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PubMed1996

Taurine induces a long-lasting increase of synaptic efficacy and axon excitability in the hippocampus.

The physiological role of taurine, one of the most abundant free amino acids in the mammalian brain, is still poorly understood. We have found that bath application of the amino acid taurine induces two opposite actions on field excitatory synaptic potentials (fEPSP) recorded in the CA1 area of hippocampal slices: a decrease in fEPSP slope prevented by GABAA antagonists, and a long-lasting potentiation of fEPSP independent of GABAA or NMDA receptor activation. Two long-lasting processes account for this taurine-induced potentiation: (1) an increase in synaptic efficacy that is accompanied neither by modifications in the basic postsynaptic membrane electrical properties nor by those presynaptic changes involved in fEPSP paired-pulse facilitation; and (2) an increase in the axon excitability revealed by a reduction on the threshold for antidromic action potential activation. In addition, taurine perfusion also induces a long-lasting increase in intracellularly recorded EPSPs and monosynaptically activated IPSPs. A number of experimental observations such as temperature dependence, extracellular Na+ concentration dependence, and saturation studies, although they are not unequivocally conclusive, suggest that the taurine uptake system is required for the taurine-induced fEPSP potentiation. Our data describe a new taurine action defined as a potentiation of synaptic transmission due in part to an increment in presynaptic axon excitability and in synaptic efficacy.

Animals↗
PubMed1975

Some effects of 5-hydroxytryptamine, dopamine and noradrenaline on neurones in the submucous plexus of guinea-pig small intestine.

1. Responses to the iontophoretic application of 5-hydroxytryptamine (5-HT), dopamine and noradrenaline were examined in neurones of the submucous plexus of guinea-pig small intestine. 2. Every neurone was excited by 5-HT. 3. In a proportion of cells, dopamine or noradrenaline caused an increase in membrane potential. This response was only observed in cells which received in inhibitory innervation. The responses closely resembled inhibitory synaptic potentials evoked by transmural stimulation. 4. Both inhibitory synaptic potentials and inhibitory responses to dopamine and noradrenaline were blocked by methysergide. 5. It seems possible that these two catecholamines may interact with similar receptors to those activated by inhibitory transmitter.

Animals↗
PubMed1989

Hypoxic changes in hippocampal neurons.

1. Reversible effects of brief periods of anoxia (replacing 95% O2-5% CO2 with 95% N2-5% CO2 for 2-4 min) were studied in CA1 neurons in hippocampal slices (from Sprague-Dawley rats), kept in an interface-type chamber at 33.5 degree. 2. The predominant voltage change during anoxia (N2) was a hyperpolarization, accompanied by a marked fall in resistance and excitability; synaptic potentials were also depressed, especially inhibitory postsynaptic potentials (IPSPs). 3. In voltage-current (V-I) plots, the N2-evoked hypolarization had a reversal potential below -90mV, even when recording with 2 M KCl electrodes and after substituting 90% of medium Cl- with isethionate. The accompanying fall in input resistance (RN) is therefore probably caused by an increase in K conductance (in agreement with previous reports). There was evidence that anomalous rectification enhances the fall in RN but limits the hyperpolarization. 4. These effects of anoxia were not fully blocked by any of the K-channel antagonists tested, including Cs, TEA, 4-AP, quinine and apamin. 5. Intracellular injections of Ca chelators caused a variable depression of N2-evoked reductions in RN. 6. It is unlikely that N2 activates ATP-sensitive K channels as tolbutamide enhanced rather than depressed the hyperpolarization and fall in RN. 7. When early depletion of cellular ATP was prevented by incubation in creatine (25 mM for greater than 1 h), even longer anoxic periods produced only minor changes in potential, RN, and synaptic transmission. 8. It was concluded that activation of K conductance by a rise in cytosolic-free Ca2+ is the most plausible of several possible underlying mechanisms.

4-Aminopyridine↗
PubMed1985

Long-term potentiation of synaptic acetylcholine release in the superior cervical ganglion of the rat.

The release of endogenous acetylcholine (ACh) from the in vitro rat superior cervical ganglion was measured by assaying the bathing medium. Simultaneously, synaptic transmission in the ganglion was assessed by recording post-ganglionic compound action potentials. A brief period of tetanic preganglionic stimulation (20 Hz for 20 s) induced a long-term potentiation of the post-ganglionic compound action potential. The same tetanic stimulation also consistently induced a long-term potentiation of stimulated ACh release. Spontaneous (non-stimulated) ACh release was not enhanced after tetanic stimulation. The content of ACh in the ganglion was not measurably increased after tetanic stimulation. These results suggest that the long-term increase in synaptic efficacy is due, at least in part, to an increase in the amount of ACh released by the afferent impulse.

