPSP can undergo robust long-term potentiation (LTP) following tetanic stimulation. These results suggest that the NMDA receptor-mediated s-EPSP may play an important role in epileptogenesis and synaptic plasticity in the amygdala.

2-Amino-5-phosphonovalerate↗
PubMed1995

The involvement of metabotropic glutamate receptors in long-term depression of N-methyl-D-aspartate receptor-mediated synaptic potential in the rat hippocampus.

The frequency-dependent long-term modifications of pharmacologically isolated N-methyl-D-aspartate (NMDA) receptor-mediated excitatory postsynaptic potential (EPSPNMDA) was studied. Intracellular recordings were obtained from CA1 cells of rat hippocampal slices and in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM) and bicuculline (20 microM) which block non-NMDA and GABAA receptors, respectively. Low-frequency stimulation at 5 Hz resulted in a long-term depression (LTD) of EPSPNMDA in 12 of 17 cells. However, when the stimulus frequency was increased to 30 Hz, a long-term potentiation (LTP) of EPSPNMDA was observed in 7 out of 9 cells. The LTD was not affected by pretreating the slices with okadaic acid (0.5-1 microM) suggesting that activation of endogenous protein phosphatase is not responsible for this process. In the presence of L-2-amino-3-phosphonopropionic acid (50 microM) or (RS)-alpha-methyl-4-carboxyphenylglycine (200 microM), 5 Hz tetanization resulted in LTP instead of LTD. These results suggest that activation of metabotropic glutamate receptor (mGluR) is necessary for the induction of EPSPNMDA LTD and blockade of mGluR unmasks a LTP.

Animals↗
PubMed1991

Pharmacological evidence that NMDA receptors contribute to mono- and di-synaptic potentials in slices of mouse olfactory cortex.

Experiments have been carried out using slices of olfactory cortex of the mouse perfused in solution containing Mg2+ (1 mM) and in which the lateral olfactory tract was stimulated at a frequency of 1 pulse/5 sec to avoid polysynaptic activity. Application of the N-methyl-D-aspartate antagonist D-(-)-2-amino-5-phosphonopentanoic acid (APP, 25 microM) suppressed a low amplitude component of the potential, the latency to onset of which corresponded with that of the monosynaptically evoked N-wave in 14 of the 17 slices tested and duration of which exceeded that of the N-wave. A residual potential, recorded in slices to which the quisqualate-/kainate-selective antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) had been applied at a concentration of 10microM, was identical to the potential suppressed by APP. The residual potential in the presence of DNQX was blocked by APP, 7-chlorokynurenate (25 microM) and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK801, 0.125-2 microM). It was potentiated in area by exogenous D-serine (1 mM) and in slices preincubated and perfused with Mg(2+)-free solution. It is concluded that, in addition to receptors of the quisqualate/kainate categories, N-methyl-D-aspartate receptors also contribute to both mono- and di-synaptic excitations in the olfactory cortex.

2-Amino-5-phosphonovalerate↗
PubMed1985

[Multi-component synaptic potentials of rubrospinal neurons of the cat induced by corticofugal spike trains].

Compound nature of EPSPs in rubrospinal neurons evoked by stimulation of the sensorimotor and associative parietal region of the cerebral cortex was shown in acute experiments on nembutalized cats by means of intracellular technique. Monosynaptic nature of the first two components of EPSPs evoked by corticofugal impulses propagating with an average velocity of 18.5 m/s and 7.5 m/s was revealed. These components are supposed to arise as a result of activation of slow conducting pyramidal and corticorubral neurons. In some rubrospinal neurons the first EPSP component evoked by corticofugal impulsation had a fast rising phase and reflected activation of axo-somatic synapses. The results are discussed in the light of the mechanisms of reorganization of cortical synaptic inputs to the red nucleus neurons.

Animals↗
PubMed2000

Suppression of inhibitory synaptic potentiation by presynaptic activity through postsynaptic GABA(B) receptors in a Purkinje neuron.

At inhibitory synapses on a cerebellar Purkinje neuron, the depolarization caused by heterosynaptic climbing fiber activation induces long-lasting potentiation accompanied by an increase in GABA(A) receptor responsiveness. Here we show that activation of a presynaptic inhibitory interneuron during the conditioning postsynaptic depolarization suppresses the potentiation. The suppression is due to postsynaptic GABA(B) receptor activation by GABA released from presynaptic terminals. The results suggest that GABA(B) receptor activation decreases the activity of cAMP-dependent protein kinase through the G(i)/G(o) proteins. The presynaptic activity-dependent suppression of synaptic plasticity is a novel regulatory mechanism of synaptic efficacy at individual synapses and may contribute to the learning and computational ability of the cerebellar cortex.

Animals↗
PubMed2001

Conditional restoration of hippocampal synaptic potentiation in Glur-A-deficient mice.