Acetylcholine↗
PubMed1992

Long-term Potentiation in the Striatum is Unmasked by Removing the Voltage-dependent Magnesium Block of NMDA Receptor Channels.

We have studied the effects of tetanic stimulation of the corticostriatal pathway on the amplitude of striatal excitatory synaptic potentials. Recordings were obtained from a corticostriatal slice preparation by utilizing both extracellular and intracellular techniques. Under the control condition (1.2 mM external Mg2+), excitatory postsynaptic potentials (EPSPs) evoked by cortical stimulation were reversibly blocked by 10 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an antagonist of dl-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) ionotropic glutamate receptors, while they were not affected by 30 - 50 microM 2-amino-5-phosphonovalerate (APV), an antagonist of N-methyl-d-aspartate (NMDA) glutamate receptors. In the presence of 1.2 mM external Mg2+, tetanic activation of cortical inputs produced long-term depression (LTD) of both extracellularly and intracellularly recorded synaptic potentials. When Mg2+ was removed from the external medium, EPSP amplitude and duration increased. In Mg2+-free medium, cortically evoked EPSPs revealed an APV-sensitive component; in this condition tetanic stimulation produced long-term potentiation (LTP) of synaptic transmission. Incubation of the slices in 30 - 50 microM APV blocked striatal LTP, while it did not affect LTD. In Mg2+-free medium, incubation of the slices in 10 microM CNQX did not block the expression of striatal LTP. Intrinsic membrane properties (membrane potential, input resistance and firing pattern) of striatal neurons were altered neither by tetanic stimuli inducing LTD and LTP, nor by removal of Mg2+ from the external medium. These findings show that repetitive activation of cortical inputs can induce long-term changes of synaptic transmission in the striatum. Under control conditions NMDA receptor channels are inactivated by the voltage-dependent Mg2+ block and repetitive cortical stimulation induces LTD which does not require activation of NMDA channels. Removal of external Mg2+ deinactivates these channels and reveals a component of the EPSP which is potentiated by repetitive activation. Since the striatum has been involved in memory and in the storage of motor skills, LTD and LTP of synaptic transmission in this structure may provide the cellular substrate for motor learning and underlie the physiopathology of some movement disorders.

Journal Article↗
PubMed2004

Pacemaker potentials are the physiologic basis of epileptiform activity in the buccal ganglia of Helix pomatia.

Mechanisms of epileptic activity in nervous systems were studied using the identified neurons B1 through B4 in the buccal ganglia of the snail Helix pomatia as a model system. Activities were recorded with intracellular microelectrodes. Epileptiform activity was induced by bath application of an epileptogenic drug (pentylenetetrazol: 1 mM to 40 mM, or etomidate: 0.1 mM to 1.0 mM). Epileptiform potentials recorded from the somata of neurons consisted of paroxysmal depolarization shifts (PDSs). With increasing concentration of an epileptogenic drug, pacemaker potentials in neuron B3 developed into PDS. Simultaneously several types of chemical post-synaptic potentials were suppressed in amplitude. Since on the one hand epileptic seizures only appear when PDS are synchronized in many neurons and since on the other hand synaptic potentials were found to be suppressed during epileptic conditions, mechanisms underlying neuronal synchronization were studied. Evidence was found that, under epileptogenic conditions only, neurons were synchronized by an non-synaptic release of substances. Strong depolarizations accompanied by an increase in intracellular calcium concentration are known to induce an unspecific exocytosis. Thus, an unspecific exocytosis from the dendrites of PDS-generating neurons probably appears under epileptic conditions and synchronizes neighbouring neurons.

Action Potentials↗
PubMed1987

Glial potentials in hippocampus.

In rats under urethane anaesthesia, intracellular recordings were made from 36 cells, mainly in CA1, that had all the characteristics of glia: unusually high and stable resting potentials (-79.6 +/- 6.0 mV, mean +/- SD) and total absence of spikes or synaptic potentials. They were exceptionally sensitive to surrounding neuronal activity, being readily depolarized by very low frequency stimulation (0.5-2 Hz) of the fimbria. In the range 0.5-2 Hz, the mean peak depolarizations increased linearly with frequency of fimbrial stimulation (9.1 +/- 0.53 mV/Hz). At frequencies of 5 Hz or more, the depolarizations were highly variable, sometimes reaching a maximum of 25-30 mV, but the overall mean was not significantly greater than for 2 Hz stimulation. The depolarizations decayed slowly, with a half-time of 4.2 +/- 1.22 s and were often followed by a prolonged undershoot (lasting over 1 min). Alvear and especially septal stimulation were much less effective in evoking glial depolarizations. One cell that initially had all the characteristics of a glia, during very prolonged stable recording, developed responses, such as synaptic potentials and 20-40 mV action potentials evoked by fimbrial or alvear stimulation, consistent with strong electrical coupling to at least one neighbouring neuron.

Animals↗
PubMed1988

Persistent protein kinase activity underlying long-term potentiation.

Long-term potentiation (LTP) of synaptic transmission in the hippocampus is a much-studied example of synaptic plasticity. Although the role of N-methyl-D-aspartate (NMDA) receptors in the induction of LTP is well established, the nature of the persistent signal underlying this synaptic enhancement is unclear. Involvement of protein phosphorylation in LTP has been widely proposed, with protein kinase C (PKC) and calcium-calmodulin kinase type II (CaMKII) as leading candidates. Here we test whether the persistent signal in LTP is an enduring phosphoester bond, a long-lived kinase activator, or a constitutively active protein kinase by using H-7, which inhibits activated protein kinases and sphingosine, which competes with activators of PKC (ref. 17) and CaMKII (ref. 18). H-7 suppressed established LTP, indicating that the synaptic potentiation is sustained by persistent protein kinase activity rather than a stably phosphorylated substrate. In contrast, sphingosine did not inhibit established LTP, although it was effective when applied before tetanic stimulation. This suggests that persistent kinase activity is not maintained by a long-lived activator, but is effectively constitutive. Surprisingly, the H-7 block of LTP was reversible; evidently, the kinase directly underlying LTP remains activated even though its catalytic activity is interrupted indicating that such kinase activity does not sustain itself simply through continual autophosphorylation (see refs 9, 13, 15).

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1989

Inhibition of postsynaptic PKC or CaMKII blocks induction but not expression of LTP.

Long-term potentiation (LTP) of synaptic transmission is a widely studied cellular example of synaptic plasticity. However, the identity, localization, and interplay among the biochemical signals underlying LTP remain unclear. Intracellular microelectrodes have been used to record synaptic potentials and deliver protein kinase inhibitors to postsynaptic CA1 pyramidal cells. Induction of LTP is blocked by intracellular delivery of H-7, a general protein kinase inhibitor, or PKC(19-31), a selective protein kinase C (PKC) inhibitor, or CaMKII(273-302), a selective inhibitor of the multifunctional Ca2+-calmodulin-dependent protein kinase (CaMKII). After its establishment, LTP appears unresponsive to postsynaptic H-7, although it remains sensitive to externally applied H-7. Thus both postsynaptic PKC and CaMKII are required for the induction of LTP and a presynaptic protein kinase appears to be necessary for the expression of LTP.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Postsynaptic Hebbian and non-Hebbian long-term potentiation of synaptic efficacy in the entorhinal cortex in slices and in the isolated adult guinea pig brain.

Long-term potentiation (LTP) was investigated in the mammalian entorhinal cortex by using two in vitro preparations, the isolated brain and the entorhinal cortex slice. Hebbian and non-Hebbian types of LTP appear to be present in layer II entorhinal cortex cells as demonstrated using two protocols: (i) tetanic stimulation of the piriform-entorhinal cortex afferent pathway to generate homosynaptic potentiation and (ii) postsynaptic subthreshold rhythmic membrane potential manipulation not paired to presynaptic activation, which gives rise to non-Hebbian LTP. The induction and the expression of both types of LTP were found to be dependent on activation of N-methyl-D-aspartate receptors as shown by their sensitivity to the receptor agonist D-2-amino-5-phosphonovalerate. This is in contrast to LTP in the hippocampus [Zalutsky, R. A. & Nicoll, R. A. (1990) Science 248, 1619-1624], where LTP is expressed by quisqualate receptors. Since, in the entorhinal cortex, LTP is linked to a selective increase of the N-methyl-D-aspartate-receptor-mediated synaptic responses, this enhancement is most likely due to postsynaptic factors.

2-Amino-5-phosphonovalerate↗
PubMed1990

Mandibular motor neurons of the caterpillar of the hawk moth Manduca sexta.