Plasticity of mature hippocampal CA1 synapses is dependent on l-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors containing the glutamate receptor A (GluR-A) subunit. In GluR-A-deficient mice, plasticity could be restored by controlled expression of green fluorescent protein (GFP)-tagged GluR-A, which contributes to channel formation and displayed the developmental redistribution of AMPA receptors in CA1 pyramidal neurons. Long-term potentiation (LTP) induced by pairing or tetanic stimulation was rescued in adult GluR-A(-/-) mice when (GFP)GluR-A expression was constitutive or induced in already fully developed pyramidal cells. This shows that GluR-A-independent forms of synaptic plasticity can mediate the establishment of mature hippocampal circuits that are prebuilt to express GluR-A-dependent LTP.

Aging↗
PubMed1986

Prenatal protein malnutrition affects synaptic potentiation in the dentate gyrus of rats in adulthood.

Long-term potentiation (LTP) was studied in the dentate gyrus of anesthetized normal and prenatally protein malnourished rats in adulthood. LTP was initiated by high-frequency stimulation of the perforant path. Potentiation of both population excitatory postsynaptic potential (EPSP) slope and population spike was studied at various times after conditioning out to 5 h. The results indicate that prenatal protein malnutrition has a differential effect on LTP. Although potentiation of the population spike was relatively unaffected, prenatal protein malnutrition did lead to a significant reduction in potentiation of the population EPSP. Several possibilities are proposed as to the cause of the differential effect.

Animals↗
PubMed2005

Slow excitatory post-synaptic potentials in myenteric AH neurons of the guinea-pig ileum are reduced by the 5-hydroxytryptamine7 receptor antagonist SB 269970.

Serotonin (5-HT) is a key modulator of neuronal excitability in the central and peripheral nervous system. In the enteric nervous system, 5-HT causes a slow depolarization in the intrinsic sensory neurons, but the receptor responsible for this has not been correlated with known gene products. The aim of this study was to determine whether the newly characterized 5-HT7 receptor may participate in the 5-HT-mediated depolarization of, and synaptic transmission to, the intrinsic sensory neurons of the guinea-pig ileum. Intracellular electrophysiological recordings were made from intrinsic sensory neurons identified as myenteric AH neurons from guinea-pig ileum. 5-HT (5 microM) applied to the cell body evoked both a fast depolarization (5-HT3 mediated) and/or a slow depolarization (5-HT1P-like). The 5-HT1/5/7 receptor agonist 5-carboxamidotryptamine (5-CT) (5 microM) evoked only a slow depolarization. When the fast depolarization evoked by 5-HT was blocked with granisetron (1 microM, 5-HT3 receptor antagonist), only a slow depolarization remained; this was abolished by the 5-HT7 receptor antagonist SB 269970 (1 microM, control: 14+/-2 mV, granisetron+SB 269970: -1+/-2 mV). The slow depolarization evoked by 5-CT was also significantly reduced by SB 269970 (control: 14+/-1 mV, SB 269970: 5+/-2 mV) suggesting a 5-HT7 receptor was activated by exogenous application of 5-CT and 5-HT. Slow excitatory postsynaptic potentials evoked by stimulating descending neural pathways (containing serotonergic fibers) were reduced by SB 269970 (control: 8+/-3 mV, SB 269970: 3+/-1 mV). However, SB 269970 had no effect on slow excitatory postsynaptic potentials evoked by stimulation of circumferential (tachykinergic) pathways (control: 7+/-1 mV, SB 269970: 6+/-1 mV). These data are consistent with the presence on enteric AH neurons of functional 5-HT7 receptors that participate in slow synaptic transmission.

Animals↗
PubMed1989

Glycine enhances NMDA-receptor mediated synaptic potentials in neocortical slices.

One class of excitatory amino-acid receptors, the N-methyl-D-aspartate (NMDA) receptors, mediates transmission at a small, but important, group of synapses in the neocortex. These receptors are implicated in neuronal plasticity during development in young mammals and in memory acquisition in adults. Recently, responses of isolated membrane patches to NMDA were shown to be greatly enhanced by glycine. This, together with the demonstration that the strychnine-insensitive glycine-binding site is distinct from, but linked to, the NMDA receptor has excited intense interest in glycine as a synaptic modulator. Before proposing a physiological function, however, it is important to determine whether glycine could enhance synaptic responses to NMDA receptor activation in intact, adult tissue. An earlier study failed to demonstrate enhancement of NMDA responses when glycine was applied and it was proposed that in intact tissue the high-affinity glycine site was already saturated by endogenous glycine. It remained possible that glycine concentrations can be maintained at low levels close to synaptic receptors. We have examined responses of neurons in slices of adult neocortex to focal applications of excitatory amino acids and glycine and report enhancement by glycine of NMDA receptor-mediated excitatory postsynaptic potentials.