As part of a planned study of the central neural basis of feeding behaviour in larval Manduca sexta, the morphology and physiology of the mandibular motor system is here described. The gross neuroanatomy of the postoral head segments has been investigated, especially the course and structure of the mandibular nerves. The electrophysiology of the mandibular opener and closer muscles has been investigated by extra- and intracellular recording during feeding behaviour and during electrical stimulation of the motor nerve. All the muscle fibres examined are of the "fast," twitch type. Contraction is associated exclusively with locally or completely propagated overshooting action potentials, never with local junctional potentials. Control of the muscles is by recruitment of more motor units and/or an increase of frequency of action potentials. No inhibitory synaptic potentials could be found. The motor neurons of the mandibular muscles have been identified by cobalt backfills of the mandibular nerve, and characterized by intracellular recording and dye injection. There are 12 closer and 8 opener motor neurons. All motor neurons recorded so far evoke 1:1 twitches in the muscle, and none appear to be inhibitory. No GABA-immunoreactive axons could be found in the mandibular nerve.

Action Potentials↗
PubMed1995

Long-term potentiation of C-fiber-evoked potentials in the rat spinal dorsal horn is prevented by spinal N-methyl-D-aspartic acid receptor blockage.

Long-term potentiation (LTP) of synaptic potentials is a fundamental mechanism of memory formation in the hippocampus. Here, we have characterized long-term changes of field potentials which were evoked in the lumbar spinal dorsal horn by supramaximal electrical stimulation of the sciatic nerve in urethane anesthetized rats. The field potentials had high thresholds (> or = 7 V), long latencies (90-130 ms, corresponding to conduction velocities between 1.2 and 0.85 m/s) and were not affected by spinalization (at C5-C6) or muscle relaxation (with pancuronium), i.e. the potentials were probably evoked by afferent C-fibers. Tetanic electrical stimulation (0.5 ms pulses, 30-40 V, 100 Hz, given in 4 trains of 1 s duration at 10 s intervals) of sciatic nerve induced in all 9 rats tested a LTP of amplitude of the C-fiber-evoked potential throughout recording periods which lasted between 4 and 9 h. Mean potentiation ranged from +71% to +174%. Superfusion of spinal cord with N-methyl-D-aspartic acid (NMDA) receptor antagonist D-(-)-4-(3-phosphonopropyl)piperazine-2-carboxylic (500 nM), which has little effect on the amplitude of C-fiber-evoked potentials, completely blocked LTP induced by tetanic stimulation in all five rats tested. Superfusion of spinal cord with NMDA (1 microM, 10 microM or 50 microM) induced LTP in only 2 out of 8 rats. This is the first report showing that LTP of C-fiber-evoked field potentials in the spinal dorsal horn in vivo may last for more than 8 h. This LTP in the spinal dorsal horn may underlie plastic changes of spinal nociception.

Animals↗
PubMed1997

Cellular mechanism for the temperature sensitive spatial orientation in Clione.

The swimming mollusk Clione is normally oriented vertically. As water is warmed, this orientation is lost or reversed. CPB3 interneurons, which transmit signals from the statocyst receptors (SRCs) to the tail motoneurons and play a key role in space orientation, were strongly depolarized upon warming. Normally, intracellular stimulation of the rostro-dorsal SRC (DSRC) excited CPB3b. Upon warming the excitation gradually decreased and in some cases was even replaced by inhibition. The reversal potential for the synaptic potentials (PSP) produced in CPB3b by DSRC stimulation is depolarized relative to the normal membrane potential at lower temperature. Warming causes depolarization of the membrane potential such that the PSP reversal potential is approached and even passed, with attenuant effects on PSP amplitude and polarity. This effect provides a mechanism for the temperature sensitive changes in the orientation of Clione.

Animals↗
PubMed1976

The formation of synapses between chick embryo skeletal muscle and ciliary ganglia grown in vitro.

1. Chick embryo ciliary ganglia (explanted) and skeletal muscle (dissociated) were grown together in vitro for up to 3 weeks. Nerve processes sprouted from the ganglia and contacted neighbouring myotubes and striated muscle fibres. 2. Spontaneous action potentials and subthreshold e.p.p.s. were recorded from muscle fibres with intracellular micropipettes. Similar potentials could be evoked by electrical stimulation of the ganglion. The pharmacological effects of curare and tetrodotoxin were identical to those observed at adult vertebrate neuromuscular junctions. 3. The amplitude, but not the frequency, of the spontaneous potentials was affected by changing the muscle fibre membrane potential. The reversal potential of evoked synaptic potentials occurred at a membrane potential of about 0 mV.

Action Potentials↗
PubMed1983

Long-term potentiation in commissural and Schaffer projections to hippocampal CA1 cells: an in vivo study in the rat.

Rats were given unilateral injections of kainic acid into the lateral ventricle to produce a unilateral lesion of CA3 pyramidal cells in the hippocampus. This procedure allowed the commissural and associational Schaffer projections of the surviving contralateral CA3 field to be studied separately for their ability to sustain long-term potentiation (l.t.p.) of synaptic efficacy. Both Schaffer and commissural projections showed l.t.p. of the population excitatory post-synaptic potential (e.p.s.p.) and the population spike. No significant difference was seen in the degree or duration of l.t.p. sustained by the two projections.

Afferent Pathways↗
PubMed2004

Recycling endosomes supply AMPA receptors for LTP.

Long-term potentiation (LTP) of synaptic strength, the most established cellular model of information storage in the brain, is expressed by an increase in the number of postsynaptic AMPA receptors. However, the source of AMPA receptors mobilized during LTP is unknown. We report that AMPA receptors are transported from recycling endosomes to the plasma membrane for LTP. Stimuli that triggered LTP promoted not only AMPA receptor insertion but also generalized recycling of cargo and membrane from endocytic compartments. Thus, recycling endosomes supply AMPA receptors for LTP and provide a mechanistic link between synaptic potentiation and membrane remodeling during synapse modification.

Animals↗
PubMed2004

Spike synchronization in the cortex/basal-ganglia networks of Parkinsonian primates reflects global dynamics of the local field potentials.

Cortical local field potentials (LFPs) reflect synaptic potentials and accordingly correlate with neuronal discharge. Because LFPs are coherent across substantial cortical areas, we hypothesized that cortical spike correlations could be predicted from them. Because LFPs recorded in the basal ganglia (BG) are also correlated with neuronal discharge and are clinically accessible in Parkinson's disease patients, we were interested in testing this hypothesis in the BG, as well. We recorded LFPs and unit discharge from multiple electrodes, which were placed in primary motor cortex or in the basal ganglia (striatum and pallidum) of two monkeys before and after rendering them parkinsonian with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. We used the method of partial spectra to construct LFP predictors of the spike cross-correlation functions (CCFs). The predicted CCF is an estimate of the correlation between two neurons under the assumption that their association is explained solely by the association of each with the LFP recorded on a third electrode. In the normal condition, the predictors account for cortical rate covariations but not for the association among the tonically active neurons of the striatum. In the parkinsonian condition, with the appearance of 10 Hz oscillations throughout the cortex-basal ganglia networks, the LFP predictors account remarkably better for the CCFs in both the cortex and the basal ganglia. We propose that, in the parkinsonian condition, the cortex-basal ganglia networks are more tightly related to global modes of brain dynamics that are echoed in the LFP.

Action Potentials↗
PubMed1993

IP3 receptor-mediated spatial and temporal Ca2+ signaling of the cell.

It is now revealed that "intracellular Ca2+ excitation" exists for the generation of spatial and temporal Ca2+ signals based on Ca2+ release from stores. It could be understood in analogy with electrical excitation in the cell surface, the plasma membrane. A local Ca2+ response is generated by the second messenger IP3 following agonist/receptor binding and PI turnover, corresponsing to the receptor potential or excitatory synaptic potential in neurons. The local Ca2+ response triggers a regenerative "intracellular Ca2+ spike" corresponding to the action potential. The regenerative process is the inherent property of the IP3R/Ca2+ release channel which is under positive and negative feedback controls by cytosolic and luminal Ca2+, like activation and inactivation of the voltage-gated Na+ channel. An intracellular Ca2+ spike can be induced artificially by local application of Ca2+, like induction of the action potential by a depolarizing pulse. The Ca2+ spike propagates as a spatial Ca2+ signal throughout the cell, as the action potential does. The excitation is followed by a refractory period. Repeated Ca2+ spikes are generated, depending on the magnitude of stimulus. Interval between Ca2+ spikes depends on the readiness of Ca2+ stores in terms of the sensitivity of the IP3R and extent of Ca2+ accumulation. The cycle of Ca2+ mobilization includes extracellular medium. The intracellular Ca2+ signals are thus frequency-encoded. The temporal pattern of transient Ca2+ pulses may be favorable for accomplishing cellular functions without the side effect of cell toxicity.

Animals↗