Action Potentials↗
PubMed1992

Mechanisms of gastric rhythm generation in the isolated stomatogastric ganglion of spiny lobsters: bursting pacemaker potentials, synaptic interactions, and muscarinic modulation.

1. The gastric central pattern generator (CPG), located in the stomatogastric ganglion (STG) of the spiny lobster (Panulirus interruptus), is nonrhythmic when deprived of neuromodulatory inputs from anterior ganglia. Leaving these inputs intact in vitro can sustain a gastric rhythm but also introduces numerous, uncontrolled and largely unknown modulatory and synaptic influences that greatly complicate analysis of this CPG. 2. Here we induced gastric rhythms in the isolated STG, by superfusing a specific modulator, the muscarinic agonist, pilocarpine. Muscarinic agents sustain vigorous gastric rhythms in the isolated STG. Our aim was to analyze the pattern-generating functions of the restricted gastric circuit, free of complicating influences from other ganglia, and under specific (muscarinic) modulation. 3. We used combinations of multiple cell hyperpolarizations, photodeletions, and synaptic blockade by picrotoxin to assess the pattern-generating role of individual gastric neurons and to study the activity of subcircuits. 4. Four identified gastric neurons [lateral gastric (LG), dorsal gastric (DG), 2 electrically coupled lateral posterior gastric (2LPGs)] acted as pattern-generating cells. They showed bursting pacemaker potentials (BPPs), i.e., plateau (or driver) potentials that underlay bursts of axonal spikes and slow, interburst depolarizing potentials that underlay repetitive burst activity. LG and DG, at least, became conditional bursters, able to burst repetitively because of intrinsic oscillations. The other gastric neurons behaved mainly as follower cells and derived their rhythmic bursting from synaptic coupling to the pattern-generator cells and from their own intrinsic (but nonoscillatory) properties. 5. The pattern-generating neurons form a novel "kernel" circuit that works by the cooperative interaction of cellular properties and synaptic connectivity. 6. This study constitutes the first complete and fully consistent analysis of pattern generation in the gastric network of the isolated STG. These mechanisms pertain to muscarinic rhythms in particular but also, we suggest, to gastric rhythm generation and CPG function in general. We suggest that 1) rhythmicity normally depends on the induction of bursty membrane properties in at least some component neurons; 2) different subcircuits can produce rhythmic patterns and may be activated by different modulators; and 3) the gastric network shares several important "building blocks" with CPGs that have been analyzed in other systems. 7. Muscarinic inputs are implicated as an important gastric regulator. We compare these responses with the reported modulatory actions of the anterior pyloric modulator (AMP), an identified, putatively cholinergic input interneuron that may act via muscarinic mechanisms.

Animals↗
PubMed1998

Synaptic potentials in respiratory neurones during evoked phase switching after NMDA receptor blockade in the cat.

1. Blockade of NMDA receptors by dizocilpine impairs the inspiratory off-switch (IOS) of central origin but not the IOS evoked by stimulation of sensory afferents. To investigate whether this difference was due to the effects of different patterns of synaptic interactions on respiratory neurones, we stimulated electrically the superior laryngeal nerve (SLN) or vagus nerve in decerebrate cats before and after i.v. administration of dizocilpine, whilst recording intracellularly. 2. Phrenic nerve responses to ipsilateral SLN or vagal stimulation were: at mid-inspiration, a transient inhibition often followed by a brief burst of activity; at late inspiration, an IOS; and at mid-expiration, a late burst of activity. 3. In all neurones (n = 16), SLN stimulation at mid-inspiration evoked an early EPSP during phase 1 (latency to the arrest of phrenic nerve activity), followed by an IPSP in inspiratory (I) neurones (n = 8) and by a wave of EPSPs in post-inspiratory (PI) neurones (n = 8) during phase 2 (inhibition of phrenic activity). An EPSP in I neurones and an IPSP in PI neurones occurred during phase 3 (brief phrenic burst) following phase 2. 4. Evoked IOS was associated with a fast (phase 1) activation of PI neurones, whereas during spontaneous IOS, a progressive (30-50 ms) depolarization of PI neurones preceded the arrest of phrenic activity. 5. Phase 3 PSPs were similar to those occurring during the burst of activity seen at the start of spontaneous inspiration. 6. Dizocilpine did not suppress the evoked phrenic inhibition and the late burst of activity. The shapes and timing of the evoked PSPs and the changes in membrane potential in I and PI neurones during the phase transition were not altered. 7. We hypothesize that afferent sensory pathways not requiring NMDA receptors (1) terminate inspiration through a premature activation of PI neurones, and (2) evoke a late burst of phrenic activity which might be the first stage of the inspiratory on-switch.

Animals↗